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This study aimed to explore the efficacy and potential mechanisms of rechallenge therapy with Microtubule-targeting agents (MTAs) in patients with HER2-low metastatic breast cancer (MBC). We performed a systematic review to investigate the rechallenge treatment concept in the field of HER2-low MBC treatment and utilized a series of cases identified in the literature to illustrate the concept.

本研究旨在探讨微管靶向药物（MTA）对HER2低转移性乳腺癌（MBC）患者再次攻击治疗的疗效和潜在机制。我们进行了系统评价，以调查HER2低MBC治疗领域的再次挑战治疗概念，并利用文献中确定的一系列病例来说明这一概念。

Here, we reported two clinical cases of HER2-low MBC patients whose disease progressed after prior treatment with MTAs such as docetaxel and vincristine. When rechallenged with Disitamab Vedotin ((RC48-antibody-drug conjugate (ADC), a monomethyl auristatin (MMAE) MTA)), both patients achieved a partial response and the final progression-free survival (PFS) was 13.5 or 9 months, respectively.

在这里，我们报告了两例HER2低MBC患者的临床病例，这些患者在接受多西他赛和长春新碱等MTA治疗后疾病进展。当用地西他单抗Vedotin（（RC48抗体-药物偶联物（ADC），一种单甲基auristatin（MMAE）MTA））再次攻击时，两名患者均获得部分缓解，最终无进展生存期（PFS）分别为13.5或9个月。

Genomic profiling detected a PIK3CA H1047R mutation in the patients. Patients were treated with everolimus before being rechallenged with RC48, which may lead to a better response. This study further summarizes and analyzes the potential mechanism of the PI3K-AKT signaling pathway in MTAs resistance and reveals that the PIK3CA H1047R mutation may be a potential molecular marker for the efficacy prediction of mTOR inhibitors, providing new insights and potential therapeutic strategies for the application of MTAs to MBC patients. .

基因组分析在患者中检测到PIK3CA H1047R突变。患者在接受RC48再次攻击之前接受了依维莫司治疗，这可能会导致更好的反应。本研究进一步总结和分析了PI3K-AKT信号通路在MTAs耐药中的潜在机制，揭示了PIK3CA H1047R突变可能是mTOR抑制剂疗效预测的潜在分子标记，为MTAs在MBC患者中的应用提供了新的见解和潜在的治疗策略。。。