TIM-3 / HAVCR2 / CD366 (BSB-163), MMab

Summary and Explanation

Upregulation has been observed in tumors progressing after anti-PD-1 therapy. It has been reported that early breast cancer patients with TIM-3+ iTILs have significantly improved breast cancer-specific survival whereas TIM-3+ sTILs did not reach statistical significance and it was concluded that the presence of TIM-3+ iTILs is an independent favorable prognostic factor in the whole cohort as well as among ER negative patients. In myelogenous leukemia (AML), upregulated TIM-3 during AML could reduce cytokine production. Co-expression of PD-1 and TIM-3 was correlated with AML progression. In follicular B-cell non-Hodgkin lymphoma, TIM-3 was expressed on nearly 35% of lymph node CD4+ and CD8+ T cells and could mediate T-cells exhaustion. In glioma patients, TIM-3 was correlated with cancer immune escape and might be a potent target. In colorectal cancer, upregulation of TIM-3 could restrict T-cell responses and might participate in tumorigenesis. The expression of TIM-3 antibody might be an independent prognostic factor for colorectal cancer.

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Synonyms: tim-3. tim3, anti-tim-3, anti-tim3, HAVCR2, anti-HAVCR2, CD366, anti-CD366, anti havcr2, anti cd366