Impacts of activation of the mitogen-activated protein kinase pathway in pancreatic cancer.

Impacts of activation of the mitogen-activated protein kinase pathway in pancreatic cancer.
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DOI:
10.3389/fonc.2015.00023
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发表时间:
2015
影响因子:
4.7
通讯作者:
Furukawa T
Furukawa T
中科院分区:
医学3区
文献类型:
--
作者:
Furukawa T

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胰腺癌的特征在于丝裂原活化蛋白激酶(MAPK)途径的组成性活化。KRAS或BRAF的突变和DUSP6的表观遗传废除协同地有助于MAPK的组成型激活。活性MAPK诱导被认为在胰腺癌的恶性表型中起作用的多种基因的表达。通过阻断这种诱导基因的功能,可以减弱恶性表型。针对MAPK下游基因的药物开发可能为胰腺癌的治疗提供新的选择。
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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