What question did this study set out to answer?

To determine how KIT oncogene activity and targeted inhibition regulate tumor-associated macrophage polarization in gastrointestinal stromal tumors.

December 9, 2013The Journal of Experimental MedicineOpen Access

KIT oncogene inhibition drives intratumoral macrophage M2 polarization

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Authors

MCMichael J. CavnarUniversity of Kentucky HealthCare SZShan ZengCentral South University TKTeresa S. KimUniversity of Washington

Discussion

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Implication

Preclinical study reveals that KIT inhibition shifts macrophages to a pro-tumor M2 state in gastrointestinal stromal tumors, highlighting oncogene control over immune cell polarization.

Key Points

To determine how KIT oncogene activity and targeted inhibition regulate tumor-associated macrophage polarization in gastrointestinal stromal tumors.
Evaluated macrophage phenotypes using a spontaneous mouse model of gastrointestinal stromal tumor (GIST) and 57 freshly procured human GIST specimens.
Investigated the phenotypic and transcriptional impact of the KIT inhibitor imatinib on tumor-associated macrophages during active treatment and upon the emergence of drug resistance.
Tumor-associated macrophages (TAMs) in untreated mouse and human GISTs displayed an M1-like antitumor phenotype and function at baseline.
Imatinib treatment polarized TAMs toward a tumor-promoting M2-like phenotype through macrophage interaction with apoptotic tumor cells and induction of C/EBP transcription factors.
Imatinib-resistant human GISTs reverted to an M1-like TAM phenotype with gene expression profiles resembling untreated tumors.

Cite This Study

Cavnar et al. (2013) studied this question.

synapsesocial.com/papers/6a7ddab933dcb27c99cb5dae https://doi.org/10.1084/jem.20130875

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December 9, 2013The Journal of Experimental MedicineOpen Access

KIT oncogene inhibition drives intratumoral macrophage M2 polarization

View Full Paper

Ask AI

Bookmark

Authors

MCMichael J. CavnarUniversity of Kentucky HealthCare SZShan ZengCentral South University TKTeresa S. KimUniversity of Washington

Discussion

Member takes

Implication

Preclinical study reveals that KIT inhibition shifts macrophages to a pro-tumor M2 state in gastrointestinal stromal tumors, highlighting oncogene control over immune cell polarization.

Key Points

To determine how KIT oncogene activity and targeted inhibition regulate tumor-associated macrophage polarization in gastrointestinal stromal tumors.
Evaluated macrophage phenotypes using a spontaneous mouse model of gastrointestinal stromal tumor (GIST) and 57 freshly procured human GIST specimens.
Investigated the phenotypic and transcriptional impact of the KIT inhibitor imatinib on tumor-associated macrophages during active treatment and upon the emergence of drug resistance.
Tumor-associated macrophages (TAMs) in untreated mouse and human GISTs displayed an M1-like antitumor phenotype and function at baseline.
Imatinib treatment polarized TAMs toward a tumor-promoting M2-like phenotype through macrophage interaction with apoptotic tumor cells and induction of C/EBP transcription factors.
Imatinib-resistant human GISTs reverted to an M1-like TAM phenotype with gene expression profiles resembling untreated tumors.

Cite This Study

Cavnar et al. (2013) studied this question.

synapsesocial.com/papers/6a7ddab933dcb27c99cb5dae https://doi.org/10.1084/jem.20130875

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