title: Prognostic relevance of 20q13 gains in sporadic colorectal cancers: a FISH analysis.
abstract: BACKGROUND
  Amplification of 20q13 is a frequent chromosomal alteration in solid tumors and harbors a number of putative oncogenes (CAS/CSE1-L, NABC1, or Aurora2). Amplifications on 20q13 have been identified as an independent prognostic marker indicating worse survival in breast and ovarian cancer. However, little is known about the prognostic significance of 20q13 gains in sporadic colorectal cancers. The aim of this study was to correlate 20q13 gains in sporadic colorectal cancers with other known prognostic factors, tumor progression, and overall survival.
  
  
  METHODS
  Nuclei were extracted from 146 paraffin-embedded colorectal cancers of different UICC stages and used for fluorescence in situ hybridization (FISH) with a directly labeled probe for 20q13.2 (VYSIS). Signals were counted in 120 nuclei per sample. 20q13 was considered gained when > or =40% of the nuclei showed 3 or more FISH signals. Statistical correlations were tested with log-rank tests and Kaplan-Meier survival curves.
  
  
  RESULTS
  Signal numbers for 20q13.2 were gained in 78 cases (53%). Cases with gains on 20q13.2 showed worse outcome than cases without: the gain of 20q13.2 was an independent prognostic marker for overall survival (P=0.006) as well as tumor progression (P=0.012) in univariate and multivariate analyses. Gains on 20q13.2 did not correlate with tumor stage. However, there was a significant association between 20q13.2 gains and tumor location in the left-sided colon and an inverse correlation between histologic grade and 20q13.2 gains.
  
  
  CONCLUSIONS
  These data indicate that gains on 20q13.2 correlate with faster tumor progression and worse patient survival independent from tumor size and lymph node involvement. Therefore, alterations on 20q13 are an important biological event in colorectal tumor progression with independent prognostic relevance.
authors.affiliation: Pathologisches Institut der Ludwig-Maximilians-Universität, München, Germany. Daniela.Aust@pathologie.med.tu-dresden.de
authors.forename: D E
authors.initials: DE
authors.lastname: Aust
authors.forename: M
authors.initials: M
authors.lastname: Muders
authors.forename: A
authors.initials: A
authors.lastname: Köhler
authors.forename: M
authors.initials: M
authors.lastname: Schmidt
authors.forename: J
authors.initials: J
authors.lastname: Diebold
authors.forename: C
authors.initials: C
authors.lastname: Müller
authors.forename: U
authors.initials: U
authors.lastname: Löhrs
authors.forename: F M
authors.initials: FM
authors.lastname: Waldman
authors.forename: G B
authors.initials: GB
authors.lastname: Baretton
mesh_terms: D000236:Adenoma / Q000235:genetics; D002890:Chromosomes, Human, Pair 20 / Q000235:genetics*; D015179:Colorectal Neoplasms / Q000737:chemistry / Q000235:genetics*; D005260:Female; D005784:Gene Amplification; D006801:Humans; D007150:Immunohistochemistry; D017404:In Situ Hybridization, Fluorescence; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
chemical_list: D016159:Tumor Suppressor Protein p53