Mapping of genetic deletions on the long arm of chromosome 22 in human pancreatic adenocarcinomas

M. E. Handel-Fernandez, M. Nassiri, M. Arana, M. M. Perez, M. Fresno, M. Nadji, V. Vincek

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


The molecular mechanisms of carcinogenesis in pancreatic cancer are still poorly understood, although the inactivation of tumor suppressor genes at multiple loci is suspected. We investigated the loss of heterozygosity (LOH) on chromosome 22 in pancreatic cancer by means of a PCR-based microsatellite analysis of archival paraffin-embedded histological sections in order to better define deleted region(s) and to test whether the NF-2 gene is involved. Using a panel of thirteen markers that spanned the long arm of chromosome 22, loss of heterozygosity was identified for at least one locus in 37% of investigated pancreatic adenocarcinomas. These deletions are clustered into two separate areas of the chromosome 22 - one proximal to the NF-2 gene and one distal. The NF-2 gene itself is not involved. These regions are likely locations of tumor suppressor genes that may contribute to the development of pancreatic cancer.

Original languageEnglish (US)
Pages (from-to)4451-4456
Number of pages6
JournalAnticancer research
Issue number6 B
StatePublished - 2000


  • Chromosome 22
  • Microsatellite
  • Pancreatic cancer
  • Tumor suppressor gene

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


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