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Frequent microsatellite alterations of chromosome locus 4q13.1 in oral squamous cell carcinomas
Author(s) -
Lin ShuChun,
Chang MeiFong,
Chung MingYi,
Chang CheShoa,
Kao ShouYen,
Liu ChungJi,
Chang KuoWei
Publication year - 2005
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.2004.00296.x
Subject(s) - locus (genetics) , microsatellite , biology , allele , loss of heterozygosity , microsatellite instability , epidermoid carcinoma , head and neck squamous cell carcinoma , chromosome , basal cell , genetics , cancer research , pathology , carcinoma , gene , cancer , head and neck cancer , medicine
Background: Studies have revealed that losses of chromosome 4q24–25 regions are frequent in cancers including head and neck squamous cell carcinoma. Our previous comparative genomic hybridization analysis showed extensive losses of chromosome arm 4q in oral squamous cell carcinoma (OSCC). Methods: To be more precise in mapping the potential regions of allelic losses and to understand the microsatellite instability (MSI) on 4q involving in oral pathogenesis, we performed allelotypings using eight polymorphic markers. Microsatellite analyses were first performed on 100 randomly selected controls to confirm the high informative rates of markers. Twenty OSCC tissues were microdissected from surgical specimens for microsatellite alterations (MA) analysis. Results: MA was observed in 95% OSCC cases. The most eminently altered locus was 4q13.1 (75%), followed by 4q22.2 and 4q32.1 (55%). Allelic losses also occurred most frequently on these loci. Thirty‐five percent cases had MA spanning 4q13.1 to 4q21.1. MSI occurred in 35% OSCC, at a lesser extent compared with allelic losses. The most common locus for MSI was 4q21.2 (20%). In addition, 4q MSI was significantly associated with the lymph node metastasis of OSCC ( P = 0.01). So far, most tumor suppressor genes on 4q have not been specified. Conclusion: Our results were additive to previous findings and proposed novel scenario of suppressor loci located at 4q13.1–21.1 whose inactivation could be important for progression of OSCC.