A. Gillenwater et al., MICROSATELLITE ALTERATIONS AT CHROMOSOME 8Q LOCI IN PLEOMORPHIC ADENOMA, Otolaryngology and head and neck surgery, 117(5), 1997, pp. 448-452
OBJECTIVE: To determine the extent, localization, and clinical signifi
cance of microsatellite loci alterations at sites of reported cytogene
tic abnormalities in pleomorphic adenomas. BACKGROUND: Pleomorphic ade
noma is a benign salivary gland tumor with a propensity for recurrence
and potential for malignant conversion. Although its cause remains un
clear, clonal cytogenetic abnormalities have been reported consistentl
y. DESIGN: DNA extracted from paired normal and tumor tissue specimens
from 1 patient with carcinoma ex pleomorphic adenoma and 17 patients
with pleomorphic adenoma (3 contained foci of carcinoma ex pleomorphic
adenoma) was evaluated for loss of heterozygosity at microsatellite l
oci with a multiplex polymerase chain reaction-based analysis. Correla
tion with clinical and pathologic features was performed. RESULTS: Ove
rall 10 (56%) of 18 cases manifested loss of heterozygosity at the loc
i tested. The frequency of loss of heterozygosity noted on 3p, 6q, 8p,
8q, and 12q microsatellite loci was 17%, 12%, 8%, 47%, and 27% of inf
ormative cases, respectively. Specimens from patients with carcinoma e
x pleomorphic adenoma showed a similar loss of heterozygosity incidenc
e at these loci. No apparent association between molecular abnormaliti
es and clinical-pathologic features was observed in this cohort. CONCL
USIONS: Loss of heterozygosity at microsatellite loci on 8q, a breakpo
int at which translocations have been previously documented in pleomor
phic adenoma, is a frequent event in this tumor. The incidence is not
increased in patients with focal carcinoma ex pleomorphic adenoma, sug
gesting that loss of heterozygosity at 8q is an early event in tumorig
enesis. Further evaluation at these loci is needed to identify potenti
al tumor suppressor genes that may be associated with the initiation a
nd progression of pleomorphic adenomas.