ArticleCancer medicine2026
Effects of Vemurafenib ± Cobimetinib on Intratumoral and Host Immunity in Patients With BRAFV600 Mutant Melanoma: Implications for Combination With Immunotherapy.
Article in Cancer medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Multi-tyrosine kinase inhibitors: exploring immunomodulatory effects on various immune cell types in cancer.Cancer cell international · 2026Review
- Effects of Vemurafenib ± Cobimetinib on Intratumoral and Host Immunity in Patients With BRAFV600 Mutant Melanoma: Implications for Combination With Immunotherapy.Cancer medicine · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
backgroundPrior studies in patients with BRAF-mutant melanoma have shown increased density of tumor infiltrating lymphocytes (TIL) after 2 weeks of BRAF (BRAFi) ± MEK inhibition (MEKi), but did not characterize the functional state or clonal diversity of TIL over time. We evaluated sequential tumor biopsies during therapy to test the hypotheses that BRAF/MEKi would increase TIL to day 29, with increases in IFNγ signatures and T-cell homing receptor ligands and expansion of functional intratumoral tumor-reactive CD8 T-cells and TIL clonality in the tumor microenvironment.
methodsSubjects with biopsy-accessible BRAF-mutant advanced melanoma received vemurafenib+/-cobimetinib. Tumor biopsies were obtained at baseline and days 8, 15, and 29 on therapy. Tumors were analyzed by quantitative immunofluorescence (QIF), NanoString, and TCRseq.
resultsFive patients were enrolled. All had an initial tumor response followed by subsequent progression. In four patients, both CD8
conclusionsData from this study provides provocative evidence that, while BRAF+/-MEK inhibitor therapy produces an increase in overall and clonal T cell infiltrates, there is limited evidence for generation of new or persistent tumor immunity. Thus, BRAFi/MEKi therapy may enable tumor-reactive T cells to infiltrate tumors but tumor control does not appear to depend on priming new immune responses.
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