BRAF and KRAS mutations in prostatic adenocarcinoma
BRAF and KRAS mutations in prostatic adenocarcinoma
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DOI：
10.1002/ijc.22071
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发表时间：
2006-10-15
影响因子：
6.4
通讯作者：
Kang, Gyeong Hoon
中科院分区：
文献类型：
--
作者：
Cho, Nam-Yun;Choi, Minhee;Kang, Gyeong Hoon
Ras、RAF、MEK和ERK信号通路的结构性激活在人类癌症中是常见的，KRAS和Bray突变是相互排斥的，可以替代激活Ras/RAF/ERK信号通路。已知RAS突变发生在前列腺癌中，但对这些肿瘤中的BRAF突变知之甚少。在本研究中，应用增强型聚合酶链式反应-限制性片段长度多态性和直接测序技术对206例前列腺癌患者的Bray和KRAS基因突变进行了研究。然后根据术前血清PSA水平、Gleason评分和肿瘤分期对已识别的KRAS和Bray突变进行分析。在206例前列腺癌中，21例(10.2%)检测到BRAF第600位密码子突变。在206例前列腺癌中，有15例(7.3%)存在KRAS基因第12或13密码子突变。然而，没有肿瘤标本同时含有BRAF和KRAS突变。BRAF基因突变的前列腺癌患者术前血清PSA水平、Gleason评分和肿瘤分期均高于KRAS基因突变的前列腺癌患者。结果表明，在前列腺癌中，BRAF突变和KRAS突变一样罕见。虽然BRAF和KRAS是相同的Ras/ERK信号通路成员，但BRAF突变的前列腺癌表现出不同于KRAS突变的前列腺癌的临床病理特征。(C)2006年Wiley-Liss，Inc.
Constitutive activation of the kinase cascade involving RAS, RAF, MEK and ERK is common to human cancers, and mutations of KRAS and BRAY are mutually exclusive and serve as alternatives to activate the RAS/RAF/ERK signaling pathway. RAS mutations are known to occur in prostate adenocarcinomas, hut little is known about BRAF mutations in these tumors. In the present study, BRAY and KRAS mutations were characterized in 206 prostate adenocarcinomas by enhanced PCR-RFLP and direct sequencing. The identified KRAS and BRAY mutations were then analyzed with respect to preoperative serum PSA levels, Gleason scores and tumor stages. Mutations in codon 600 of BRAF were identified in 21 (10.2%) of 206 prostate adenocarcinomas. KRAS mutations in codons 12 or 13 were found in 15 (7.3%) of 206 prostate adenocarcinomas. However, no tumor specimen contained both BRAF and KRAS mutations. Prostate adenocarcinomas with a BRAF mutation tended to show higher preoperative serum PSA levels, Gleason scores and tumor stages than prostate adenocarcinomas with a KRAS mutation. The results obtained show that BRAF mutations are as uncommon as KRAS mutations in prostate adenocarcinoma. Although BRAF and KRAS are members of the same RAS/ERK signaling pathway, prostate adenocarcinomas with a BRAF mutation showed clinicopathologic features that differed from those of prostate adenocarcinoma with a KRAS mutation. (c) 2006 Wiley-Liss, Inc.