TY - JOUR
T1 - Hypoxia and pancreatic ductal adenocarcinoma
AU - Yamasaki, Akio
AU - Yanai, Kosuke
AU - Onishi, Hideya
N1 - Funding Information:
This study was supported by the Japan Society for the Promotion of Science KAKENHI Grant Numbers JP17H04283 JP18K08620 , and JP19K09124 .
Funding Information:
This study was supported by the Japan Society for the Promotion of Science KAKENHI Grant Numbers JP17H04283 , JP18K08620 , and JP19K09124 .
Publisher Copyright:
© 2020 Elsevier B.V.
PY - 2020/8/1
Y1 - 2020/8/1
N2 - 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.
AB - 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.
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U2 - 10.1016/j.canlet.2020.04.018
DO - 10.1016/j.canlet.2020.04.018
M3 - Review article
C2 - 32380129
AN - SCOPUS:85084418478
SN - 0304-3835
VL - 484
SP - 9
EP - 15
JO - Cancer Letters
JF - Cancer Letters
ER -