前列腺癌
雄激素剥夺疗法
恶性肿瘤
间质细胞
肿瘤微环境
雄激素受体
癌症
癌症研究
疾病
医学
前列腺
肿瘤进展
生物
肿瘤科
内科学
出处
期刊:Cancer Research
[American Association for Cancer Research]
日期:2023-07-28
卷期号:83 (18): 2990-2992
被引量:7
标识
DOI:10.1158/0008-5472.can-23-2260
摘要
Abstract Prostate cancer is a common malignancy driven by the androgen receptor (AR) pathway, with androgen deprivation therapy (ADT) being a standard treatment. However, the development of castration-resistant prostate cancer (CRPC) poses a significant challenge. CRPC is characterized by significantly increased tumor heterogeneity and lineage plasticity. Current research has primarily emphasized intrinsic tumor mechanisms, paying less attention to the role of the tumor microenvironment in cancer recurrence and drug resistance. In their recent study published in Cancer Cell, Wang and colleagues used single-cell RNA sequencing in genetically engineered mouse models with prostate tumors at different stages. They revealed that SPP1+ myofibroblastic cancer-associated fibroblasts (myCAF), induced by ADT, play an instrumental role in CRPC development. Their work also underscores the association between therapy-induced phenotypic alterations of CAFs and disease progression. This discovery highlights the potential for stromal compartment targeting as a means to mitigate CRPC development and overcome treatment resistance.
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