IF 48.8 1区 医学 Q1 CELL BIOLOGY
Mathieu Desaunay, Poulikos I. Poulikakos
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引用次数: 0

摘要

皮肤黑色素瘤经常由BRAF(V600X)突变驱动,常常对丝裂原活化蛋白激酶(MAPK)靶向疗法和免疫检查点抑制剂产生抗药性。在本期《癌细胞》(Cancer Cell)杂志上,Lubrano 等人将 RhoA-FAK-AKT 信号转导确定为一种耐药机制,并证明将 RAF-MEK 胶与 FAK 抑制剂结合可增强肿瘤消退和免疫反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Overcoming melanoma therapy resistance with RAF-MEK and FAK inhibition
Cutaneous melanoma, frequently driven by BRAF (V600X) mutations, often develops resistance to mitogen-activated protein kinase (MAPK)-targeted therapies and immune checkpoint inhibitors. In this issue of Cancer Cell, Lubrano et al. identify RhoA-FAK-AKT signaling as a resistance mechanism and demonstrate that combining RAF-MEK glue with a FAK inhibitor enhances tumor regression and immune response.
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来源期刊
Cancer Cell
Cancer Cell 医学-肿瘤学
CiteScore
55.20
自引率
1.20%
发文量
179
审稿时长
4-8 weeks
期刊介绍: Cancer Cell is a journal that focuses on promoting major advances in cancer research and oncology. The primary criteria for considering manuscripts are as follows: Major advances: Manuscripts should provide significant advancements in answering important questions related to naturally occurring cancers. Translational research: The journal welcomes translational research, which involves the application of basic scientific findings to human health and clinical practice. Clinical investigations: Cancer Cell is interested in publishing clinical investigations that contribute to establishing new paradigms in the treatment, diagnosis, or prevention of cancers. Insights into cancer biology: The journal values clinical investigations that provide important insights into cancer biology beyond what has been revealed by preclinical studies. Mechanism-based proof-of-principle studies: Cancer Cell encourages the publication of mechanism-based proof-of-principle clinical studies, which demonstrate the feasibility of a specific therapeutic approach or diagnostic test.
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