Mutational activation of FGFR3 is not involved in the development of prostate cancer.

OBJECTIVE: The mutational constitutive activation of FGFR3 has been discovered in several malignancies but only limited data on FGFR3 mutations in prostate cancer are available. Most recently, activating FGFR3 mutations were described as being associated with low-grade prostate tumors. Therefore, we investigated the FGFR3 mutation status in a comprehensive series of prostate tumors.
METHODS: 102 archival formalin-fixed paraffin-embedded prostate tumors of patients treated with radical prostatectomy [with a low-grade subgroup (Gleason score ≤6) of 29 patients] as well as 29 incidental prostate tumors [low-grade tumors (Gleason score ≤6); n = 22] and 16 benign prostatic hyperplasia samples obtained by transurethral resection of the prostate were investigated. After microdissection and DNA isolation, all FGFR3 mutation hotspots discovered in human malignancies were analyzed using the SNaPshot(©) approach or restriction fragment length polymorphism (RFLP) analysis.
RESULTS: All cases could successfully be analyzed by SNaPshot; 80 cases were investigated using RFLP. No mutation in FGFR3 could be detected in any of the analyzed cases.
CONCLUSION: The most recently reported FGFR3 mutations in low-grade prostate tumors could not be verified in our series. There were also no mutations in prostate tumors from patients with concomitant bladder tumors as reported previously. These data suggest that the mutational activation of FGFR3 plays no important role in prostate carcinogenesis, which is in accordance with previous studies performed on smaller tumor cohorts.