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KMID : 1001020100080010032
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Journal of Urologic Oncology
2010 Volume.8 No. 1 p.32 ~ p.39
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The Correlation of Survivals with BRAF and KRAS Mutations in Prostatic Adenocarcinoma
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Sung Byung-Ju
Chung Jae-Min
Chang Hee-Kyung
Choi Seong
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Abstract
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Purpose: KRAS and BRAF are members of the MAP kinase (MAPK) pathway, which is hyperactive in approximately 30% of all cancers. We evaluated the mutational status of KRAS and BRAF in adenocarcinomas of the prostate.
Materials and Methods : BRAF and KRAS mutations were characterized in 103 prostate adenocarcinomas using PCR/sequencing. The identified KRAS and BRAF mutations were analyzed via pre-treatment serum PSA, Gleason score, clinical tumor staging, and overall survival. Chi square testing, one-way ANOVA testing, and the Kaplan Meier method were used to perform association studies.
Results: BRAF mutations were identified in 7 (6.8%) of 103 prostate adenocarcinomas. All mutations in codon 600 of the BRAF gene were Val600Glu (c.1799T＞A) mutations. Mutations in codons 12 and 13 of KRAS were found in 30 (29.1%) of 103 prostate adenocarcinomas. All 30 KRAS mutations were Gly12Asp (c.35G＞A) mutations. There was no concordant mutation of BRAF and KRAS in any single tumor specimen. Tumors with KRAS mutations, tumors with BRAF mutations, and tumors with neither mutation were no different statistically based on the Gleason score, clinical tumor stage, and pre-treatment serum PSA level. Prostate adenocarcinomas with BRAF mutations tended to be associated with lower overall survival than those with KRAS mutations and those with neither mutation (12.6 months vs. 32.2 months, 40.9 months, p=0.006).
Conclusions : Prostate adenocarcinomas with BRAF mutations tended to be associated with a lower overall survival compared to those with KRAS mutations and those with neither mutation.
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KEYWORD
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BRAF, KRAS, Prostate adenocarcinoma
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