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癌症中的丝裂原活化蛋白激酶信号通路。

MAP kinase signalling pathways in cancer.

作者信息

Dhillon A S, Hagan S, Rath O, Kolch W

机构信息

The Beatson Institute for Cancer Research, Bearsden, Glasgow, UK.

出版信息

Oncogene. 2007 May 14;26(22):3279-90. doi: 10.1038/sj.onc.1210421.

DOI:10.1038/sj.onc.1210421
PMID:17496922
Abstract

Cancer can be perceived as a disease of communication between and within cells. The aberrations are pleiotropic, but mitogen-activated protein kinase (MAPK) pathways feature prominently. Here, we discuss recent findings and hypotheses on the role of MAPK pathways in cancer. Cancerous mutations in MAPK pathways are frequently mostly affecting Ras and B-Raf in the extracellular signal-regulated kinase pathway. Stress-activated pathways, such as Jun N-terminal kinase and p38, largely seem to counteract malignant transformation. The balance and integration between these signals may widely vary in different tumours, but are important for the outcome and the sensitivity to drug therapy.

摘要

癌症可被视为一种细胞间及细胞内通讯的疾病。这些异常具有多效性,但丝裂原活化蛋白激酶(MAPK)通路尤为突出。在此,我们讨论关于MAPK通路在癌症中作用的最新发现和假说。MAPK通路中的癌性突变通常主要影响细胞外信号调节激酶通路中的Ras和B-Raf。应激激活通路,如Jun氨基末端激酶和p38,在很大程度上似乎会对抗恶性转化。这些信号之间的平衡与整合在不同肿瘤中可能差异很大,但对治疗结果和药物治疗敏感性很重要。

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