Avoiding Extinction: Cancer-Associated Fibroblasts Help Triple-Negative Breast Cancer Outrun Chemotherapy.
Avoiding Extinction: Cancer-Associated Fibroblasts Help Triple-Negative Breast Cancer Outrun Chemotherapy.
复制标题
避免灭绝：癌症相关成纤维细胞帮助三阴性乳腺癌战胜化疗。
DOI：
10.1158/0008-5472.can-23-2770
复制
发表时间：
2023
期刊：
影响因子：
11.2
通讯作者：
Echeverria,GloriaV
中科院分区：
文献类型：
--
作者：
Wall,StevenW;Echeverria,GloriaV
新辅助化疗是三阴性乳腺癌（TNBC）治疗的主要方法。基于部分细胞杀伤的原理，化疗方案通常是短时间药物暴露的周期，然后是从毒副作用中恢复的一段时间。然而，许多患者由于各种原因而经历化疗耐药性，导致肿瘤不能通过治疗充分减少。手术切除前对化疗的反应是患者预后的一个强有力的预测因素;因此，寻找提高疗效的方法是一个关键的需求。人们已经做出了巨大的努力来了解肿瘤微环境与许多肿瘤类型的治疗敏感性之间的关系。在这一期的《癌症研究》中，Miroshnychenko及其同事研究了癌症相关成纤维细胞（CAF）诱导的肿瘤细胞增殖的良好特征化现象如何使TNBC在多个细胞毒性化疗周期后逃避灭绝。他们的发现意味着CAF促进的肿瘤细胞增殖允许肿瘤细胞通过治疗引起的压力条件，并避免肿瘤消除。这种“间接”化学抗性的机制与肿瘤细胞增殖增强化学敏感性的教条形成对比。这项研究为发现机制和治疗靶点打开了大门，以限制CAF将肿瘤细胞从灭绝边缘拯救出来的能力。第3681页
Neoadjuvant chemotherapy is a staple of triple-negative breast cancer (TNBC) treatment. Predicated on the principle of fractional cell killing, chemotherapy regimens are typically cycles of short drug exposure followed by a period of recovery from the toxic side effects. However, many patients experience chemotherapy resistance for a variety of reasons, resulting in tumors that are not sufficiently reduced with treatment. Response to chemotherapy prior to surgical resection is a strong predictor of patient prognosis; therefore, finding ways to improve efficacy is a critical need. Tremendous effort has gone into understanding the relationship between the tumor microenvironment and treatment sensitivity in many tumor types. In this issue ofCancer Research, Miroshnychenko and colleagues investigate how the well-characterized phenomenon of cancer-associated fibroblast (CAF)–induced proliferation of tumor cells allows TNBC to evade extinction after multiple cycles of cytotoxic chemotherapies. Their findings imply CAF-promoted tumor cell proliferation allows tumor cells to push through stressful conditions caused by treatment and to avoid tumor elimination. This mechanism of ‘indirect’ chemoresistance contrasts with the dogma that tumor cell proliferation enhances chemosensitivity. This study opens the door for the discovery of mechanisms and therapeutic targets to limit the ability of CAFs to rescue tumor cells from the brink of extinction.See related article by Miroshnychenko et al., p. 3681