No evidence for fibroblast growth factor receptor 3 (FGFR-3) R248C/S249C mutations in human prostate cancer
2000; Wiley; Volume: 87; Issue: 3 Linguagem: Inglês
10.1002/1097-0215(20000801)87
ISSN1097-0215
AutoresBenyoussef Naïmi, Alain Latil, Philippe Berthon, Olivier Cussenot,
Tópico(s)Urological Disorders and Treatments
ResumoInternational Journal of CancerVolume 87, Issue 3 p. 455-456 Letter to the editorFree Access No evidence for fibroblast growth factor receptor 3 (FGFR-3) R248C/S249C mutations in human prostate cancer Benyoussef Naimi, Corresponding Author Benyoussef Naimi b.naimi@cerepp.org CeRePP-Université Paris, Paris France UroGène, Génopole, Evry, FranceCeRePP-Université Paris VII EA3104 and UroGène, Génopole, 4 rue Pierre Fontaine, 91000 Evry, France. Fax: +33(0)160878989Search for more papers by this authorAlain Latil, Alain Latil CeRePP-Université Paris, Paris FranceSearch for more papers by this authorPhilippe Berthon, Philippe Berthon CeRePP-Université Paris, Paris FranceSearch for more papers by this authorOlivier Cussenot, Olivier Cussenot CeRePP-Université Paris, Paris FranceSearch for more papers by this author Benyoussef Naimi, Corresponding Author Benyoussef Naimi b.naimi@cerepp.org CeRePP-Université Paris, Paris France UroGène, Génopole, Evry, FranceCeRePP-Université Paris VII EA3104 and UroGène, Génopole, 4 rue Pierre Fontaine, 91000 Evry, France. Fax: +33(0)160878989Search for more papers by this authorAlain Latil, Alain Latil CeRePP-Université Paris, Paris FranceSearch for more papers by this authorPhilippe Berthon, Philippe Berthon CeRePP-Université Paris, Paris FranceSearch for more papers by this authorOlivier Cussenot, Olivier Cussenot CeRePP-Université Paris, Paris FranceSearch for more papers by this author First published: 10 July 2000 https://doi.org/10.1002/1097-0215(20000801)87:3 3.0.CO;2-QCitations: 5AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Dear Sir, Several genetic studies show that specific point mutations in fibroblast growth factor receptor 3 (FGFR-3) are associated with autosomal dominant human skeletal dysplasia and craniosynostosis syndromes (Meyers et al., 1995; Rousseau et al., 1994). Mutations leading to ligand independence prompt constitutive activation of FGFR-3 and show that FGFR-3 acts as a negative regulator of bone growth (Colvin et al., 1996; Deng et al., 1996). Conversely, the same FGFR-3 mutations have been found in multiple melanoma (MM) and in bladder and cervical carcinomas, suggesting that FGFR-3 may act as an oncogenic factor (Cappellen et al., 1999; Chesi et al., 1997). The FGFs have been associated with prostate cancer progression. Stroma–epithelium interactions may be disrupted during prostate cancer tumorigenesis, leading to independent growth of more aggressive epithelial clones in which autocrine expression of FGFs is required (Ropiquet et al., 1999). To investigate whether the FGF autocrine pathway is acquired through FGFR-3 mutation-dependent activation in human prostate cancer, we analyzed the mutational status of the junction (517 bp) between the immunoglobulin-like domains II and III of FGFR-3. This region has been described as the most frequently mutated in bladder and cervical carcinomas, specifically with the missense mutation S249C (Cappellen et al., 1999). We analyzed 20 human prostate tumors from patients undergoing surgery (Table I). The FGFR-3 sequence (517 bp) was amplified using the forward primer 5′-AGGACGAGGCTGAGGACA-3′ and the reverse primer 5′-CTTGAGCACGGTAACGTA-3′. The PCR product was purified to remove primer dimers and excess nucleotides and sequenced using the ABI Prism Dye Terminator Cycle Sequencing Kit on the ABI377 sequencer (PE Biosystem). The resulting sequences compared to wild-type sequences using CLUSTAL W. software, version 1.8 (Thompson et al., 1994), revealed no mutations in the subset of tumors analyzed. Table I. Characterization of Human Prostate Tumors Analyzed for FGFR-3 Mutations Sample Gleason score Clinical stage Histopathological stage T1 7 A pT3N0M0 T2 7 B pT3N1M0 T3 7 B pT3N0M0 T4 7 A pT3N0M0 T5 6 B pT2N0M0 T6 7 C pT2N0M0 T7 6 A pT3N0M0 T8 7 B pT2N0M0 T9 7 B pT2N0M0 T10 8 D3 pT3NXM+ T11 7 D3 pT3NXM+ T12 8 D3 pT3NXM+ T13 — C pT3NxM0 T14 7 D3 pT3NXM+ T16 9 D3 pT3NXM+ T17 8 D3 pT3NXM+ T18 8 D3 pT3NXM+ T20 7 A pT2cN0M0 T21 7 B pT2bN0M0 T22 7 B pT2cN0M0 Capellen and colleagues (1999) reported frequent activating mutations of FGFR-3 in human bladder and cervical carcinomas, with >30% of cases in the bladder. The S249C mutation was the most common, affecting 5 of 9 bladder cancers and 3 of 3 cervical cancers carrying mutations. We found no evidence for similar mutations in human prostate tumors. From these data, therefore, it appears that FGFR-3 mutations may be restricted to particular types of human malignancy. Additional studies are required on other types of cancer, to determine the exact contribution and distribution of FGFR-3 mutations in human carcinomas. Yours sincerely, REFERENCES REFERENCES Cappellen, D., De Oliveira, C., Ricol, D., De Medina, S., Bourdin, J., Sastre-garau, X., Chopin, D., Thiery, J.P. and Radvanyi, F., Frequent activating mutations of FGFR-3 in human bladder and cervix carcinomas. Nature (Genet.), 23, 18- 20 (1999). 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