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Updated: Aug 8, 2026
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Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein
Published on: January 16, 2020
BRAF and KRAS mutations in prostatic adenocarcinoma
Nam-Yun Cho1, Minhee Choi, Baek-Hee Kim
1Laboratory of Epigenetics, Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
International Journal of Cancer
|May 25, 2006
Summary
BRAF and KRAS mutations are uncommon in prostate cancer, occurring in about 10% and 7% of tumors, respectively. BRAF mutations were linked to more advanced disease features compared to KRAS mutations.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- RAS/RAF/ERK signaling pathway activation is common in human cancers.
- KRAS mutations are known in prostate adenocarcinomas, but BRAF mutations are less understood.
- BRAF and KRAS mutations are mutually exclusive activators of the RAS/RAF/ERK pathway.
Purpose of the Study:
- To characterize BRAF and KRAS mutations in prostate adenocarcinomas.
- To analyze the clinicopathologic significance of these mutations.
- To compare the features of tumors with BRAF versus KRAS mutations.
Main Methods:
- Enhanced PCR-RFLP and direct sequencing were used to detect mutations.
- BRAF and KRAS mutations were analyzed in 206 prostate adenocarcinoma specimens.
- Mutation status was correlated with serum PSA, Gleason score, and tumor stage.
Main Results:
- BRAF mutations (codon 600) were found in 10.2% of tumors.
- KRAS mutations (codons 12 or 13) were found in 7.3% of tumors.
- No co-occurrence of BRAF and KRAS mutations was observed.
- BRAF-mutated tumors showed higher PSA, Gleason scores, and tumor stages than KRAS-mutated tumors.
Conclusions:
- BRAF mutations are as uncommon as KRAS mutations in prostate adenocarcinoma.
- BRAF and KRAS mutations, despite activating the same pathway, are associated with distinct clinicopathologic features in prostate cancer.
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