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- W30541128 abstract "The anti-angiogenic drug sunitinib is a receptor tyrosine-kinase (RTK) inhibitor with significant, yet not curative, therapeutic impacts in metastatic renal cell carcinoma (mRCC). Sunitinib is also an immunomodulator, potently reversing myeloid-derived suppressor cell (MDSC) accumulation and T-cell inhibition in the peripheral blood even of non-responder RCC patients. We observed that sunitinib similarly prevented massive MDSC accumulation and restored normal T-cell function in the spleens of tumor-bearing mice, even when sunitinib had negligible impacts upon tumor progression itself. Both monocytic and neutrophilic splenic MDSC were highly inhibitable by sunitinib. In contrast, MDSC in bone marrow and tumor proved highly resistant to sunitinib, and ambient T-cell function remained suppressed in these compartments. Proteomic analyses comparing tumor to peripheral compartments demonstrated that GM-CSF predicted sunitinib resistance, and recombinant GM-CSF could confer sunitinib resistance to MDSC in vitro. MDSC conditioning with GM-CSF inhibited STAT3 and promoted STAT5 activation, whereas other hematopoietic support factors preferentially preserved both STAT3 activation and sunitinib susceptibility. We conclude that compartmentaldependent GM-CSF exposure may account for sunitinib’s regionalized impact upon host MDSC modulation, and hypothesize that ancillary strategies to decrease such" @default.
- W30541128 created "2016-06-24" @default.
- W30541128 creator A5079994196 @default.
- W30541128 date "2009-01-01" @default.
- W30541128 modified "2023-09-23" @default.
- W30541128 title "MECHANISM OF MYELOID-DERIVED SUPPRESSOR CELL ACCUMULATION IN CANCER AND SUSCEPTIBILITY TO REVERSAL BY SUNITINIB" @default.
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