Treatment of feline colonic adenocarcinoma

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Arteaga TA, McKnight J and Bergman PJ. A review of 18 cases of feline colonic adenocarcinoma treated with subtotal colectomies and adjuvant carboplatin. J Am Anim Hosp Assoc. 2012; 48: 399-404.

Adenocarcinoma is the second most common gastrointestinal tumor in cats and the most common tumor found in the colon. Colonic adenocarcinoma is both locally invasive and frequently has advanced metastasis at the time of presentation. Aggressive local surgery (subtotal colectomy) improves survival time in cats, but patients eventually succumb to metastasis, warranting adjuvant treatment with chemotherapy. Carboplatin is an alkylating platinum-based chemotherapeutic agent and has been shown to have efficacy in humans and dogs with carcinomas. Limited previous studies have shown mild to moderate efficacy and safety of carboplatin in cats with carcinomas, meriting its investigation as an adjuvant therapy for colonic adenocarcinomas.
 
This retrospective study evaluated signalment, diagnostic findings, disease-free interval, survival time, chemotherapeutic toxicoses, and prognostic factors for 18 cats with colonic adenocarcinoma treated with subtotal colectomy and monthly carboplatin. Interestingly, cats initially presenting with weight loss had a longer median disease-free interval (290 days versus 75 days), suggesting that a more chronic disease course occurs when weight loss is present. Four cats without weight loss had distant metastasis and a more acute presentation. Median survival time for all cats was 269 days, with cats without distant metastasis surviving 340 days and cats with distant metastasis surviving 200 days. For comparison, in a previous study, cats treated with subtotal colectomy alone lived only 56 days. Carboplatin toxicities reported included low-grade neutropenia, thrombocytopenia, and gastrointestinal toxicity, none of which required reduction or delay in treatment. One cat developed azotemia and carboplatin treatment was stopped after the fifth monthly dose. In conclusion, cats with colonic adenocarcinoma commonly present with colonic obstruction and usually remain patent after subtotal colectomy, but in the end, they are often euthanized due to metastasis, warranting early adjuvant chemotherapy. In this study, carboplatin was shown to have minimal toxicity and to be a viable adjunct for treating this disease. [GO]

See also: Green ML, Smith JD and Kass PH. Surgical versus non-surgical treatment of feline small intestinal adenocarcinoma and the influence of metastasis on long-term survival in 18 cats (2000-2007). Can Vet J. 2011; 52: 1101-5. [Free, full text article]

Related blog articles:
Feline intestinal cancer (March 2011)

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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

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

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

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

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

Efficacy of intranasal vaccination in cats

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Bradley A, Kinyon J, Frana T, Bolte D, Hyatt DR and Lappin MR. Efficacy of intranasal administration of a modified live feline herpesvirus 1 and feline calicivirus vaccine against disease caused by Bordetella bronchiseptica after experimental challenge. J Vet Intern Med. 2012; 26: 1121-5.

Upper respiratory tract infections (URTI) are common problems affecting cats in shelters, boarding facilities, breeding catteries, and pet homes. The most common causes of URTI include feline herpesvirus 1 (FHV), feline calicivirus (FCV), Bordetella bronchiseptica, Chlamydophila felis, Mycoplasma spp, and some bacteria. However, vaccines are only available for FHV, FCV, B. bronchiseptica, and C. felis. No single product is available to provide protection against all 4 agents in one vaccine.
 
Most feline vaccines are formulated for parenteral use, but there are 2 products on the market in the United States designed for intranasal administration. Intranasal administration of vaccines stimulates a nonspecific immune response in addition to the specific immune response against the agent in the vaccine. These investigators examined the effect of intranasal vaccination against FHV and FCV on disease caused by B. bronchiseptica. Two groups of 10 cats each were either inoculated intranasally with the vaccine or left unvaccinated. They were then exposed to B. bronchiseptica seven days later. Vaccinated cats were found to be less likely to be clinically ill than unvaccinated cats. Thus, intranasal vaccination with FHV and FCV decreased disease caused by a different pathogen due to its stimulation of nonspecific immunity. [MK]

See also: Egberink H, Addie D, Belak S, et al. Bordetella bronchiseptica infection in cats ABCD guidelines on prevention and management. J Feline Med Surg. 2009; 11: 610-4.
Free, full text article updated 2012

Related blog articles:
Treatment of feline upper respiratory tract disease (August 2012)
Upper respiratory tract disease in shelters (November 2009)
Understanding chronic respiratory disease in cats (August 2009)

More on cat health:
Winn Feline Foundation Library
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