Mapping of genetic deletions on the long arm of chromosome 22 in human pancreatic adenocarcinomas.
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.
Handel-Fernandez
M E
ME
Department of Microbiology and Immunology, University of Miami School of Medicine, Miami, FL 33136, USA.
Nassiri
M
M
Arana
M
M
Perez
M M
MM
Fresno
M
M
Nadji
M
M
Vincek
V
V
D000230:Adenocarcinoma / Q000235:genetics*; D002874:Chromosome Mapping; D002892:Chromosomes, Human, Pair 22 / Q000235:genetics*; D017353:Gene Deletion; D016515:Genes, Neurofibromatosis 2 / Q000235:genetics; D016147:Genes, Tumor Suppressor / Q000235:genetics; D005819:Genetic Markers; D006801:Humans; D019656:Loss of Heterozygosity / Q000235:genetics*; D018895:Microsatellite Repeats; D010190:Pancreatic Neoplasms / Q000235:genetics*; D016133:Polymerase Chain Reaction
D005819:Genetic Markers