Genetic and epigenetic alterations of the cyclin-dependent kinase inhibitors p15(INK4b) and p16(INK4a) in human thyroid carcinoma cell lines and primary thyroid carcinomas Academic Article Article uri icon

Overview

MeSH Major

  • Carcinoma
  • Thyroid Neoplasms

abstract

  • The high prevalence of p15 and p16 mutations in the cell lines described suggests involvement of these genes in immortalization in vitro. The p16 defects may have preexisted in a small subclone of the primary tumor that were selected for in vitro. Alternatively, p16 mutations may have arisen de novo during cell culture. Mutations of p15INK4b and p16INK4a do not appear to be critical events in the development of follicular adenomas or papillary carcinomas. However, de novo methylation of the 5' CpG island of p16 is common in primary tumors, indicating that the function of this gene may be lost as an epigenetic event during disease progression.

publication date

  • November 15, 1998

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1002/(SICI)1097-0142(19981115)83:10<2185::AID-CNCR18>3.0.CO;2-4

PubMed ID

  • 9827724

Additional Document Info

start page

  • 2185

end page

  • 93

volume

  • 83

number

  • 10