Yeh, C.W., Huang, S.S., Lee, R.P. and Yung, B.Y. (2006) Ras-Dependent Recruitment of c-myc for Transcriptional Activation of Nucleophosmin/B23 in Highly Malignant U1 Bladder Cancer Cells. Molecular Pharmacology, 70(4), 1443-1453.

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.