剖析 STAT 罕见突变：STAT3 突变髓样肿瘤的特征

IF 10 1区医学 Q1 ONCOLOGY

Clinical Cancer Research Pub Date : 2024-10-15 DOI:10.1158/1078-0432.CCR-24-1692

Michael J Hochman, David A Frank

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引用次数: 0

摘要

转录因子 STAT3 驱动着促进细胞增殖、存活和多能性的基因表达。在急性髓性白血病和骨髓增生异常综合征等骨髓肿瘤中发现的 STAT3 基因突变及其临床相关性，为这些疾病的发病机制和靶向治疗提供了新的思路。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

Dissecting Out a Rare Mutation, STAT: Features of STAT3-Mutant Myeloid Neoplasms.

The transcription factor STAT3 drives the expression of genes promoting cellular proliferation, survival, and pluripotency. The description of STAT3 mutations and their clinical correlates in myeloid neoplasms, such as acute myeloid leukemia and myelodysplastic syndromes, raises new insights into both the pathogenesis and the targeted therapy of these diseases. See related article by Ye et al., p. 4681.

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来源期刊

Clinical Cancer Research 医学-肿瘤学

CiteScore

20.10

自引率

1.70%

发文量

1207

审稿时长

2.1 months

期刊介绍： Clinical Cancer Research is a journal focusing on groundbreaking research in cancer, specifically in the areas where the laboratory and the clinic intersect. Our primary interest lies in clinical trials that investigate novel treatments, accompanied by research on pharmacology, molecular alterations, and biomarkers that can predict response or resistance to these treatments. Furthermore, we prioritize laboratory and animal studies that explore new drugs and targeted agents with the potential to advance to clinical trials. We also encourage research on targetable mechanisms of cancer development, progression, and metastasis.