To contact us Click HERE
Added the Journal of the Canadian Dental Association's Clinical Question and Answer Blog to our blog reading list. It is a tremendous resource for clinicians and worth a view from patients if you are so inclined. We are also honoured to be recognized by them as a top dental blog. Thanks!! :)
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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
31 Aralık 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
27 Aralık 2012 Perşembe
Added a New Blog to my Reading List: JCDA's Question and Answer Blog
To contact us Click HERE
Added the Journal of the Canadian Dental Association's Clinical Question and Answer Blog to our blog reading list. It is a tremendous resource for clinicians and worth a view from patients if you are so inclined. We are also honoured to be recognized by them as a top dental blog. Thanks!! :)
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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
Evaluating natriuretic peptides in hyperthyroid cats
To contact us Click HERE
Menaut P, Connolly DJ, Volk A, et al. Circulating natriuretic peptide concentrations in hyperthyroid cats. J Small Anim Pract. 2012; 53: 673-8.
Natriuretic peptides (NPs) are neurohormones stored in heart muscle cells (atrial cardiomyocytes) and released in response to atrial stretch. They possess potent natriuretic and vasorelaxant properties. They have been shown to be chronically up-regulated in cats with underlying heart disease and have thus been used as a biomarker to detect occult heart disease and differentiate cardiac from non-cardiac dyspnea in emergency situations. In particular, the non-biologically active N-terminal fragment from atrial natriuretic peptide, (NT-proANP), and from brain natriuretic peptide, NT-proBNP, have commonly been studied due to their stability in plasma.
Hyperthyroidism is the most common endocrine disease of cats. In humans with hyperthyroidism, a number of studies have shown NP concentrations to be elevated. Therefore, since NP measurement is increasingly being used to assess feline cardiac disease, determining the influence of elevated thyroid function on NP concentrations is essential.
In this study, 61 hyperthyroid cats were assessed before and after treatment for hyperthyroidism. Treatment included using methimazole or methimazole and subsequent surgical thyroidectomy. Cats with overt heart failure or systemic hypertension were excluded from the study due to previous reports showing these conditions to be associated with an increase in NT-proBNP. Assessment included full physical examination, systolic blood pressure (SBP), plasma biochemistries, total thyroid level (TT4), packed cell volume (PCV), and urinalysis, as well as measurement of NT-proBNP and NT-proANP concentrations. The length of time between pre- and post-treatment evaluation was 35 days and the length of time that the cats were on treatment before post-treatment sample was 28 days. Total T4, heart rate, SBP, and PCV all decreased and body weight and creatinine concentrations increased once euthyroidism was established. In addition, NT-proBNP significantly declined, but no change in NT-proANP concentrations was noted. In conclusion, hyperthyroidism has a modest but significant effect on elevating NT-proBNP with little effect on NT-proANP. Therefore, thyroid status should be taken into account when interpreting NT-proBNP results. [GO]
See also: Singletary GE, Rush JE, Fox PR, Stepien RL and Oyama MA. Effect of NT-pro-BNP assay on accuracy and confidence of general practitioners in diagnosing heart failure or respiratory disease in cats with respiratory signs. J Vet Intern Med. 2012; 26: 542-6.
Related blog articles:
Biochemical testing for feline heart disease (March 2009)
Cardiac biomarkers in feline heart disease (July 2011)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Natriuretic peptides (NPs) are neurohormones stored in heart muscle cells (atrial cardiomyocytes) and released in response to atrial stretch. They possess potent natriuretic and vasorelaxant properties. They have been shown to be chronically up-regulated in cats with underlying heart disease and have thus been used as a biomarker to detect occult heart disease and differentiate cardiac from non-cardiac dyspnea in emergency situations. In particular, the non-biologically active N-terminal fragment from atrial natriuretic peptide, (NT-proANP), and from brain natriuretic peptide, NT-proBNP, have commonly been studied due to their stability in plasma.
Hyperthyroidism is the most common endocrine disease of cats. In humans with hyperthyroidism, a number of studies have shown NP concentrations to be elevated. Therefore, since NP measurement is increasingly being used to assess feline cardiac disease, determining the influence of elevated thyroid function on NP concentrations is essential.In this study, 61 hyperthyroid cats were assessed before and after treatment for hyperthyroidism. Treatment included using methimazole or methimazole and subsequent surgical thyroidectomy. Cats with overt heart failure or systemic hypertension were excluded from the study due to previous reports showing these conditions to be associated with an increase in NT-proBNP. Assessment included full physical examination, systolic blood pressure (SBP), plasma biochemistries, total thyroid level (TT4), packed cell volume (PCV), and urinalysis, as well as measurement of NT-proBNP and NT-proANP concentrations. The length of time between pre- and post-treatment evaluation was 35 days and the length of time that the cats were on treatment before post-treatment sample was 28 days. Total T4, heart rate, SBP, and PCV all decreased and body weight and creatinine concentrations increased once euthyroidism was established. In addition, NT-proBNP significantly declined, but no change in NT-proANP concentrations was noted. In conclusion, hyperthyroidism has a modest but significant effect on elevating NT-proBNP with little effect on NT-proANP. Therefore, thyroid status should be taken into account when interpreting NT-proBNP results. [GO]
See also: Singletary GE, Rush JE, Fox PR, Stepien RL and Oyama MA. Effect of NT-pro-BNP assay on accuracy and confidence of general practitioners in diagnosing heart failure or respiratory disease in cats with respiratory signs. J Vet Intern Med. 2012; 26: 542-6.
Related blog articles:
Biochemical testing for feline heart disease (March 2009)
Cardiac biomarkers in feline heart disease (July 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
20 Aralık 2012 Perşembe
Added a New Blog to my Reading List: JCDA's Question and Answer Blog
To contact us Click HERE
Added the Journal of the Canadian Dental Association's Clinical Question and Answer Blog to our blog reading list. It is a tremendous resource for clinicians and worth a view from patients if you are so inclined. We are also honoured to be recognized by them as a top dental blog. Thanks!! :)
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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
Treatment for insecticide toxicosis in cats
To contact us Click HERE
Haworth MD and Smart L. Use of intravenous lipid therapy in three cases of feline permethrin toxicosis. J Vet Emerg Crit Care. 2012; 22: 697-702.
Permethrin is a synthetic pyrethroid insecticide and acaricide commonly used for flea and tick control in dogs. Permethrin toxicosis in cats usually occurs when owners inadvertently apply over-the-counter spot-on flea insecticides intended for dogs to their cats or when cats are exposed secondarily to the product used on dogs that share the same environment. Permethrin exerts its toxic effect on ectoparasite and host by modulating sodium ion channels, causing them to remain open longer, resulting in repetitive excitable cell discharge. While this leads to paralysis and death of the parasite, toxicosis in the host manifests primarily as central nervous system effects including tremors, hyperesthesia, ataxia, mydriasis, pyrexia, seizures, and possibly death. Cats are highly susceptible to permethrin toxicity possibly due to their innate deficiency in glucoronyl transferase and slower hepatic detoxification of the compound.
No antidote exists for permethrin toxicosis, therefore treatment is aimed at decontamination and control of neurological symptoms while allowing time for the toxin to be metabolized and excreted. Clinical signs typically last from 1 to 3 days. Mortality rates vary from 5-45%. Lengthy hospitalization times and cost often contribute to an owner’s decision for euthanasia.
Intravenous lipid emulsion (IVLE) has shown promise as an emerging adjuvant treatment for certain lipophilic toxicants such as ivermectin, local anesthetics, and permethrin. Although the exact mechanism of action of IVLE is unknown, it has been postulated that the lipid creates a “sink” for fat-soluble drugs, decreasing their tissue availability. This report describes treatment of 3 cats with permethrin toxicosis with IVLE administration in addition to standard treatment. All 3 cats appeared to show accelerated resolution of clinical signs following lipid administration. The authors suggest that lipid administration may also reduce hospitalization time and cost, and possibly prevent the decision to euthanize. A prospective, controlled clinical trial to confirm these findings is warranted. In circumstances where euthanasia, or death is imminent, the use of IVLE is justified. [GO]
See also: Bruckner M and Schwedes CS. Successful treatment of permethrin toxicosis in two cats with an intravenous lipid administration. Tierarztl Prax Ausg K Kleintiere Heimtiere. 2012; 40: 129-34.
Malik R, Ward MP, Seavers A, et al. Permethrin spot-on intoxication of cats: Literature review and survey of veterinary practitioners in Australia. J Feline Med Surg. 2010; 12: 5-14.
Related blog articles:
Feline permethrin toxicity (March 2010)
Cats and permethrin toxicity (February 2009)
Feline permethrin spot-on toxicity (May 2008)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Permethrin is a synthetic pyrethroid insecticide and acaricide commonly used for flea and tick control in dogs. Permethrin toxicosis in cats usually occurs when owners inadvertently apply over-the-counter spot-on flea insecticides intended for dogs to their cats or when cats are exposed secondarily to the product used on dogs that share the same environment. Permethrin exerts its toxic effect on ectoparasite and host by modulating sodium ion channels, causing them to remain open longer, resulting in repetitive excitable cell discharge. While this leads to paralysis and death of the parasite, toxicosis in the host manifests primarily as central nervous system effects including tremors, hyperesthesia, ataxia, mydriasis, pyrexia, seizures, and possibly death. Cats are highly susceptible to permethrin toxicity possibly due to their innate deficiency in glucoronyl transferase and slower hepatic detoxification of the compound.
No antidote exists for permethrin toxicosis, therefore treatment is aimed at decontamination and control of neurological symptoms while allowing time for the toxin to be metabolized and excreted. Clinical signs typically last from 1 to 3 days. Mortality rates vary from 5-45%. Lengthy hospitalization times and cost often contribute to an owner’s decision for euthanasia.
Intravenous lipid emulsion (IVLE) has shown promise as an emerging adjuvant treatment for certain lipophilic toxicants such as ivermectin, local anesthetics, and permethrin. Although the exact mechanism of action of IVLE is unknown, it has been postulated that the lipid creates a “sink” for fat-soluble drugs, decreasing their tissue availability. This report describes treatment of 3 cats with permethrin toxicosis with IVLE administration in addition to standard treatment. All 3 cats appeared to show accelerated resolution of clinical signs following lipid administration. The authors suggest that lipid administration may also reduce hospitalization time and cost, and possibly prevent the decision to euthanize. A prospective, controlled clinical trial to confirm these findings is warranted. In circumstances where euthanasia, or death is imminent, the use of IVLE is justified. [GO]
See also: Bruckner M and Schwedes CS. Successful treatment of permethrin toxicosis in two cats with an intravenous lipid administration. Tierarztl Prax Ausg K Kleintiere Heimtiere. 2012; 40: 129-34.
Malik R, Ward MP, Seavers A, et al. Permethrin spot-on intoxication of cats: Literature review and survey of veterinary practitioners in Australia. J Feline Med Surg. 2010; 12: 5-14.
Related blog articles:
Feline permethrin toxicity (March 2010)
Cats and permethrin toxicity (February 2009)
Feline permethrin spot-on toxicity (May 2008)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Lomustine for treatment of feline lymphoma
To contact us Click HERE
Dutelle AL, Bulman-Fleming JC, Lewis CA and Rosenberg MP. Evaluation of lomustine as a rescue agent for cats with resistant lymphoma. J Feline Med Surg. 2012; 14: 694-700.
Treating cases of resistant lymphoma is very challenging for veterinarians. The study reported here evaluated the use of lomustine as a rescue agent for 39 cases of resistant lymphoma in cats. The aims of the study were to evaluate lomustine as a rescue agent in this scenario, to determine prognostic factors for progression-free interval, and to detail toxicities noted in the course of the study. Progression-free interval (PFI) was defined as the time from when a cat was placed on lomustine to subsequent progression of disease necessitating a protocol change or euthanasia. The different parameters evaluated were lymphocyte cell size, number of previous chemotherapy drugs and number of chemotherapy protocols received, time from lymphoma diagnosis to initiation of lomustine therapy, body weight, and anatomic location of lymphoma.
The results demonstrated that the significant prognostic factors for PFI were cell size, number of previous chemotherapeutic drugs, number of previous chemotherapeutic protocols, and anatomic location. Cats with large cell lymphoma were 9.8 times more likely to have disease progression. Twenty-one cats (54%) received more than 1 dose of lomustine. Cats that had received 3 to 4 prior protocols were 3.6 times more likely to have disease progression than cats receiving 1 or 2 prior protocols. And cats with non-GI lymphoma were 4.7 times more likely to have progression of disease as ones with GI lymphoma. The most commonly noted toxicities in this study were vomiting, diarrhea, thrombocytopenia, leukopenia, and elevated ALT. It was noted that strict monitoring of the CBC while cats are on this drug is very important. [VT]
See also: Musser ML, Quinn HT and Chretin JD. Low apparent risk of CCNU (lomustine)-associated clinical hepatotoxicity in cats. J Feline Med Surg. 2012; 14: 871-5.
Related blog articles:
Pulmonary fibrosis in a cat receiving lomustine (July 2008)
Treatment for mast cell tumors in cats (April 2008)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Treating cases of resistant lymphoma is very challenging for veterinarians. The study reported here evaluated the use of lomustine as a rescue agent for 39 cases of resistant lymphoma in cats. The aims of the study were to evaluate lomustine as a rescue agent in this scenario, to determine prognostic factors for progression-free interval, and to detail toxicities noted in the course of the study. Progression-free interval (PFI) was defined as the time from when a cat was placed on lomustine to subsequent progression of disease necessitating a protocol change or euthanasia. The different parameters evaluated were lymphocyte cell size, number of previous chemotherapy drugs and number of chemotherapy protocols received, time from lymphoma diagnosis to initiation of lomustine therapy, body weight, and anatomic location of lymphoma.
The results demonstrated that the significant prognostic factors for PFI were cell size, number of previous chemotherapeutic drugs, number of previous chemotherapeutic protocols, and anatomic location. Cats with large cell lymphoma were 9.8 times more likely to have disease progression. Twenty-one cats (54%) received more than 1 dose of lomustine. Cats that had received 3 to 4 prior protocols were 3.6 times more likely to have disease progression than cats receiving 1 or 2 prior protocols. And cats with non-GI lymphoma were 4.7 times more likely to have progression of disease as ones with GI lymphoma. The most commonly noted toxicities in this study were vomiting, diarrhea, thrombocytopenia, leukopenia, and elevated ALT. It was noted that strict monitoring of the CBC while cats are on this drug is very important. [VT]
See also: Musser ML, Quinn HT and Chretin JD. Low apparent risk of CCNU (lomustine)-associated clinical hepatotoxicity in cats. J Feline Med Surg. 2012; 14: 871-5.
Related blog articles:
Pulmonary fibrosis in a cat receiving lomustine (July 2008)
Treatment for mast cell tumors in cats (April 2008)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
16 Aralık 2012 Pazar
Added a New Blog to my Reading List: JCDA's Question and Answer Blog
To contact us Click HERE
Added the Journal of the Canadian Dental Association's Clinical Question and Answer Blog to our blog reading list. It is a tremendous resource for clinicians and worth a view from patients if you are so inclined. We are also honoured to be recognized by them as a top dental blog. Thanks!! :)
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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
Dental Did You Know: Success Rates of Veneers vs Composite Buildups
To contact us Click HERE
A small study has revealed that the 5 year survival rate of direct composite buildups was 79% (which was lower than the 6 year survival rate of veneers of 92%).
Source: Sevels I, Clinical Abstracts, Ontario Dentist, Dec 2012, Vol 89, No 10, pg 20-21.
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: Sevels I, Clinical Abstracts, Ontario Dentist, Dec 2012, Vol 89, No 10, pg 20-21.
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
Which diet is best for chronic diarrhea in cats?
To contact us Click HERE
Laflamme DP, Xu H, Cupp CJ, Kerr WW, Ramadan Z and Long GM. Evaluation of canned therapeutic diets for the management of cats with naturally occurring chronic diarrhea. J Feline Med Surg. 2012; 14: 669-77.
Dietary therapy has been considered important in the management of many feline gastrointestinal disorders. Low fat diets were for a long period of time the major recommendation for feeding cats with acute and chronic diarrhea. However, a recent double-blinded clinical trial showed that dietary fat did not affect the outcome of diarrhea in cats.
The current study, conducted by Nestle Purina PetCare Co., looked at the clinical efficacy of a new therapeutic diet for cats with diarrhea. Researchers assigned 16 cats with chronic diarrhea to be fed diet X (Hill’s Prescription i/d Feline) or diet Y (Purina Veterinary Diets EN Gastrointestinal Feline Formula) for 4 weeks while fecal scores were recorded daily for the last week on each diet. The process was then repeated by switching each cat to the alternate diet. Diet Y is a canned food formulated to contain high protein, low carbohydrate, moderate fiber (with both soluble and insoluble fibers), and a source of long-chain omega-3 fatty acids. Omega-3 fatty acids provide a relative anti-inflammatory effect and may be beneficial in some types of GI disease. Fecal scores improved significantly when both therapeutic diets were fed, but diet Y showed the best results. When fed diet Y, 47% of the cats developed normal stools with dietary change alone. [VT]
See also: Hart ML, Suchodolski JS, Steiner JM and Webb CB. Open-label trial of a multi-strain synbiotic in cats with chronic diarrhea. J Feline Med Surg. 2012; 14: 240-5.
Related blog articles:
Dietary therapy for chronic diarrhea in cats (April 2011)
Intestinal biopsies in cats (April 2010)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Dietary therapy has been considered important in the management of many feline gastrointestinal disorders. Low fat diets were for a long period of time the major recommendation for feeding cats with acute and chronic diarrhea. However, a recent double-blinded clinical trial showed that dietary fat did not affect the outcome of diarrhea in cats.
The current study, conducted by Nestle Purina PetCare Co., looked at the clinical efficacy of a new therapeutic diet for cats with diarrhea. Researchers assigned 16 cats with chronic diarrhea to be fed diet X (Hill’s Prescription i/d Feline) or diet Y (Purina Veterinary Diets EN Gastrointestinal Feline Formula) for 4 weeks while fecal scores were recorded daily for the last week on each diet. The process was then repeated by switching each cat to the alternate diet. Diet Y is a canned food formulated to contain high protein, low carbohydrate, moderate fiber (with both soluble and insoluble fibers), and a source of long-chain omega-3 fatty acids. Omega-3 fatty acids provide a relative anti-inflammatory effect and may be beneficial in some types of GI disease. Fecal scores improved significantly when both therapeutic diets were fed, but diet Y showed the best results. When fed diet Y, 47% of the cats developed normal stools with dietary change alone. [VT]
See also: Hart ML, Suchodolski JS, Steiner JM and Webb CB. Open-label trial of a multi-strain synbiotic in cats with chronic diarrhea. J Feline Med Surg. 2012; 14: 240-5.
Related blog articles:
Dietary therapy for chronic diarrhea in cats (April 2011)
Intestinal biopsies in cats (April 2010)
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
12 Aralık 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
Added a New Blog to my Reading List: JCDA's Question and Answer Blog
To contact us Click HERE
Added the Journal of the Canadian Dental Association's Clinical Question and Answer Blog to our blog reading list. It is a tremendous resource for clinicians and worth a view from patients if you are so inclined. We are also honoured to be recognized by them as a top dental blog. Thanks!! :)
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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
11 Aralık 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
Added a New Blog to my Reading List: JCDA's Question and Answer Blog
To contact us Click HERE
Added the Journal of the Canadian Dental Association's Clinical Question and Answer Blog to our blog reading list. It is a tremendous resource for clinicians and worth a view from patients if you are so inclined. We are also honoured to be recognized by them as a top dental blog. Thanks!! :)
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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
Nice Dental Website: Region of Peel Oral Health Website
To contact us Click HERE
The region of Peel (Mississauga and area) has an informative oral health website. I'll quote from their press release:
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
This resource has been designed to provide parents/caregivers with clear messaging to guide proper brushing patterns as well as direct parents/caregivers to the Region of Peel oral health website (www.peelregion.ca/dental). At this website they will find additional information on caring for children's teeth and information on Region of Peel dental services including the Children in Need of Treatment (CINOT) Program and the Healthy Smiles Ontario (HSO) Program.I've added a screenshot of the website below:
.png "Region of Peel Oral Health Website - Screenshot by Promenade Court Dental") |
| Screenshot of the Peel Region Oral Health Website (www.peelregion.ca/dental) |
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
Renal secondary hyperparathyroidism in cats
To contact us Click HERE
Finch NC, Syme HM and Elliott J. Parathyroid hormone concentration in geriatric cats with various degrees of renal function. J Am Vet Med Assoc. 2012; 241: 1326-35.
Chronic kidney disease (CKD) in cats is commonly associated with an increase in plasma parathyroid hormone (PTH) and is known as renal secondary hyperparathyroidism. PTH is a primary regulator of calcium and phosphorus homeostasis. PTH secretion is stimulated when parathyroid gland calcium-sensing receptors detect a low ionized calcium plasma concentration. Cats with CKD have decreased glomerular filtration rate resulting in phosphate retention. Retained phosphate complexes with ionized calcium leading to reduction in ionized calcium concentration and an increase in PTH. The prevalence of hyperparathyroidism in cats with CKD has previously been reported to be as high as 84%. PTH is regarded as a uremic toxin and elevated levels are suggested to contribute to renal damage and increase morbidity and mortality. Clinical consequences of increased PTH concentration include renal osteodystrophy, soft tissue calcification, glucose and lipid metabolic disturbances, contribution to immunosuppression and anemia, and neurologic and cardiovascular dysfunction. Therefore, recognition of the stage of CKD at which plasma PTH concentrations increase and management of renal secondary hyperparathyroidism is important in cats.
The authors of this paper enrolled 118 clinically normal geriatric cats (over 9 years) with various degrees of renal disease. Cats were monitored for 12 months after which time they were categorized into 1 of 3 groups. Group 1 cats were basically non-azotemic with adequate urine concentrating ability, group 2 cats were mildly azotemic (creatinine between 1.6-2 mg/dL, or creatinine > 2.0 mg/dL with USG > 1.035), and group 3 cats were azotemic (creatinine > 2.0 mg/dL with USG < 1.035). This study revealed that plasma PTH concentration could increase in non-azotemic cats that subsequently developed azotemia, compared with cats remaining non-azotemic, in the absence of concurrent hypocalcemia or hyperphosphatemia. Traditionally, the pathophysiologic mechanism for the development of renal secondary hyperparathyroidism in cats with CKD was thought to only involve disturbances in calcium and phosphate homeostasis. Therefore, this study suggests other factors are involved in the development of renal secondary hyperparathyroidism. Other factors discussed included age, decreased ionized calcium rather than total calcium concentrations, hypomagnesemia, decreased expression of calcium-sensing receptors, and increased fibroblast growth factor-23 concentration. A positive correlation was noted between increased PTH and calcitriol concentrations, but the role of calcitriol in the development of renal secondary hyperparathyroidism in cats remains unclear. [GO]
See also: Kidder AC and Chew D. Treatment options for hyperphosphatemia in feline CKD: What's out there? Journal of Feline Medicine & Surgery. 2009; 11: 913-24.
Related blog articles:
Survival of cats with kidney disease (September 2008)
Predictors of feline kidney disease (August 2009)
Improving treatment of feline kidney disease; 2012 Winn grant (May 2012)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Chronic kidney disease (CKD) in cats is commonly associated with an increase in plasma parathyroid hormone (PTH) and is known as renal secondary hyperparathyroidism. PTH is a primary regulator of calcium and phosphorus homeostasis. PTH secretion is stimulated when parathyroid gland calcium-sensing receptors detect a low ionized calcium plasma concentration. Cats with CKD have decreased glomerular filtration rate resulting in phosphate retention. Retained phosphate complexes with ionized calcium leading to reduction in ionized calcium concentration and an increase in PTH. The prevalence of hyperparathyroidism in cats with CKD has previously been reported to be as high as 84%. PTH is regarded as a uremic toxin and elevated levels are suggested to contribute to renal damage and increase morbidity and mortality. Clinical consequences of increased PTH concentration include renal osteodystrophy, soft tissue calcification, glucose and lipid metabolic disturbances, contribution to immunosuppression and anemia, and neurologic and cardiovascular dysfunction. Therefore, recognition of the stage of CKD at which plasma PTH concentrations increase and management of renal secondary hyperparathyroidism is important in cats.
The authors of this paper enrolled 118 clinically normal geriatric cats (over 9 years) with various degrees of renal disease. Cats were monitored for 12 months after which time they were categorized into 1 of 3 groups. Group 1 cats were basically non-azotemic with adequate urine concentrating ability, group 2 cats were mildly azotemic (creatinine between 1.6-2 mg/dL, or creatinine > 2.0 mg/dL with USG > 1.035), and group 3 cats were azotemic (creatinine > 2.0 mg/dL with USG < 1.035). This study revealed that plasma PTH concentration could increase in non-azotemic cats that subsequently developed azotemia, compared with cats remaining non-azotemic, in the absence of concurrent hypocalcemia or hyperphosphatemia. Traditionally, the pathophysiologic mechanism for the development of renal secondary hyperparathyroidism in cats with CKD was thought to only involve disturbances in calcium and phosphate homeostasis. Therefore, this study suggests other factors are involved in the development of renal secondary hyperparathyroidism. Other factors discussed included age, decreased ionized calcium rather than total calcium concentrations, hypomagnesemia, decreased expression of calcium-sensing receptors, and increased fibroblast growth factor-23 concentration. A positive correlation was noted between increased PTH and calcitriol concentrations, but the role of calcitriol in the development of renal secondary hyperparathyroidism in cats remains unclear. [GO]
See also: Kidder AC and Chew D. Treatment options for hyperphosphatemia in feline CKD: What's out there? Journal of Feline Medicine & Surgery. 2009; 11: 913-24.
Related blog articles:
Survival of cats with kidney disease (September 2008)
Predictors of feline kidney disease (August 2009)
Improving treatment of feline kidney disease; 2012 Winn grant (May 2012)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
8 Aralık 2012 Cumartesi
Added a New Blog to my Reading List: JCDA's Question and Answer Blog
To contact us Click HERE
Added the Journal of the Canadian Dental Association's Clinical Question and Answer Blog to our blog reading list. It is a tremendous resource for clinicians and worth a view from patients if you are so inclined. We are also honoured to be recognized by them as a top dental blog. Thanks!! :)
Source: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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: Canadian Dental Association's Clinical Question and Answer Blog: http://www.jcdablogs.ca/, read Dec 7, 2012
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
7 Aralık 2012 Cuma
Dental Did You Know: Colon Cancer and Proposed Breath Screening
To contact us Click HERE
A small study from Italy has determined that it is possible to use breath analysis of volatile compounds to identify people with colorectal cancer.
Source: CBC News website, http://www.cbc.ca/news/health/story/2012/12/04/colon-cancer-breath-test.html, first posted Dec 5, 2012, read Dec 6, 2012.
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: CBC News website, http://www.cbc.ca/news/health/story/2012/12/04/colon-cancer-breath-test.html, first posted Dec 5, 2012, read Dec 6, 2012.
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
Infectious diseases in cat shelters
To contact us Click HERE
DiGangi BA, Levy JK, Griffin B, et al. Prevalence of serum antibody titers against feline panleukopenia virus, feline herpesvirus 1, and feline calicivirus in cats entering a Florida animal shelter. J Am Vet Med Assoc. 2012; 241: 1320-5.
Feline panleukopenia virus (FPV), feline herpes virus 1 (FHV-1), and feline calicivirus (FCV) are widespread in the cat population, and particularly in shelter environments. The American Association of Feline Practitioners guidelines recommend that all cats at or over 4 weeks of age be vaccinated against these three viruses upon admission to animal shelters. However, the proportion of cats entering shelters that are already protected (i.e., seropositive) against infection (FPV) or disease (FHV-1 and FCV) because of prior vaccination or natural exposure is usually unknown. The objective of this study was to determine the prevalence of and factors associated with seropositivity for FPV, FHV-1, and FCV in cats entering a Florida animal shelter.
Of 347 cats enrolled in this study, prevalence of seropositivity was 39.8%, 11.0% and 36.6% against FPV, FHV-1, and FCV, respectively. Factors associated with seropositivity included sterilization, age equal to or greater than 6 months, and relinquishment by an owner. Surprisingly, community origin (i.e., rural or urban), health status, signs of previous caregiving aside from sterilization, and outcome (i.e., adopted, transferred, euthanized, or reclaimed by owner) were not associated with seropositivity and should not be used to determine an individual cat’s need for vaccination. This study suggests that most cats admitted to an animal shelter do not have adequate antibody protection against infection or disease; therefore, the recommendation to vaccinate all cats admitted to an animal shelter is reasonable and vaccination should not be withheld due to signs of previous veterinary care. [GO]
See also: DiGangi BA, Gray LK, Levy JK, Dubovi EJ and Tucker SJ. Detection of protective antibody titers against feline panleukopenia virus, feline herpesvirus-1, and feline calicivirus in shelter cats using a point-of-care ELISA. J Feline Med Surg. 2011; 13: 912-8.
Related blog articles:
Upper respiratory tract disease in shelters (November 2009)
Disease control in animal shelters (May 2011)
Coronavirus in California shelter cats (April 2012)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Feline panleukopenia virus (FPV), feline herpes virus 1 (FHV-1), and feline calicivirus (FCV) are widespread in the cat population, and particularly in shelter environments. The American Association of Feline Practitioners guidelines recommend that all cats at or over 4 weeks of age be vaccinated against these three viruses upon admission to animal shelters. However, the proportion of cats entering shelters that are already protected (i.e., seropositive) against infection (FPV) or disease (FHV-1 and FCV) because of prior vaccination or natural exposure is usually unknown. The objective of this study was to determine the prevalence of and factors associated with seropositivity for FPV, FHV-1, and FCV in cats entering a Florida animal shelter.
Of 347 cats enrolled in this study, prevalence of seropositivity was 39.8%, 11.0% and 36.6% against FPV, FHV-1, and FCV, respectively. Factors associated with seropositivity included sterilization, age equal to or greater than 6 months, and relinquishment by an owner. Surprisingly, community origin (i.e., rural or urban), health status, signs of previous caregiving aside from sterilization, and outcome (i.e., adopted, transferred, euthanized, or reclaimed by owner) were not associated with seropositivity and should not be used to determine an individual cat’s need for vaccination. This study suggests that most cats admitted to an animal shelter do not have adequate antibody protection against infection or disease; therefore, the recommendation to vaccinate all cats admitted to an animal shelter is reasonable and vaccination should not be withheld due to signs of previous veterinary care. [GO]
See also: DiGangi BA, Gray LK, Levy JK, Dubovi EJ and Tucker SJ. Detection of protective antibody titers against feline panleukopenia virus, feline herpesvirus-1, and feline calicivirus in shelter cats using a point-of-care ELISA. J Feline Med Surg. 2011; 13: 912-8.
Related blog articles:
Upper respiratory tract disease in shelters (November 2009)
Disease control in animal shelters (May 2011)
Coronavirus in California shelter cats (April 2012)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Kidney disease in cats and people
To contact us Click HERE
Poli A, Tozon N, Guidi G and Pistello M. Renal alterations in feline immunodeficiency virus (FIV)-infected cats: a natural model of lentivirus-induced renal disease changes. Viruses. 2012; 4: 1372-89. [Free, full text article]
Human immunodeficiency virus (HIV) is associated with severe kidney disease including acute and chronic renal failure, but the underlying pathogenic mechanisms are unclear. HIV and feline immunodeficiency virus (FIV) are closely related viruses so that disease in cats may be a model for disease in humans. Both human and feline patients may live for many years after infection and suffer from chronic diseases. While kidney disease has been documented in cats with FIV, no detailed description of the kidney lesions has been published.
The investigators, working at the University of Pisa in Italy, examined kidneys from 72 cats infected with FIV. They found and described pathologic changes in the kidneys of cats with FIV that are similar to those in humans with HIV. A high proportion of the cats were affected. Thus they conclude that FIV may cause kidney changes, perhaps leading to kidney disease in infected cats. [MK]
See also: 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.
Related blog articles:
FIV and kidney disease in cats (February 2010)
FIV and kidney disease (October 2012)
More on cat health:
Winn Feline Foundation Library
Find us on Facebook
Follow us on Twitter
Join us on Google+
Human immunodeficiency virus (HIV) is associated with severe kidney disease including acute and chronic renal failure, but the underlying pathogenic mechanisms are unclear. HIV and feline immunodeficiency virus (FIV) are closely related viruses so that disease in cats may be a model for disease in humans. Both human and feline patients may live for many years after infection and suffer from chronic diseases. While kidney disease has been documented in cats with FIV, no detailed description of the kidney lesions has been published.
The investigators, working at the University of Pisa in Italy, examined kidneys from 72 cats infected with FIV. They found and described pathologic changes in the kidneys of cats with FIV that are similar to those in humans with HIV. A high proportion of the cats were affected. Thus they conclude that FIV may cause kidney changes, perhaps leading to kidney disease in infected cats. [MK]
See also: 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.
Related blog articles:
FIV and kidney disease in cats (February 2010)
FIV and kidney disease (October 2012)
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.
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.
30 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
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
Find us on Facebook
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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
To contact us Click HERE
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
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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)
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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
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
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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
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
19 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
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
Find us on Facebook
Follow us on Twitter
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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+
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