To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
30 Kasım 2012 Cuma
29 Kasım 2012 Perşembe
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Does coat color predict cat personality?
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Delgado MM, Munera JD and Reevy GM. Human perceptions of coat color as an indicator of domestic cat personality. Anthrozoos. 2012; 25: 427-40.
Did you ever wonder what was behind the stereotype of black cats being evil or unlucky now that we have passed the Halloween season? Or if there was a real reason why black cats might be adopted less from shelters than other cats? A recent study by researchers at California State University and the New College of Florida explored where these biases originate by using an Internet-based study of about 200 individuals. The survey used a 7-point scale to assign 10 terms (active, aloof, bold, calm, friendly, intolerant, shy, stubborn, tolerant, and trainable) to five different colors of cats (orange, tri-color, white, black, and bi-color). Significant differences were found in that people tended to assign “friendliness” to orange cats, “intolerance” to tricolored cats, and “aloofness” to white and tricolored cats. “Stubbornness” was not assigned in any color of cats.
White cats were considered less bold and active and more shy and calm than other colors. Orange cats were also considered more trainable than white cats. There was a glimmer of hope from the survey in that respondents placed more importance on personality than color when they selected a cat companion, though some evidence shows they believe the two qualities are linked. The study’s information will be beneficial for shelters and those in cat rescue to help promote adoption of different color cats, how to educate potential adopters, and how to avoid relinquishment of some cats due to coat color bias. [VT]
See also: McConnell AR, Brown CM, Shoda TM, Stayton LE and Martin CE. Friends with benefits: on the positive consequences of pet ownership. J Pers Soc Psychol. 2011; 101: 1239-52.
Related blog articles:
How the tabby cat got its stripes (October 2012)
More on cat health:
Winn Feline Foundation Library
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Did you ever wonder what was behind the stereotype of black cats being evil or unlucky now that we have passed the Halloween season? Or if there was a real reason why black cats might be adopted less from shelters than other cats? A recent study by researchers at California State University and the New College of Florida explored where these biases originate by using an Internet-based study of about 200 individuals. The survey used a 7-point scale to assign 10 terms (active, aloof, bold, calm, friendly, intolerant, shy, stubborn, tolerant, and trainable) to five different colors of cats (orange, tri-color, white, black, and bi-color). Significant differences were found in that people tended to assign “friendliness” to orange cats, “intolerance” to tricolored cats, and “aloofness” to white and tricolored cats. “Stubbornness” was not assigned in any color of cats.
White cats were considered less bold and active and more shy and calm than other colors. Orange cats were also considered more trainable than white cats. There was a glimmer of hope from the survey in that respondents placed more importance on personality than color when they selected a cat companion, though some evidence shows they believe the two qualities are linked. The study’s information will be beneficial for shelters and those in cat rescue to help promote adoption of different color cats, how to educate potential adopters, and how to avoid relinquishment of some cats due to coat color bias. [VT]
See also: McConnell AR, Brown CM, Shoda TM, Stayton LE and Martin CE. Friends with benefits: on the positive consequences of pet ownership. J Pers Soc Psychol. 2011; 101: 1239-52.
Related blog articles:
How the tabby cat got its stripes (October 2012)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
28 Kasım 2012 Çarşamba
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
27 Kasım 2012 Salı
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
26 Kasım 2012 Pazartesi
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
FIV in African lions
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Maas M, Keet DF, Rutten VP, Heesterbeek JA and Nielen M. Assessing the impact of feline immunodeficiency virus and bovine tuberculosis co-infection in African lions. Proceedings Biological sciences / The Royal Society. 2012; 279: 4206-14.
South Africa has about 2,700 free-ranging lions, living mostly around Kruger National Park (KNP). Bovine tuberculosis (BTB), caused by Mycobacterium bovis, is a disease that was introduced relatively recently into the KNP lion population, probably through domestic cattle brought by European settlers at the end of the 18th century. About 25 lions die of BTB every year in KNP.
Feline immunodeficiency virus (FIV) infects domestic cats and at least 20 other species of non-domestic felids around the world. FIV subtype Ple is thought to have been endemic in lions for a much longer time than BTB and infection is common. There is concern that these infections, especially when they occur together, may increase disease and affect lion conservation programs. These researchers collected data from lions in KNP from 1993-2008. BTB was more common in lions in the south of KNP than the north, but infection rate increased over time in the north. A large percentage (31%) of lions were infected with both pathogens. Both infections caused changes in blood test results, with FIV having a greater impact than BTB. However, it did not appear that these co-infections were synergistic (i.e., making disease worse), unlike the situation in humans infected with HIV and M. tuberculosis. This may be due to a different pathogenesis of FIV in African lions than HIV in humans. [MK]
See also: Troyer JL, Roelke ME, Jespersen JM, et al. FIV diversity: FIV Ple subtype composition may influence disease outcome in African lions. Vet Immunol Immunopathol. 2011; 143: 338-46. [Free, full text article]
Related blog articles:
Feline immunodeficiency virus in African lions: October 2009
FeLV and FIV affect blood values in cats: October 2009
Risk factors for FIV infection: July 2009
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
South Africa has about 2,700 free-ranging lions, living mostly around Kruger National Park (KNP). Bovine tuberculosis (BTB), caused by Mycobacterium bovis, is a disease that was introduced relatively recently into the KNP lion population, probably through domestic cattle brought by European settlers at the end of the 18th century. About 25 lions die of BTB every year in KNP.
Feline immunodeficiency virus (FIV) infects domestic cats and at least 20 other species of non-domestic felids around the world. FIV subtype Ple is thought to have been endemic in lions for a much longer time than BTB and infection is common. There is concern that these infections, especially when they occur together, may increase disease and affect lion conservation programs. These researchers collected data from lions in KNP from 1993-2008. BTB was more common in lions in the south of KNP than the north, but infection rate increased over time in the north. A large percentage (31%) of lions were infected with both pathogens. Both infections caused changes in blood test results, with FIV having a greater impact than BTB. However, it did not appear that these co-infections were synergistic (i.e., making disease worse), unlike the situation in humans infected with HIV and M. tuberculosis. This may be due to a different pathogenesis of FIV in African lions than HIV in humans. [MK]
See also: Troyer JL, Roelke ME, Jespersen JM, et al. FIV diversity: FIV Ple subtype composition may influence disease outcome in African lions. Vet Immunol Immunopathol. 2011; 143: 338-46. [Free, full text article]
Related blog articles:
Feline immunodeficiency virus in African lions: October 2009
FeLV and FIV affect blood values in cats: October 2009
Risk factors for FIV infection: July 2009
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
25 Kasım 2012 Pazar
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
24 Kasım 2012 Cumartesi
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
23 Kasım 2012 Cuma
Treatment of feline colonic adenocarcinoma
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Arteaga TA, McKnight J and Bergman PJ. A review of 18 cases of feline colonic adenocarcinoma treated with subtotal colectomies and adjuvant carboplatin. J Am Anim Hosp Assoc. 2012; 48: 399-404.
Adenocarcinoma is the second most common gastrointestinal tumor in cats and the most common tumor found in the colon. Colonic adenocarcinoma is both locally invasive and frequently has advanced metastasis at the time of presentation. Aggressive local surgery (subtotal colectomy) improves survival time in cats, but patients eventually succumb to metastasis, warranting adjuvant treatment with chemotherapy. Carboplatin is an alkylating platinum-based chemotherapeutic agent and has been shown to have efficacy in humans and dogs with carcinomas. Limited previous studies have shown mild to moderate efficacy and safety of carboplatin in cats with carcinomas, meriting its investigation as an adjuvant therapy for colonic adenocarcinomas.
This retrospective study evaluated signalment, diagnostic findings, disease-free interval, survival time, chemotherapeutic toxicoses, and prognostic factors for 18 cats with colonic adenocarcinoma treated with subtotal colectomy and monthly carboplatin. Interestingly, cats initially presenting with weight loss had a longer median disease-free interval (290 days versus 75 days), suggesting that a more chronic disease course occurs when weight loss is present. Four cats without weight loss had distant metastasis and a more acute presentation. Median survival time for all cats was 269 days, with cats without distant metastasis surviving 340 days and cats with distant metastasis surviving 200 days. For comparison, in a previous study, cats treated with subtotal colectomy alone lived only 56 days. Carboplatin toxicities reported included low-grade neutropenia, thrombocytopenia, and gastrointestinal toxicity, none of which required reduction or delay in treatment. One cat developed azotemia and carboplatin treatment was stopped after the fifth monthly dose. In conclusion, cats with colonic adenocarcinoma commonly present with colonic obstruction and usually remain patent after subtotal colectomy, but in the end, they are often euthanized due to metastasis, warranting early adjuvant chemotherapy. In this study, carboplatin was shown to have minimal toxicity and to be a viable adjunct for treating this disease. [GO]
See also: Green ML, Smith JD and Kass PH. Surgical versus non-surgical treatment of feline small intestinal adenocarcinoma and the influence of metastasis on long-term survival in 18 cats (2000-2007). Can Vet J. 2011; 52: 1101-5. [Free, full text article]
Related blog articles:
Feline intestinal cancer (March 2011)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
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Adenocarcinoma is the second most common gastrointestinal tumor in cats and the most common tumor found in the colon. Colonic adenocarcinoma is both locally invasive and frequently has advanced metastasis at the time of presentation. Aggressive local surgery (subtotal colectomy) improves survival time in cats, but patients eventually succumb to metastasis, warranting adjuvant treatment with chemotherapy. Carboplatin is an alkylating platinum-based chemotherapeutic agent and has been shown to have efficacy in humans and dogs with carcinomas. Limited previous studies have shown mild to moderate efficacy and safety of carboplatin in cats with carcinomas, meriting its investigation as an adjuvant therapy for colonic adenocarcinomas.
This retrospective study evaluated signalment, diagnostic findings, disease-free interval, survival time, chemotherapeutic toxicoses, and prognostic factors for 18 cats with colonic adenocarcinoma treated with subtotal colectomy and monthly carboplatin. Interestingly, cats initially presenting with weight loss had a longer median disease-free interval (290 days versus 75 days), suggesting that a more chronic disease course occurs when weight loss is present. Four cats without weight loss had distant metastasis and a more acute presentation. Median survival time for all cats was 269 days, with cats without distant metastasis surviving 340 days and cats with distant metastasis surviving 200 days. For comparison, in a previous study, cats treated with subtotal colectomy alone lived only 56 days. Carboplatin toxicities reported included low-grade neutropenia, thrombocytopenia, and gastrointestinal toxicity, none of which required reduction or delay in treatment. One cat developed azotemia and carboplatin treatment was stopped after the fifth monthly dose. In conclusion, cats with colonic adenocarcinoma commonly present with colonic obstruction and usually remain patent after subtotal colectomy, but in the end, they are often euthanized due to metastasis, warranting early adjuvant chemotherapy. In this study, carboplatin was shown to have minimal toxicity and to be a viable adjunct for treating this disease. [GO]
See also: Green ML, Smith JD and Kass PH. Surgical versus non-surgical treatment of feline small intestinal adenocarcinoma and the influence of metastasis on long-term survival in 18 cats (2000-2007). Can Vet J. 2011; 52: 1101-5. [Free, full text article]
Related blog articles:
Feline intestinal cancer (March 2011)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
22 Kasım 2012 Perşembe
Let's immune system help
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Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
21 Kasım 2012 Çarşamba
Let's immune system help
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Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
20 Kasım 2012 Salı
Let's immune system help
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Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
19 Kasım 2012 Pazartesi
Let's immune system help
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Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Efficacy of intranasal vaccination in cats
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Bradley A, Kinyon J, Frana T, Bolte D, Hyatt DR and Lappin MR. Efficacy of intranasal administration of a modified live feline herpesvirus 1 and feline calicivirus vaccine against disease caused by Bordetella bronchiseptica after experimental challenge. J Vet Intern Med. 2012; 26: 1121-5.
Upper respiratory tract infections (URTI) are common problems affecting cats in shelters, boarding facilities, breeding catteries, and pet homes. The most common causes of URTI include feline herpesvirus 1 (FHV), feline calicivirus (FCV), Bordetella bronchiseptica, Chlamydophila felis, Mycoplasma spp, and some bacteria. However, vaccines are only available for FHV, FCV, B. bronchiseptica, and C. felis. No single product is available to provide protection against all 4 agents in one vaccine.
Most feline vaccines are formulated for parenteral use, but there are 2 products on the market in the United States designed for intranasal administration. Intranasal administration of vaccines stimulates a nonspecific immune response in addition to the specific immune response against the agent in the vaccine. These investigators examined the effect of intranasal vaccination against FHV and FCV on disease caused by B. bronchiseptica. Two groups of 10 cats each were either inoculated intranasally with the vaccine or left unvaccinated. They were then exposed to B. bronchiseptica seven days later. Vaccinated cats were found to be less likely to be clinically ill than unvaccinated cats. Thus, intranasal vaccination with FHV and FCV decreased disease caused by a different pathogen due to its stimulation of nonspecific immunity. [MK]
See also: Egberink H, Addie D, Belak S, et al. Bordetella bronchiseptica infection in cats ABCD guidelines on prevention and management. J Feline Med Surg. 2009; 11: 610-4.
Free, full text article updated 2012
Related blog articles:
Treatment of feline upper respiratory tract disease (August 2012)
Upper respiratory tract disease in shelters (November 2009)
Understanding chronic respiratory disease in cats (August 2009)
More on cat health:
Winn Feline Foundation Library
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Upper respiratory tract infections (URTI) are common problems affecting cats in shelters, boarding facilities, breeding catteries, and pet homes. The most common causes of URTI include feline herpesvirus 1 (FHV), feline calicivirus (FCV), Bordetella bronchiseptica, Chlamydophila felis, Mycoplasma spp, and some bacteria. However, vaccines are only available for FHV, FCV, B. bronchiseptica, and C. felis. No single product is available to provide protection against all 4 agents in one vaccine.
Most feline vaccines are formulated for parenteral use, but there are 2 products on the market in the United States designed for intranasal administration. Intranasal administration of vaccines stimulates a nonspecific immune response in addition to the specific immune response against the agent in the vaccine. These investigators examined the effect of intranasal vaccination against FHV and FCV on disease caused by B. bronchiseptica. Two groups of 10 cats each were either inoculated intranasally with the vaccine or left unvaccinated. They were then exposed to B. bronchiseptica seven days later. Vaccinated cats were found to be less likely to be clinically ill than unvaccinated cats. Thus, intranasal vaccination with FHV and FCV decreased disease caused by a different pathogen due to its stimulation of nonspecific immunity. [MK]
See also: Egberink H, Addie D, Belak S, et al. Bordetella bronchiseptica infection in cats ABCD guidelines on prevention and management. J Feline Med Surg. 2009; 11: 610-4.
Free, full text article updated 2012
Related blog articles:
Treatment of feline upper respiratory tract disease (August 2012)
Upper respiratory tract disease in shelters (November 2009)
Understanding chronic respiratory disease in cats (August 2009)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
18 Kasım 2012 Pazar
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
17 Kasım 2012 Cumartesi
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
16 Kasım 2012 Cuma
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
15 Kasım 2012 Perşembe
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Developing new therapies for feline mammary cancer
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Figueira AC, Teodosio AS, Carvalheira J, Lacerda M, de Matos A and Gartner F. P-cadherin expression in feline mammary tissues. Veterinary Medicine International. 2012; 2012. [Free, full text article}
Feline mammary gland tumors are the third most common neoplasia in the domestic cat after skin and lymphohematopoietic tumors, accounting for 17% of all neoplasms in female cats (but rare in male cats). Mammary epithelial tumors are the most common type of feline mammary tumor, with adenocarcinomas (i.e., tubular, papillary, or solid) predominating. Tumors occur at a mean age between 10 to 12 years with Siamese, domestic short-haired, and tri-colored cats having an increased risk. Unfortunately, most cats have advanced disease when first presented to veterinarians, averaging 5 months after the neoplasia is first noticed. Treatment of choice is radical mastectomy of all glands on the affected side or bilateral mastectomy if possible, because of the high local recurrence rate, high rate of metastasis, and the frequent multicentric origin of feline mammary gland tumors. Often surgery for the opposite side is staged 2-4 weeks later. Also, all regional lymph nodes should be palpated and removed if enlarged. Ovariohysterectomy at an early age (< 6 months old) has a significant sparing effect. Significant factors affecting survival include the size, extent of surgery, and histologic grade of the tumor. The overall average time from detection of tumor to death is about 1 year with surgery alone. Due to the high metastatic potential of mammary carcinoma, adjuvant chemotherapy may improve survival times, but additional studies are needed.
Cadherins are cellular adhesion proteins that play an important role in the formation and maintenance of normal tissue architecture. Placental cadherin (P-cadherin) is a classical cadherin expressed by myoepithelial cells of the mammary gland. Changes in P-cadherin expression in mammary tissue have been implicated in human mammary carcinogenesis. Feline mammary tumors have similar histological and clinical course as human breast cancer; therefore, similar changes in aberrant P-cadherin expression are expected in cats. The present study included histological examination and P-cadherin immunolabelling chemistry of mammary tissue from cats with normal (n=4), hyperplastic (n=12), benign (n=6), and various malignancies (n=39). P-cadherin was aberrantly expressed only in mammary epithelial cells in malignant tumors as similarly observed in human breast cancer. Degree of expression was also positively correlated with histological grade.
Abnormal expression of P-cadherin may provide a promising antibody therapeutic target for humans and cats with mammary neoplasia, in particular in cases with metastatic disease. Disease conditions similar in humans and cats, such as mammary neoplasia, provide an excellent example of the “one world, one health, one medicine” paradigm. [GO]
See also: Hughes K and Dobson JM. Prognostic histopathological and molecular markers in feline mammary neoplasia. Vet J. 2012; 194: 19-26.
Related blog articles:
Treatment of feline mammary cancer with combination therapy (Feb. 2010)
Treatment of feline mammary cancer using surgery and chemotherapy (May 2009)
More on cat health:
Winn Feline Foundation Library
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Feline mammary gland tumors are the third most common neoplasia in the domestic cat after skin and lymphohematopoietic tumors, accounting for 17% of all neoplasms in female cats (but rare in male cats). Mammary epithelial tumors are the most common type of feline mammary tumor, with adenocarcinomas (i.e., tubular, papillary, or solid) predominating. Tumors occur at a mean age between 10 to 12 years with Siamese, domestic short-haired, and tri-colored cats having an increased risk. Unfortunately, most cats have advanced disease when first presented to veterinarians, averaging 5 months after the neoplasia is first noticed. Treatment of choice is radical mastectomy of all glands on the affected side or bilateral mastectomy if possible, because of the high local recurrence rate, high rate of metastasis, and the frequent multicentric origin of feline mammary gland tumors. Often surgery for the opposite side is staged 2-4 weeks later. Also, all regional lymph nodes should be palpated and removed if enlarged. Ovariohysterectomy at an early age (< 6 months old) has a significant sparing effect. Significant factors affecting survival include the size, extent of surgery, and histologic grade of the tumor. The overall average time from detection of tumor to death is about 1 year with surgery alone. Due to the high metastatic potential of mammary carcinoma, adjuvant chemotherapy may improve survival times, but additional studies are needed.
Cadherins are cellular adhesion proteins that play an important role in the formation and maintenance of normal tissue architecture. Placental cadherin (P-cadherin) is a classical cadherin expressed by myoepithelial cells of the mammary gland. Changes in P-cadherin expression in mammary tissue have been implicated in human mammary carcinogenesis. Feline mammary tumors have similar histological and clinical course as human breast cancer; therefore, similar changes in aberrant P-cadherin expression are expected in cats. The present study included histological examination and P-cadherin immunolabelling chemistry of mammary tissue from cats with normal (n=4), hyperplastic (n=12), benign (n=6), and various malignancies (n=39). P-cadherin was aberrantly expressed only in mammary epithelial cells in malignant tumors as similarly observed in human breast cancer. Degree of expression was also positively correlated with histological grade.Abnormal expression of P-cadherin may provide a promising antibody therapeutic target for humans and cats with mammary neoplasia, in particular in cases with metastatic disease. Disease conditions similar in humans and cats, such as mammary neoplasia, provide an excellent example of the “one world, one health, one medicine” paradigm. [GO]
See also: Hughes K and Dobson JM. Prognostic histopathological and molecular markers in feline mammary neoplasia. Vet J. 2012; 194: 19-26.
Related blog articles:
Treatment of feline mammary cancer with combination therapy (Feb. 2010)
Treatment of feline mammary cancer using surgery and chemotherapy (May 2009)
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14 Kasım 2012 Çarşamba
End of Year Reminder: Take Advantage of your Dental Insurance Benefits!
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Just a reminder to everyone with dental insurance benefits that renew in January:
Take advantage your benefits by scheduling your hygiene or restorative appointments before the year is up to preserve the full amounts of your insurance for the following year. Statements for this year's dental expenditures for tax purposes will be ready anytime after January 1st, just phone Jodie with your request.
Hans Skariah, B.Sc., DMD
Promenade Court Dental Health Group in Mississauga
2233 Hurontario St., Mississauga, ON, Canada
(1/2 km north of the QEW in the Dome Building)
(905) 273-7100
Take advantage your benefits by scheduling your hygiene or restorative appointments before the year is up to preserve the full amounts of your insurance for the following year. Statements for this year's dental expenditures for tax purposes will be ready anytime after January 1st, just phone Jodie with your request.
Hans Skariah, B.Sc., DMD
Promenade Court Dental Health Group in Mississauga
2233 Hurontario St., Mississauga, ON, Canada
(1/2 km north of the QEW in the Dome Building)
(905) 273-7100
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
13 Kasım 2012 Salı
Let's immune system help
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Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
12 Kasım 2012 Pazartesi
Inherited hemolytic anemia in cats
To contact us Click HERE
Grahn R, Grahn J, Penedo M, Helps C and Lyons L. Erythrocyte pyruvate kinase deficiency mutation identified in multiple breeds of domestic cats. BMC Vet Res. 2012; 8: 207. [Free, full text article]
In the Abyssinian and Somali breeds as well as random bred domestic shorthair cats there is a form of inherited hemolytic anemia caused by alterations in the enzyme erythrocyte pyruvate kinase. This enzyme is essential for normal function of red blood cells (erythrocytes). Mutations in PKLR, the gene encoding regulatory glycolytic enzyme pyruvate kinase (PK), result in the disease. The first documented case of feline PK deficiency was in an Abyssinian cat. Subsequent reports demonstrated that Somalis, a longhaired variety of the Abyssinian, as well as random bred domestic shorthairs, may also suffer from PK deficiency. The disturbance of PK results in decreased erythrocyte life span resulting in anemia. The anemia exhibits as a chronic, intermittent, hemolytic anemia. The most common clinical signs are lethargy, diarrhea, pale mucous membranes, poor appetite, poor coat quality, weight loss, icterus, and sporadic splenomegaly.
In looking at an affected group of 25 cats, clinical signs were first noted as early as 6 months and as late as 5 years of age. PK deficiency has an autosomal recessive inheritance with variability of onset and severity of clinical signs. In this study, sequence analysis of PKLR revealed an intron 5 single nucleotide polymorphism (SNP) at position 304 consistent with the disease phenotype in Abyssinian and Somali cats. The disease-associated SNP presence and frequency was determined by analysis in 14,179 cats representing 40 breeds or populations. Based on the study’s findings, the authors recommend PK testing for several breeds including the Bengal, Egyptian Mau, La Perm, Maine Coon, Norwegian Forest Cat, Savannah, Siberian, and Singapura, in addition to Abyssinian and Somali. Breeds known to have been derived from Abyssinian crosses such as the Ocicat, and new breeds developed with out-crossing programs using affected breeds should be tested as well. In time, expanded testing methods along with removal of affected individuals from the breeding population may enable the selective elimination of the PK deficiency-associated SNP in domestic cat populations. [VT]
See also: Barrs V, Giger U, Wilson B, et al. Erythrocytic pyruvate kinase deficiency and AB blood types in Australian Abyssinian and Somali cats. Aust Vet J. 2009; 87: 39-44. [Free, full text article]
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In the Abyssinian and Somali breeds as well as random bred domestic shorthair cats there is a form of inherited hemolytic anemia caused by alterations in the enzyme erythrocyte pyruvate kinase. This enzyme is essential for normal function of red blood cells (erythrocytes). Mutations in PKLR, the gene encoding regulatory glycolytic enzyme pyruvate kinase (PK), result in the disease. The first documented case of feline PK deficiency was in an Abyssinian cat. Subsequent reports demonstrated that Somalis, a longhaired variety of the Abyssinian, as well as random bred domestic shorthairs, may also suffer from PK deficiency. The disturbance of PK results in decreased erythrocyte life span resulting in anemia. The anemia exhibits as a chronic, intermittent, hemolytic anemia. The most common clinical signs are lethargy, diarrhea, pale mucous membranes, poor appetite, poor coat quality, weight loss, icterus, and sporadic splenomegaly.
In looking at an affected group of 25 cats, clinical signs were first noted as early as 6 months and as late as 5 years of age. PK deficiency has an autosomal recessive inheritance with variability of onset and severity of clinical signs. In this study, sequence analysis of PKLR revealed an intron 5 single nucleotide polymorphism (SNP) at position 304 consistent with the disease phenotype in Abyssinian and Somali cats. The disease-associated SNP presence and frequency was determined by analysis in 14,179 cats representing 40 breeds or populations. Based on the study’s findings, the authors recommend PK testing for several breeds including the Bengal, Egyptian Mau, La Perm, Maine Coon, Norwegian Forest Cat, Savannah, Siberian, and Singapura, in addition to Abyssinian and Somali. Breeds known to have been derived from Abyssinian crosses such as the Ocicat, and new breeds developed with out-crossing programs using affected breeds should be tested as well. In time, expanded testing methods along with removal of affected individuals from the breeding population may enable the selective elimination of the PK deficiency-associated SNP in domestic cat populations. [VT]
See also: Barrs V, Giger U, Wilson B, et al. Erythrocytic pyruvate kinase deficiency and AB blood types in Australian Abyssinian and Somali cats. Aust Vet J. 2009; 87: 39-44. [Free, full text article]
More on cat health:
Winn Feline Foundation Library
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Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
11 Kasım 2012 Pazar
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
10 Kasım 2012 Cumartesi
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
9 Kasım 2012 Cuma
Heart disease in pedigreed cats
To contact us Click HERE
Trehiou-Sechi E, Tissier R, Gouni V, et al. Comparative echocardiographic and clinical features of hypertrophic cardiomyopathy in 5 breeds of cats: a retrospective analysis of 344 Cases (2001–2011). J Vet Intern Med. 2012; 26: 532-41.
A common form of heart disease in cats is hypertrophic cardiomyopathy (HCM) and it is associated with risk of sudden death. HCM has been shown to be inherited in some breeds though few studies have looked at comparisons of HCM phenotype and survival according to breed. The authors performed a retrospective study of 344 cats from 5 different breeds (Persian, Domestic Shorthair, Sphynx, Maine Coon, and Chartreux) having primary HCM diagnosed by conventional echocardiography. In this group, 266 cats were asymptomatic and 78 were symptomatic. Most of the symptomatic cats exhibited congestive heart failure, aortic thromboembolism, syncope, and weakness.
The age at the first cardiac event was significantly lower in Maine Coons (2.5 years) versus other breeds (7 years). In Sphynx, the age at the time of diagnosis was 3.5 years. Concerning sudden death solely, Maine Coon cats died younger than other breeds. No sudden deaths were reported in Chartreux and Persian cats in this study. Sudden death was observed in only 3 breeds—Maine Coon, Domestic Shorthair, and Sphynx. All cats surviving longer than 15 years of age were Domestic Shorthair, Persians, or Chartreux. From the results of this study, it appears that feline HCM is characterized by marked phenotypic variability with several breed-dependent features with regard to epidemiological characteristics, left ventricular geometric patterns, age at the time of diagnosis, and decompensation events. [VT]
See also: Silverman SJ, Stern JA and Meurs KM. Hypertrophic cardiomyopathy in the Sphynx cat: A retrospective evaluation of clinical presentation and heritable etiology. J Feline Med Surg. 2012; 14: 246-9.
For more information: Other blog articles on hypertrophic cardiomyopathy
More on cat health:
Winn Feline Foundation Library
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A common form of heart disease in cats is hypertrophic cardiomyopathy (HCM) and it is associated with risk of sudden death. HCM has been shown to be inherited in some breeds though few studies have looked at comparisons of HCM phenotype and survival according to breed. The authors performed a retrospective study of 344 cats from 5 different breeds (Persian, Domestic Shorthair, Sphynx, Maine Coon, and Chartreux) having primary HCM diagnosed by conventional echocardiography. In this group, 266 cats were asymptomatic and 78 were symptomatic. Most of the symptomatic cats exhibited congestive heart failure, aortic thromboembolism, syncope, and weakness.
The age at the first cardiac event was significantly lower in Maine Coons (2.5 years) versus other breeds (7 years). In Sphynx, the age at the time of diagnosis was 3.5 years. Concerning sudden death solely, Maine Coon cats died younger than other breeds. No sudden deaths were reported in Chartreux and Persian cats in this study. Sudden death was observed in only 3 breeds—Maine Coon, Domestic Shorthair, and Sphynx. All cats surviving longer than 15 years of age were Domestic Shorthair, Persians, or Chartreux. From the results of this study, it appears that feline HCM is characterized by marked phenotypic variability with several breed-dependent features with regard to epidemiological characteristics, left ventricular geometric patterns, age at the time of diagnosis, and decompensation events. [VT]
See also: Silverman SJ, Stern JA and Meurs KM. Hypertrophic cardiomyopathy in the Sphynx cat: A retrospective evaluation of clinical presentation and heritable etiology. J Feline Med Surg. 2012; 14: 246-9.
For more information: Other blog articles on hypertrophic cardiomyopathy
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
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Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
5 Kasım 2012 Pazartesi
Let's immune system help
To contact us Click HERE
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido,
Vinod P Balachandran, et al. Nature Medicine17 (2011)
I would like to hilight this paper to our readership, as many of your are involved in the design of clinical trials and selection of potential biomarkers. This report is one of a handful of high impact papers that report the coperative role that inflammatory infiltrate and non cell autonomous effectors play in modulating response to established agents. This study demonstrates an interesting immunological mechanism of Imatininb that contributes to the antitumor effect in a Gastrointestinal Stromal Tumor (GIST) mouse model. Inflammatory infiltrate is a known finding in GIST specimens (including intratumoral CD8+ Tcells, Treg cells and macrophages). Acording to the authors, Imatinib activates CD8+ T cells and induces Treg cells apoptosis within the tumor. Imatinib is therefore able to reduce the expression of 2,3-dioxygenase (Ido) of tumor cells. Ido enzyme is involved in the catayzation of immunosuppressive metabolites from tryptophan and therefore mediates downstream immunological response. Interestingly Imatininb resistant tumors, generally as a result of a second KIT mutation, restore the overexpression of IDO and combination of Imatinib with CTLA-4 blockade (a well established immunotherapeutic strategy) act synergistically. This insight provides some hints on something we have been suspecting for a long time. It is easy to predict consequences for rational design of combination therapies and strategies to overcome resistance in Imatinib resistant tumors.TweetShare
FIV and kidney disease
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Baxter KJ, Levy JK, Edinboro CH, Vaden SL and Tompkins MB. Renal disease in cats infected with feline immunodeficiency virus. J Vet Intern Med. 2012; 26: 238-43.
In people infected with human immunodeficiency virus (HIV), renal disease is the fourth most common cause of death. Feline immunodeficiency virus (FIV) causes similar clinical syndromes to HIV in humans (e.g., immune dysregulation, opportunistic infections, inflammatory diseases, and neoplasia). The seroprevalence of FIV in cats in North America is estimated to be 3.6-4.3%, with the highest prevalence found in adult male, sick, and free-roaming cats. The authors used a mixed retrospective/prospective cross-sectional study of client-owned cats (153 FIV-infected, 306 FIV-uninfected) and specific-pathogen-free (SPF) research colony cats (95 FIV-infected, 98 FIV-uninfected). The researchers hypothesized that cats infected with FIV are at increased risk of proteinuria, and that proteinuria is associated with advanced FIV infection and comorbidity factors contribute to the prevalence of renal disease.
Comparisons were made by evaluating blood urea nitrogen, serum creatinine, urine specific gravity, and urine protein-creatinine (UPC) ratio between infected and uninfected cats. Also CD4+ and CD8+ T lymphocytes were measured and the ratio was calculated. Renal azotemia was defined as a serum creatinine > 1.9 mg/dL with urine specific gravity < 1.035. Proteinuria was defined as a UPC ratio > 0.4 with an inactive urine sediment. The results indicated that the prevalence of proteinuria was higher in client-owned FIV-infected cats than in FIV-uninfected cats. Yet, there was no significant difference in the prevalence of azotemia. The authors believe that using their classification system, being considered “diseased” was not a risk factor for proteinuria in FIV-infected cats. The primary conclusion from the study was that client-owned cats with naturally acquired FIV infection were at increased risk of proteinuria, but not renal azotemia. The cause and pathogenesis of this proteinuria is uncertain. [VT]
See also: Poli A, Abramo F, Matteucci D, et al. Renal involvement in feline immunodeficiency virus infection: p24 antigen detection, virus isolation and PCR analysis. Vet Immunol Immunopathol. 1995; 46: 13-20.
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In people infected with human immunodeficiency virus (HIV), renal disease is the fourth most common cause of death. Feline immunodeficiency virus (FIV) causes similar clinical syndromes to HIV in humans (e.g., immune dysregulation, opportunistic infections, inflammatory diseases, and neoplasia). The seroprevalence of FIV in cats in North America is estimated to be 3.6-4.3%, with the highest prevalence found in adult male, sick, and free-roaming cats. The authors used a mixed retrospective/prospective cross-sectional study of client-owned cats (153 FIV-infected, 306 FIV-uninfected) and specific-pathogen-free (SPF) research colony cats (95 FIV-infected, 98 FIV-uninfected). The researchers hypothesized that cats infected with FIV are at increased risk of proteinuria, and that proteinuria is associated with advanced FIV infection and comorbidity factors contribute to the prevalence of renal disease.
Comparisons were made by evaluating blood urea nitrogen, serum creatinine, urine specific gravity, and urine protein-creatinine (UPC) ratio between infected and uninfected cats. Also CD4+ and CD8+ T lymphocytes were measured and the ratio was calculated. Renal azotemia was defined as a serum creatinine > 1.9 mg/dL with urine specific gravity < 1.035. Proteinuria was defined as a UPC ratio > 0.4 with an inactive urine sediment. The results indicated that the prevalence of proteinuria was higher in client-owned FIV-infected cats than in FIV-uninfected cats. Yet, there was no significant difference in the prevalence of azotemia. The authors believe that using their classification system, being considered “diseased” was not a risk factor for proteinuria in FIV-infected cats. The primary conclusion from the study was that client-owned cats with naturally acquired FIV infection were at increased risk of proteinuria, but not renal azotemia. The cause and pathogenesis of this proteinuria is uncertain. [VT]
See also: Poli A, Abramo F, Matteucci D, et al. Renal involvement in feline immunodeficiency virus infection: p24 antigen detection, virus isolation and PCR analysis. Vet Immunol Immunopathol. 1995; 46: 13-20.
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New antiviral treatments for cats
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Robert-Tissot C, Ruegger VL, Cattori V, et al. Stimulation with a class A CpG oligonucleotide enhances resistance to infection with feline viruses from five different families. Vet Res. 2012; 43: 60. [free, full text article]
Viral pathogens commonly infect domestic cats, in particular in multi-cat environments such as shelters and catteries, often leading to increased morbidity and mortality. A promising addition to our armamentarium against viral infection along with vaccinations is the manipulation of innate immunity. Oligonucleotides (ODN) containing unmethylated cytosine-phosphate-guanosine motifs of class A (CpG-A) are recognized as pathogen-associated molecular patterns due to high abundance in viral genome (as well as bacterial genome) and, thus, are highly potent synthetic inducers of innate antiviral mechanisms.
This study tested in vitro CpG-A ODN ability to enhance innate immune responses and prevent viral replication. CpG-A ODN was shown to stimulate feline peripheral blood mononuclear cells (PBMCs), enhancing their proliferation, and shifting their gene expression in an antiviral orientation. In vivo, CpG-A ODN also induced a systemic antiviral state with astonishing effects of potent induction of IFNα and IFNω, with mRNA expression of these genes increased by up to 12 000 and 35 000-fold respectively in PBMCs of cats.
With regard to this, a recombinant feline type I IFN marketed in both Japan (Intercat®) and Europe (Virbagen Omega®) has made its way into therapeutic protocols for FCV, FHV, FeLV and canine parvovirus infections and has demonstrated preventive capacities in a cattery developing an outbreak of FPV. However, when compared to direct initiation of antiviral mechanisms by a recombinant IFNα protein, administration of CpG-A ODN holds the advantage of inducing the production of all type I IFN and their subtypes, which have been shown to possess differential antiviral properties and kinetics. On the other hand, CpG-A ODN stimulated PBMCs in kittens tended to develop an immunologic environment with a Th2 orientation (antibody response) corroborating the immature IFN system and impaired activation of mononuclear cells in neonates. This particular observation opens new perspectives on possible explanations for the qualitative discrepancy between innate immune responses in newborns and adults.
Overall, treatment with CpG-A ODN enhanced resistance against feline viruses from five distinct viral families, namely Coronavirdae, Herpesviridae, Caliciviridae, Parvoviridae, and Retrovridae. The data highlights the prophylactic potential of CpG-A ODN in domestic cats as a stand-alone agent and against a large range of viral pathogens simultaneously. Cats may highly benefit from such a molecule when placed in environments with strong infectious pressure such as catteries, shelters or pet shows. [GO]
See also: Medzhitov R. Recognition of microorganisms and activation of the immune response. Nature. 2007; 449: 819-26.
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Viral pathogens commonly infect domestic cats, in particular in multi-cat environments such as shelters and catteries, often leading to increased morbidity and mortality. A promising addition to our armamentarium against viral infection along with vaccinations is the manipulation of innate immunity. Oligonucleotides (ODN) containing unmethylated cytosine-phosphate-guanosine motifs of class A (CpG-A) are recognized as pathogen-associated molecular patterns due to high abundance in viral genome (as well as bacterial genome) and, thus, are highly potent synthetic inducers of innate antiviral mechanisms.
This study tested in vitro CpG-A ODN ability to enhance innate immune responses and prevent viral replication. CpG-A ODN was shown to stimulate feline peripheral blood mononuclear cells (PBMCs), enhancing their proliferation, and shifting their gene expression in an antiviral orientation. In vivo, CpG-A ODN also induced a systemic antiviral state with astonishing effects of potent induction of IFNα and IFNω, with mRNA expression of these genes increased by up to 12 000 and 35 000-fold respectively in PBMCs of cats. With regard to this, a recombinant feline type I IFN marketed in both Japan (Intercat®) and Europe (Virbagen Omega®) has made its way into therapeutic protocols for FCV, FHV, FeLV and canine parvovirus infections and has demonstrated preventive capacities in a cattery developing an outbreak of FPV. However, when compared to direct initiation of antiviral mechanisms by a recombinant IFNα protein, administration of CpG-A ODN holds the advantage of inducing the production of all type I IFN and their subtypes, which have been shown to possess differential antiviral properties and kinetics. On the other hand, CpG-A ODN stimulated PBMCs in kittens tended to develop an immunologic environment with a Th2 orientation (antibody response) corroborating the immature IFN system and impaired activation of mononuclear cells in neonates. This particular observation opens new perspectives on possible explanations for the qualitative discrepancy between innate immune responses in newborns and adults.
Overall, treatment with CpG-A ODN enhanced resistance against feline viruses from five distinct viral families, namely Coronavirdae, Herpesviridae, Caliciviridae, Parvoviridae, and Retrovridae. The data highlights the prophylactic potential of CpG-A ODN in domestic cats as a stand-alone agent and against a large range of viral pathogens simultaneously. Cats may highly benefit from such a molecule when placed in environments with strong infectious pressure such as catteries, shelters or pet shows. [GO]
See also: Medzhitov R. Recognition of microorganisms and activation of the immune response. Nature. 2007; 449: 819-26.
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Dental Did You Know: Obesity and Dental Health
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Men and women with a BMI over 30 regardless of smoking or diabetes status had a greater risk of developing periodontal disease than those with a healthy body weight.
Source: Ward W and Fritz P, Obesity and Periodontal Health: What's the Link? Should I be Concerned? Oral Health, Oct 2012, Vol 102, No 10, pg 80-83.
Hans Skariah, B.Sc., DMD
Promenade Court Dental Health Group in Mississauga
2233 Hurontario St., Mississauga, ON, Canada
(1/2 km north of the QEW in the Dome Building)
(905) 273-7100
Source: Ward W and Fritz P, Obesity and Periodontal Health: What's the Link? Should I be Concerned? Oral Health, Oct 2012, Vol 102, No 10, pg 80-83.
Hans Skariah, B.Sc., DMD
Promenade Court Dental Health Group in Mississauga
2233 Hurontario St., Mississauga, ON, Canada
(1/2 km north of the QEW in the Dome Building)
(905) 273-7100
4 Kasım 2012 Pazar
Ragdoll cats and kidney disease
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Paepe D, Saunders JH, Bavegems V, et al. Screening of ragdoll cats for kidney -disease: a retrospective evaluation. J Small Anim Pract. 2012; 53: 572-7.
A very popular cat breed worldwide is the Ragdoll. Ragdoll breeders often advise clients to watch for future renal disease in their cats. Most of these questions center around potential chronic interstitial nephritis and polycystic kidney disease (PKD). There is minimal scientific evidence regarding risk of renal disease in this breed. The Veterinary Medical College at Ghent University in Belgium performed a retrospective evaluation of Ragdolls screened for renal disease over an 8-year period. The screening methods included abdominal ultrasonography, measurement of serum creatinine and urea concentrations, and genetic testing for the PKD-1 mutation. The study population was made up of 244 Ragdoll cats: 172 females and 72 males.
In this study, 8.6% of the screened cats showed ultrasonographic abnormalities that could be compatible with chronic kidney disease (CKD). The suspected CKD cats were significantly older and had significantly higher urea and creatinine concentrations compared to cats with normal ultrasound results. Ragdolls are one of the breeds that have been outcrossed with Persians, so Ragdoll cats could be at risk for PKD. The researchers found a PKD prevalence of less than 3% in the study cats, considerably lower than the 31-42% prevalence of PKD described in European studies of Persians and related cats. Only one PKD-positive and one suspected PKD-positive Ragdoll cat were noted in the last 7 years of the study. This could mean that PKD screening before breeding is effective at eradicating PKD in this breed. All genetically tested cats tested negative for PKD.
In conclusion, almost 10% of this healthy Ragdoll population had ultrasonographic findings compatible with CKD, and PKD occurs at a low prevalence in Ragdoll cats in Belgium and the Netherlands. [VT]
See also: Heiene R, Rumsby G, Ziener M, et al. Chronic kidney disease with three cases of oxalate-like nephrosis in Ragdoll cats. Journal of Feline Medicine & Surgery. 2009; 11: 474-80.
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A very popular cat breed worldwide is the Ragdoll. Ragdoll breeders often advise clients to watch for future renal disease in their cats. Most of these questions center around potential chronic interstitial nephritis and polycystic kidney disease (PKD). There is minimal scientific evidence regarding risk of renal disease in this breed. The Veterinary Medical College at Ghent University in Belgium performed a retrospective evaluation of Ragdolls screened for renal disease over an 8-year period. The screening methods included abdominal ultrasonography, measurement of serum creatinine and urea concentrations, and genetic testing for the PKD-1 mutation. The study population was made up of 244 Ragdoll cats: 172 females and 72 males.
In this study, 8.6% of the screened cats showed ultrasonographic abnormalities that could be compatible with chronic kidney disease (CKD). The suspected CKD cats were significantly older and had significantly higher urea and creatinine concentrations compared to cats with normal ultrasound results. Ragdolls are one of the breeds that have been outcrossed with Persians, so Ragdoll cats could be at risk for PKD. The researchers found a PKD prevalence of less than 3% in the study cats, considerably lower than the 31-42% prevalence of PKD described in European studies of Persians and related cats. Only one PKD-positive and one suspected PKD-positive Ragdoll cat were noted in the last 7 years of the study. This could mean that PKD screening before breeding is effective at eradicating PKD in this breed. All genetically tested cats tested negative for PKD.
In conclusion, almost 10% of this healthy Ragdoll population had ultrasonographic findings compatible with CKD, and PKD occurs at a low prevalence in Ragdoll cats in Belgium and the Netherlands. [VT]
See also: Heiene R, Rumsby G, Ziener M, et al. Chronic kidney disease with three cases of oxalate-like nephrosis in Ragdoll cats. Journal of Feline Medicine & Surgery. 2009; 11: 474-80.
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Understanding FIP virulence
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Chang HW, Egberink HF, Halpin R, Spiro DJ and Rottier PJ. Spike protein fusion peptide and feline coronavirus virulence. Emerg Infect Dis. 2012; 18: 1089-95. [free, full text article]
Coronaviruses are enveloped RNA viruses known for their potential to change their cellular tropism. Tropism refers to the specificity of a virus for a particular host tissue, determined in part by the interaction of viral surface structures with receptors present on the surface of unique host cell (e.g., endothelial cells, macrophages). Whether tropism switching leads to cross-species transmission as happened with severe acute respiratory syndrome (SARS-CoV) jumping from bats to humans or, as in the case of feline coronaviruses, switching leads from a relatively low virulence enteric virus (FECV) to a systemic pathogenetic form (FIPV), it is clear that this family of viruses is an important public health concern and feline pathogen. In the case of FECV, identifying the genetic mutation(s) leading to this tropism switching still remains a quandary for researchers, veterinarians, and cat owners alike.
The researchers in this study compared full genome sequenced data from 11 viruses in each pathotype and identified the most distinctive site(s) by further refining sequence variation between the two pathotypes around those site(s). Two putative sites that both code for regions in the fusion peptide domain of the spike protein were found to distinguish FECV from FIPV, accounting for > 95% of cases. The S protein functions in cell entry via receptor attachment (involving the N terminus) and membrane fusion (membrane-proximal domain). These researchers further speculate that these two mutations in addition to other mutations likely within the accessory 3c gene account for switching to the virulent FIPV form. [GO]
See also: Pedersen NC, Liu H, Scarlett J, et al. Feline infectious peritonitis: Role of the feline coronavirus 3c gene in intestinal tropism and pathogenicity based upon isolates from resident and adopted shelter cats. Virus Research. 2012; 165: 17-28.
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Coronaviruses are enveloped RNA viruses known for their potential to change their cellular tropism. Tropism refers to the specificity of a virus for a particular host tissue, determined in part by the interaction of viral surface structures with receptors present on the surface of unique host cell (e.g., endothelial cells, macrophages). Whether tropism switching leads to cross-species transmission as happened with severe acute respiratory syndrome (SARS-CoV) jumping from bats to humans or, as in the case of feline coronaviruses, switching leads from a relatively low virulence enteric virus (FECV) to a systemic pathogenetic form (FIPV), it is clear that this family of viruses is an important public health concern and feline pathogen. In the case of FECV, identifying the genetic mutation(s) leading to this tropism switching still remains a quandary for researchers, veterinarians, and cat owners alike.
The researchers in this study compared full genome sequenced data from 11 viruses in each pathotype and identified the most distinctive site(s) by further refining sequence variation between the two pathotypes around those site(s). Two putative sites that both code for regions in the fusion peptide domain of the spike protein were found to distinguish FECV from FIPV, accounting for > 95% of cases. The S protein functions in cell entry via receptor attachment (involving the N terminus) and membrane fusion (membrane-proximal domain). These researchers further speculate that these two mutations in addition to other mutations likely within the accessory 3c gene account for switching to the virulent FIPV form. [GO]
See also: Pedersen NC, Liu H, Scarlett J, et al. Feline infectious peritonitis: Role of the feline coronavirus 3c gene in intestinal tropism and pathogenicity based upon isolates from resident and adopted shelter cats. Virus Research. 2012; 165: 17-28.
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Public perception of feral cats
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Loyd KAT and Hernandez SM. Public perceptions of domestic cats and preferences for feral cat management in the southeastern United States. Anthrozoos. 2012; 25: 337-51.
Millions of feral cats exist in the United States and their management is the subject of debate. Strategies range from euthanasia of these cats to trap-neuter-release programs which have been implemented in many urban areas of the country. Awareness and understanding of public attitudes and preferences for control of these feral cat populations will aid in development of management strategies. These investigators used an anonymous internet survey of randomly selected residents of Georgia.
From the article: “Results indicate that more residents have positive experiences with feral cats than negative, cat owners have greater knowledge of cats than non-cat owners, and animal welfare or conservation organization membership has a significant effect on attitudes towards cats. A majority of survey respondents agreed that more effective feral cat management is needed yet did not approve of trap-neuter-release (TNR) legislation recently passed in Athens-Clarke County. ….residents’ attitudes were found to be more important than experiences or knowledge in supporting cat management legislation. Cat sanctuaries were found to be the most acceptable option to reduce feral cat populations (56%), followed by TNR (49%) and capturing and euthanizing cats (44%).” [MK]
See also: Peterson MN, Hartis B, Rodriguez S, Green M and Lepczyk CA. Opinions from the front lines of cat colony management conflict. PLoS ONE. 2012; 7: e44616. [free, full text article]
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Millions of feral cats exist in the United States and their management is the subject of debate. Strategies range from euthanasia of these cats to trap-neuter-release programs which have been implemented in many urban areas of the country. Awareness and understanding of public attitudes and preferences for control of these feral cat populations will aid in development of management strategies. These investigators used an anonymous internet survey of randomly selected residents of Georgia.
From the article: “Results indicate that more residents have positive experiences with feral cats than negative, cat owners have greater knowledge of cats than non-cat owners, and animal welfare or conservation organization membership has a significant effect on attitudes towards cats. A majority of survey respondents agreed that more effective feral cat management is needed yet did not approve of trap-neuter-release (TNR) legislation recently passed in Athens-Clarke County. ….residents’ attitudes were found to be more important than experiences or knowledge in supporting cat management legislation. Cat sanctuaries were found to be the most acceptable option to reduce feral cat populations (56%), followed by TNR (49%) and capturing and euthanizing cats (44%).” [MK]See also: Peterson MN, Hartis B, Rodriguez S, Green M and Lepczyk CA. Opinions from the front lines of cat colony management conflict. PLoS ONE. 2012; 7: e44616. [free, full text article]
For more information: other blog articles on feral cats
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