Despite the availability of largely effective treatments for breast cancer, such as the combination of aromatase inhibitors or anti-estrogens with cdk4/6 inhibitors for estrogen receptor positive/Her 2 negative breast cancer, breast cancer remains a significant cause of morbidity and mortality. This is due, in large part, to a very limited understanding of the mechanisms underlying the failure of conventional therapies and disease recurrence after tumor dormancy.

One cellular process that is activated in response to the majority of breast cancer treatments is autophagy. Proven to be an indispensable cellular function, autophagy is largely accepted as a pro-survival mechanism in tumor cells and has consequently generated significant interest in cancer research and treatment strategies. Autophagy plays multiple and often disparate roles during different stages of tumorigenesis and in response to anti-tumor treatments; in fact, autophagy is induced by almost all conventional treatments of breast cancer and is considered a target for pharmacologic blockade in the clinic. Consequently, it is important to further our understanding of this process and its role in breast cancer.

尽管有大量有效的乳腺癌治疗方法，例如芳香酶抑制剂或抗雌激素与 cdk4/6 抑制剂的组合治疗雌激素受体阳性/Her 2 阴性乳腺癌，但乳腺癌仍然是发病率和死亡率的重要原因。这在很大程度上是由于对常规疗法失败和肿瘤休眠后疾病复发的潜在机制的了解非常有限。

响应大多数乳腺癌治疗而被激活的一种细胞过程是自噬。自噬被证明是必不可少的细胞功能，在很大程度上被认为是肿瘤细胞的促生存机制，因此引起了对癌症研究和治疗策略的极大兴趣。自噬在肿瘤发生的不同阶段和对抗肿瘤治疗的反应中发挥着多种且通常不同的作用；事实上，几乎所有传统的乳腺癌治疗都会诱导自噬，并被认为是临床上药物阻断的靶点。因此，重要的是进一步了解这一过程及其在乳腺癌中的作用。