TY - JOUR
T1 - Analysis of chromosome 9p21 deletion and p16 gene mutation in salivary gland carcinomas
AU - Cerilll, Lisa A.
AU - Swartzbaugh, Joanna R.
AU - Saadut, Rega
AU - Marshall, Carina E.
AU - Rumpel, Craig A.
AU - Moskaluk, Christopher A.
AU - Frierson, Henry F.
N1 - Funding Information:
From the Department of Pathology, The University of Virginia Health Sciences Center, Charlottesville, VA. Accepted for publication June 25, 1999. Supported by grant number 5K08CA74431-02 to C.A.M from the National Cancer Institute. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the National Cancer Institute. Address correspondence and reprint requests to Lisa A. Cerilli, MD, Department of Pathology, Box 214, University of Virginia Health Sciences Center, Charlottesville, VA 22908. Copyright © 1999 by W.B. Saunders Company 0046-8177/99/3010-0019510.00/0 salivary duct carcinoma showed a homozygous deletion of pl6 in differential polymerase chain reaction analysis. Loss of heterozygosity was fotmd in 1 of 10 adenoid cystic carcinomas and I of 8 mucoepider-moid carcinomas and was absent in the remaining subtypes. No mutations in exon 1 or exon 2 or homozygous deletion of pl6 were found in these 2 particular neoplasms with LOH. These results suggest that inactivation of pl6 is important in the development or progression of at least some salivary duct carcinomas, but we found no evidence that its alteration plays a role in the other subtypes examined. HUM PATHOL 30:1242-1246. Key words: salivary gland cancer, pl 6, 9p, salivary duct carcinoma.
PY - 1999/10
Y1 - 1999/10
N2 - The chromosomal locus 91p21 contains the p16(INK4a/CDKN2/MTS1) tumor suppressor gene that has been implicated in a variety of tumor types, including carcinomas of the head and neck, esophagus, and pancreas. To determine whether the loss of this gene is involved in salivary gland cancers, 35 carcinomas and paired nonneoplastic specimens were analyzed for loss of heterozygosity (LOH) of polymorphic genetic markers located in the region of interest. Five types of salivary gland tumors were studied: mucoepidermoid carcinoma, salivary duct carcinoma, adenoid cystic carcinoma, acinic cell carcinoma, and polymorphous low-grade adenocarcinoma. Seven of 9 salivary duct carcinomas showed LOH of 1 or more polymorphic markers. In 1 case of salivary duct carcinoma with LOH, we confirmed a deletion of bp 240- 254 within exon 2. In addition, another salivary duct carcinoma showed a homozygous deletion of p16 in differential polymerase chain reaction analysis. Loss of heterozygosity was found in 1 of 10 adenoid cystic carcinomas and 1 of 8 mucoepidermoid carcinomas and was absent in the remaining subtypes. No mutations in exon 1 or exon 2 or homozygous deletion of p16 were found in these 2 particular neoplasms with LOH. These results suggest that inactivation of p16 is important in the development or progression of at least some salivary duct carcinomas, but we found no evidence that its alteration plays a role in the other subtypes examined.
AB - The chromosomal locus 91p21 contains the p16(INK4a/CDKN2/MTS1) tumor suppressor gene that has been implicated in a variety of tumor types, including carcinomas of the head and neck, esophagus, and pancreas. To determine whether the loss of this gene is involved in salivary gland cancers, 35 carcinomas and paired nonneoplastic specimens were analyzed for loss of heterozygosity (LOH) of polymorphic genetic markers located in the region of interest. Five types of salivary gland tumors were studied: mucoepidermoid carcinoma, salivary duct carcinoma, adenoid cystic carcinoma, acinic cell carcinoma, and polymorphous low-grade adenocarcinoma. Seven of 9 salivary duct carcinomas showed LOH of 1 or more polymorphic markers. In 1 case of salivary duct carcinoma with LOH, we confirmed a deletion of bp 240- 254 within exon 2. In addition, another salivary duct carcinoma showed a homozygous deletion of p16 in differential polymerase chain reaction analysis. Loss of heterozygosity was found in 1 of 10 adenoid cystic carcinomas and 1 of 8 mucoepidermoid carcinomas and was absent in the remaining subtypes. No mutations in exon 1 or exon 2 or homozygous deletion of p16 were found in these 2 particular neoplasms with LOH. These results suggest that inactivation of p16 is important in the development or progression of at least some salivary duct carcinomas, but we found no evidence that its alteration plays a role in the other subtypes examined.
KW - 9p
KW - P16
KW - Salivary duct carcinoma
KW - Salivary gland cancer
UR - http://www.scopus.com/inward/record.url?scp=0032862936&partnerID=8YFLogxK
U2 - 10.1016/S0046-8177(99)90044-8
DO - 10.1016/S0046-8177(99)90044-8
M3 - Article
C2 - 10534174
AN - SCOPUS:0032862936
SN - 0046-8177
VL - 30
SP - 1242
EP - 1246
JO - Human Pathology
JF - Human Pathology
IS - 10
ER -