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Loss of heterozygosity at 10q in tumors of the upper respiratory tract is associated with poor prognosis
Author(s) -
Gasparotto Daniela,
Vukosavljevic Tamara,
Piccinin Sara,
Barzan Luigi,
Sulfaro Sandro,
Armellin Michela,
Boiocchi Mauro,
Maestro Roberta
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990820)84:4<432::aid-ijc18>3.0.co;2-#
Subject(s) - loss of heterozygosity , respiratory tract , medicine , respiratory system , oncology , respiratory disease , pathology , biology , lung , genetics , allele , gene
Frequent loss of a specific chromosomic region in cancers is often associated with inactivation of a tumor‐suppressor gene. The long arm of chromosome 10 is deleted in several types of tumor, among them squamous‐cell carcinomas of the head and neck (HNSCC). To determine the role of 10q deletions in the tumorigenesis of the upper respiratory tract, 47 HNSCCs were examined for loss of heterozygosity (LOH) at 10q: 43% of the cases analyzed showed LOH at 10q, and 2 distinct hot spots of deletion were identified, at 10q22‐23 and 10q25‐26. The possible involvement of pTEN/MMAC1, a tumor‐suppressor gene mapped at 10q23, was also evaluated. No mutation, homozygous deletion or loss of expression of pTEN/MMAC1 was detected, indicating that inactivation of this gene plays a minor role in HNSCC development. Interestingly, the frequency of deletion at 10q was greater in invasive carcinoma than in adjacent carcinoma in situ, and a significant association between LOH and poor prognosis was observed. Taken together, our results suggest the presence in the long arm of chromosome 10 of (a) tumor‐suppressor gene(s) other than pTEN/MMAC1 and presumably involved in the malignant progression of tumors of the upper respiratory tract. Int. J. Cancer (Pred. Oncol.) 84:432–436, 1999. © 1999 Wiley‐Liss, Inc.