Centre Hospitalier Universitaire du Sart Tilman Liège and Liège University, Domaine Universitaire du Sart Tilman, B35, 4000 Liège, Belgium.
Centre de Recherche en Cancérologie de Lyon, Inserm U1052 CNRS 5286, Centre Léon Bérard, 28 rue Laënnec, 69373 LYON cedex 08, Lyon, France.
Cancer Treat Rev. 2015 Feb;41(2):94-104. doi: 10.1016/j.ctrv.2014.12.011. Epub 2014 Dec 30.
Disease progression despite existing endocrine therapies remains a major challenge to the effective management of hormone-receptor-positive (HR(+)), human epidermal growth factor receptor-2-negative (HER2(-)), advanced breast cancer. Recent advances in elucidating the molecular mechanisms of disease progression have identified the existence of adaptive "cross-talk" between the estrogen receptor (ER) and various growth factor receptor and intracellular signaling pathways, allowing breast cancer cells to escape the inhibitory effects of endocrine therapy. These findings provide the clinical rationale for enhancing or extending endocrine sensitivity by combining endocrine therapy with a targeted agent against a compensatory pathway. In BOLERO-2, adding the mTOR inhibitor everolimus to endocrine therapy significantly improved progression-free survival (PFS) in patients with HR(+) advanced breast cancer previously treated with nonsteroidal aromatase inhibitor therapy. Notably, PFS benefits were comparable in subgroup analyses of first- and later-line settings. These results contrast with those of the large first-line HORIZON study, wherein adding the mTOR inhibitor temsirolimus to endocrine therapy did not improve PFS. Therefore, it is unclear whether a targeted agent should only be combined with endocrine therapy to restore endocrine sensitivity or whether it may also prevent or delay resistance in hormone-sensitive advanced breast cancer. Numerous additional targeted agents are currently being evaluated in combination with endocrine therapies, including PI3K, cyclin-dependent kinase 4/6, SRC, and histone deacetylase inhibitors. Appropriate patient selection based on prior treatment history will become increasingly important in maximizing the incremental benefit derived from these new agents combined with existing endocrine therapies in HR(+) advanced breast cancer.
尽管存在内分泌治疗,疾病进展仍然是激素受体阳性(HR(+))、人表皮生长因子受体 2 阴性(HER2(-))、晚期乳腺癌有效管理的主要挑战。最近在阐明疾病进展的分子机制方面的进展表明,雌激素受体(ER)与各种生长因子受体和细胞内信号通路之间存在适应性“串扰”,使乳腺癌细胞能够逃避内分泌治疗的抑制作用。这些发现为通过将内分泌治疗与针对补偿途径的靶向药物联合使用来增强或延长内分泌敏感性提供了临床依据。在 BOLERO-2 中,将 mTOR 抑制剂依维莫司加入内分泌治疗显著改善了先前接受非甾体芳香酶抑制剂治疗的 HR(+)晚期乳腺癌患者的无进展生存期(PFS)。值得注意的是,在一线和二线亚组分析中,PFS 获益相当。这些结果与大型一线 HORIZON 研究的结果形成对比,其中加入 mTOR 抑制剂替西罗莫司联合内分泌治疗并未改善 PFS。因此,尚不清楚靶向药物是否仅应与内分泌治疗联合使用以恢复内分泌敏感性,或者它是否也可以预防或延迟激素敏感的晚期乳腺癌的耐药性。目前正在评估许多其他靶向药物与内分泌疗法联合使用,包括 PI3K、细胞周期蛋白依赖性激酶 4/6、SRC 和组蛋白去乙酰化酶抑制剂。基于先前治疗史的适当患者选择将在最大限度地提高这些新药物与 HR(+)晚期乳腺癌中现有内分泌疗法联合使用所带来的增量获益方面变得越来越重要。