Increasing levels of MYC and MET co-amplification during tumor progression of a case of gastric cancer

Cancer Genet Cytogenet. 1995 Jul 15;82(2):140-5. doi: 10.1016/0165-4608(95)00033-l.

Abstract

The cytogenetic study of a nodal metastasis from a gastric carcinoma, after two passages in nude mice, revealed a large number of double minutes. Comparative genomic in situ hybridization (CGH) analysis using DNA extracted from this xenograft revealed the existence of three clear amplification units that originated from the chromosomal subregions 6q24-25, 7q31-32, and 8q24 in the xenograft DNA. Similar, though less prominent, CGH results were found with DNAs extracted from the primary tumor and its metastasis, implying that the same amplicons were also present, albeit less abundantly, in the DNAs of these neoplastic tissues. Southern analysis of the second-passage xenograft detected 18- and 10-fold amplification of MET (located at 7q31) and MYC (located at 8q24), respectively. The retrospective study of the first passage of the xenograft, as well as of the metastatic and primary tumors before xenografting, showed amplification levels of MET of, respectively, 12-, 9-, and 5-fold and MYC of, respectively, 8-, 7-, and 5-fold. Our results suggest that increased levels of co-amplification of MYC and MET correlate with enhanced growth potential in this case of gastric carcinoma.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • DNA, Neoplasm / analysis
  • Gene Amplification
  • Genes, myc / genetics*
  • Humans
  • In Situ Hybridization
  • Male
  • Proto-Oncogene Proteins c-met
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / physiopathology

Substances

  • DNA, Neoplasm
  • Proto-Oncogene Proteins c-met
  • Receptor Protein-Tyrosine Kinases