title: CLC and IFNAR1 are differentially expressed and a global immunity score is distinct between early- and late-onset colorectal cancer.
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.
authors.affiliation: Department of Cancer Prevention, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
authors.forename: T H
authors.initials: TH
authors.lastname: Ågesen
authors.forename: M
authors.initials: M
authors.lastname: Berg
authors.forename: T
authors.initials: T
authors.lastname: Clancy
authors.forename: E
authors.initials: E
authors.lastname: Thiis-Evensen
authors.forename: L
authors.initials: L
authors.lastname: Cekaite
authors.forename: G E
authors.initials: GE
authors.lastname: Lind
authors.forename: J M
authors.initials: JM
authors.lastname: Nesland
authors.forename: A
authors.initials: A
authors.lastname: Bakka
authors.forename: T
authors.initials: T
authors.lastname: Mala
authors.forename: H J
authors.initials: HJ
authors.lastname: Hauss
authors.forename: T
authors.initials: T
authors.lastname: Fetveit
authors.forename: M H
authors.initials: MH
authors.lastname: Vatn
authors.forename: E
authors.initials: E
authors.lastname: Hovig
authors.forename: A
authors.initials: A
authors.lastname: Nesbakken
authors.forename: R A
authors.initials: RA
authors.lastname: Lothe
authors.forename: R I
authors.initials: RI
authors.lastname: Skotheim
mesh_terms: D000328:Adult; D017668:Age of Onset; D000368:Aged; D000369:Aged, 80 and over; D016000:Cluster Analysis; D015179:Colorectal Neoplasms / Q000453:epidemiology / Q000235:genetics* / Q000276:immunology*; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D006023:Glycoproteins / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D008245:Lysophospholipase / Q000235:genetics* / Q000378:metabolism; D008875:Middle Aged; D009367:Neoplasm Staging; D053633:Receptor, Interferon alpha-beta / Q000235:genetics* / Q000378:metabolism
chemical_list: D006023:Glycoproteins; C507964:IFNAR1 protein, human; D053633:Receptor, Interferon alpha-beta; D008245:Lysophospholipase; C011711:lysolecithin acylhydrolase