BRAF and KRAS mutations in prostatic adenocarcinoma

Constitutive activation of the kinase cascade involving RAS, RAF, MEK and ERK is common to human cancers, and mutations of KRAS and BRAF are mutually exclusive and serve as alternatives to activate the RAS/RAF/ERK signaling pathway. RAS mutations are known to occur in prostate adenocarcinomas, but l...

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Published in:International journal of cancer 2006-10, Vol.119 (8), p.1858-1862
Main Authors: Cho, Nam‐Yun, Choi, Minhee, Kim, Baek‐Hee, Cho, Yong‐Mee, Moon, Kyung Chul, Kang, Gyeong Hoon
Format: Article
Language:English
Subjects:
Adenocarcinoma - genetics
Adenocarcinoma - pathology
Aged
Base Sequence
Biological and medical sciences
BRAF
Humans
KRAS
Male
Medical sciences
Middle Aged
Mutation - genetics
Nephrology. Urinary tract diseases
Oncogene Protein p21(ras) - genetics
prostate adenocarcinoma
Prostatic Neoplasms - genetics
Prostatic Neoplasms - pathology
Proto-Oncogene Proteins B-raf - genetics
Tumors
Tumors of the urinary system
Urinary tract. Prostate gland
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Summary:Constitutive activation of the kinase cascade involving RAS, RAF, MEK and ERK is common to human cancers, and mutations of KRAS and BRAF are mutually exclusive and serve as alternatives to activate the RAS/RAF/ERK signaling pathway. RAS mutations are known to occur in prostate adenocarcinomas, but little is known about BRAF mutations in these tumors. In the present study, BRAF and KRAS mutations were characterized in 206 prostate adenocarcinomas by enhanced PCR‐RFLP and direct sequencing. The identified KRAS and BRAF 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. © 2006 Wiley‐Liss, Inc.
ISSN:0020-7136
1097-0215
DOI:10.1002/ijc.22071