Abstract
Pancreatic cancer is characterized by constitutive activation of the mitogen-activated protein kinase (MAPK) pathway. Mutations of KRAS or BRAF and epigenetic abrogation of DUSP6 contribute synergistically to the constitutive activation of MAPK. Active MAPK induces the expression of a variety of genes that are thought to play roles in malignant phenotypes of pancreatic cancer. By blocking the functions of such induced genes, it is possible to attenuate the malignant phenotypes. The development of drugs targeting genes downstream of MAPK may provide a novel therapeutic option for pancreatic cancer.
Highlights
Pancreatic cancer is one of the leading causes of cancer mortality in Japan and many western countries [1, 2]
Pancreatic cancer is characterized by constitutive activation of the mitogen-activated protein kinase (MAPK) pathway
Mutations of KRAS observed in pancreatic cancers often occur in codons 12, 13, and 61, at most are G12D or G12R substitutions, which attenuates the intrinsic GTPase activity, such mutations result in prolonged activation of RAS [6]
Summary
Reviewed by: Robert Klein, Icahn School of Medicine at Mount Sinai, USA Yong Zhang, AntiCancer Inc., USA. Pancreatic cancer is characterized by constitutive activation of the mitogen-activated protein kinase (MAPK) pathway. Mutations of KRAS or BRAF and epigenetic abrogation of DUSP6 contribute synergistically to the constitutive activation of MAPK. Active MAPK induces the expression of a variety of genes that are thought to play roles in malignant phenotypes of pancreatic cancer. By blocking the functions of such induced genes, it is possible to attenuate the malignant phenotypes.The development of drugs targeting genes downstream of MAPK may provide a novel therapeutic option for pancreatic cancer
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