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
25 Şubat 2013 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
24 Şubat 2013 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
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 Şubat 2013 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
22 Şubat 2013 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
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