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Bournet, B., Souque, A., Senesse, P., Assenat, E., Barthet, M., Lesavre, N., Aubert, A., O’Toole, D., Hammel, P., Levy, P., Ruszniewski, P., Bouisson, M., Escourrou, J., Cordelier, P. and Buscail, L. (2009) Endoscopic ultrasound-guided fine-needle aspiration biopsy coupled with KRAS mutation assay to distinguish pancreatic cancer from pseudotumoral chronic pancreatitis. Endoscopy, 41(6), 552-557.

has been cited by the following article:

• TITLE: Promoter hypermethylation of tissue specific tumor supressor genes and point mutation in K-ras, c-myc proto-oncogenes in urinary (transitional cell) bladder carcinoma

  AUTHORS: Oztürk Ozdemir, Esin Yildiz, Semih Ayan, Eylem Gul, Gökhan Gokce, Fazilet Yildiz, Binnur Koksal

  KEYWORDS: C-myc; K-ras; Ki-67; Urinary Bladder; Urothelial Neoplasms; Promoter Hypermethylation; Tumor Supressor Genes

  JOURNAL NAME: Health, Vol.2 No.8, August 25, 2010

  ABSTRACT: In a total of 83 UN specimens were investigated for proto-oncogene mutations, tumor supressor genes promoter methylation status and c-myc and Ki-67 expression. Point mutations in c-myc were detected in cases with high grade and proliferation index. Mutated K-ras proto-onco- gene profiles were detected in 17 (21%) tumoral spiecemens that examined. Tumor specimens were also showed hypermethylated promoter domain for the SFRP2, MGMT tumor supressor genes. These findings showed the combine effect of mutated c-myc and K-ras oncogene and epigenetic inactivation of tissue specific tumor supressor genes (TS) play a crucial role in tumor progression and recurrence in UN carcinogenesis.