CLC and IFNAR1 are differentially expressed and a global immunity score is distinct between early- and late-onset colorectal cancer

Genes Immun. 2011 Dec;12(8):653-62. doi: 10.1038/gene.2011.43. Epub 2011 Jun 30.

Abstract

Colorectal cancer (CRC) incidence increases with age, and early onset of the disease is an indication of genetic predisposition, estimated to cause up to 30% of all cases. To identify genes associated with early-onset CRC, we investigated gene expression levels within a series of young patients with CRCs who are not known to carry any hereditary syndromes (n=24; mean 43 years at diagnosis), and compared this with a series of CRCs from patients diagnosed at an older age (n=17; mean 79 years). Two individual genes were found to be differentially expressed between the two groups, with statistical significance; CLC was higher and IFNAR1 was less expressed in early-onset CRCs. Furthermore, genes located at chromosome band 19q13 were found to be enriched significantly among the genes with higher expression in the early-onset samples, including CLC. An elevated immune content within the early-onset group was observed from the differentially expressed genes. By application of outlier statistics, H3F3A was identified as a top candidate gene for a subset of the early-onset CRCs. In conclusion, CLC and IFNAR1 were identified to be overall differentially expressed between early- and late-onset CRC, and are important in the development of early-onset CRC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Age of Onset
  • Aged
  • Aged, 80 and over
  • Cluster Analysis
  • Colorectal Neoplasms / epidemiology
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / immunology*
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic*
  • Glycoproteins / genetics*
  • Glycoproteins / metabolism
  • Humans
  • Lysophospholipase / genetics*
  • Lysophospholipase / metabolism
  • Middle Aged
  • Neoplasm Staging
  • Receptor, Interferon alpha-beta / genetics*
  • Receptor, Interferon alpha-beta / metabolism

Substances

  • Glycoproteins
  • IFNAR1 protein, human
  • Receptor, Interferon alpha-beta
  • Lysophospholipase
  • lysolecithin acylhydrolase