PURPOSE: Mutational activation of the MAP kinase pathway is frequently found in many types of cancer. Recently, activating mutations in the BRAF gene, an important activator of this pathway, have been described in several tumor types including melanoma, colorectal and papillary thyroid cancer. The most frequent mutation in exon 15 (V600E) as well as several other mutations within exons 11 and 15 result in constitutive activation of the oncoprotein. MATERIALS AND METHODS: Our study aimed to investigate BRAF mutations in 30 human bladder tumors and their adjacent normal tissues. The V600E mutation was screened by PCR/RFLP and exons 11, 14 and 15 of BRAF including intron-exon boundaries were sequenced. RESULTS: We detected two tumor specimens bearing two different mutations, both of which were found in exon 15. One sample showed the T1799A (V600E) and the other the G1798T (V600L) mutation. The first specimen was stage pT1a and grade II, whereas the second was stage pT2b and grade III. No mutations within the coding region of exons 11, 14, 15 and the intron-exon junctions for the remaining samples were found. CONCLUSIONS: Our results suggest that involvement of BRAF mutations in the development of transitional cell carcinoma of the bladder is infrequent.
PURPOSE: Mutational activation of the MAP kinase pathway is frequently found in many types of cancer. Recently, activating mutations in the BRAF gene, an important activator of this pathway, have been described in several tumor types including melanoma, colorectal and papillary thyroid cancer. The most frequent mutation in exon 15 (V600E) as well as several other mutations within exons 11 and 15 result in constitutive activation of the oncoprotein. MATERIALS AND METHODS: Our study aimed to investigate BRAF mutations in 30 human bladder tumors and their adjacent normal tissues. The V600E mutation was screened by PCR/RFLP and exons 11, 14 and 15 of BRAF including intron-exon boundaries were sequenced. RESULTS: We detected two tumor specimens bearing two different mutations, both of which were found in exon 15. One sample showed the T1799A (V600E) and the other the G1798T (V600L) mutation. The first specimen was stage pT1a and grade II, whereas the second was stage pT2b and grade III. No mutations within the coding region of exons 11, 14, 15 and the intron-exon junctions for the remaining samples were found. CONCLUSIONS: Our results suggest that involvement of BRAF mutations in the development of transitional cell carcinoma of the bladder is infrequent.
Authors: Apostolos Zaravinos; Maria Chatziioannou; George I Lambrou; Ioannis Boulalas; Dimitris Delakas; Demetrios A Spandidos Journal: Pathol Oncol Res Date: 2010-09-18 Impact factor: 3.201
Authors: Debyani Chakravarty; Jianjiong Gao; Sarah M Phillips; Ritika Kundra; Hongxin Zhang; Jiaojiao Wang; Julia E Rudolph; Rona Yaeger; Tara Soumerai; Moriah H Nissan; Matthew T Chang; Sarat Chandarlapaty; Tiffany A Traina; Paul K Paik; Alan L Ho; Feras M Hantash; Andrew Grupe; Shrujal S Baxi; Margaret K Callahan; Alexandra Snyder; Ping Chi; Daniel Danila; Mrinal Gounder; James J Harding; Matthew D Hellmann; Gopa Iyer; Yelena Janjigian; Thomas Kaley; Douglas A Levine; Maeve Lowery; Antonio Omuro; Michael A Postow; Dana Rathkopf; Alexander N Shoushtari; Neerav Shukla; Martin Voss; Ederlinda Paraiso; Ahmet Zehir; Michael F Berger; Barry S Taylor; Leonard B Saltz; Gregory J Riely; Marc Ladanyi; David M Hyman; José Baselga; Paul Sabbatini; David B Solit; Nikolaus Schultz Journal: JCO Precis Oncol Date: 2017-05-16
Authors: Alexander Skorokhod; Peter Helmbold; Benedikt Brors; Peter Schirmacher; Alexander Enk; Roland Penzel Journal: PLoS One Date: 2013-03-26 Impact factor: 3.240