Department of Cancer Therapy and Research, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Department of Cancer Therapy and Research, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Cancer Lett. 2020 Aug 1;484:9-15. doi: 10.1016/j.canlet.2020.04.018. Epub 2020 May 5.
Chemotherapy and immunotherapy for pancreatic ductal adenocarcinoma (PDAC) have limited success. One reason for this is thought to be the cancer microenvironment surrounding PDAC. Hypoxia is a feature of the cancer microenvironment. Under hypoxia, different various molecules and signaling pathways are activated compared with normoxia. To develop a new effective therapeutic strategy for PDAC, we need to target these hypoxic conditions to overcome PDAC. To inhibit the malignant phenotype, the cellular changes that occur under hypoxia should be elucidated. Various molecules and signaling that are activated by hypoxia may contribute to the induction of malignant phenotypes of PDAC such as proliferation, invasion, tumorigenesis, chemosensitivity, and autophagy. If we can develop therapeutic approaches to target one of these molecules or signaling pathways, we may proceed to the next therapeutic step of successfully treating refractory PDAC.
化疗和免疫疗法治疗胰腺导管腺癌 (PDAC) 的效果有限。造成这种情况的一个原因被认为是 PDAC 周围的癌症微环境。缺氧是癌症微环境的一个特征。与正常氧相比，在缺氧条件下会激活不同的分子和信号通路。为了开发治疗 PDAC 的新有效治疗策略，我们需要针对这些缺氧条件来克服 PDAC。为了抑制恶性表型，应该阐明缺氧下发生的细胞变化。缺氧激活的各种分子和信号可能有助于诱导 PDAC 的恶性表型，如增殖、侵袭、肿瘤发生、化疗敏感性和自噬。如果我们能够开发针对这些分子或信号通路之一的治疗方法，我们可能会进入下一治疗步骤，成功治疗难治性 PDAC。
