DELETION MAPPING OF CHROMOSOME 3P AND 13Q AND PRELIMINARY-ANALYSIS OFTHE FHIT GENE IN HUMAN NONMELANOMA SKIN-CANCER

Citation
Sk. Sikkink et al., DELETION MAPPING OF CHROMOSOME 3P AND 13Q AND PRELIMINARY-ANALYSIS OFTHE FHIT GENE IN HUMAN NONMELANOMA SKIN-CANCER, Journal of investigative dermatology, 109(6), 1997, pp. 801-805
Citations number
45
ISSN journal
0022202X
Volume
109
Issue
6
Year of publication
1997
Pages
801 - 805
Database
ISI
SICI code
0022-202X(1997)109:6<801:DMOC3A>2.0.ZU;2-9
Abstract
Loss of heterozygosity of chromosomes 3p and 13q occurs frequently in human cutaneous squamous cell neoplasms, suggesting the presence of on e or more tumor suppressor genes on these chromosome arms that may be involved in the pathogenesis of this tumor type, To date there is no c lear evidence in cutaneous tumors where these putative genes are locat ed, In this study we have analyzed 20 squamous cell neoplasms that sho w allelic loss at chromosome 13q, and 22 squamous cell neoplasms that show allelic loss at chromosome 3p, in an attempt to define the smalle st area of deletion, One commonly deleted region was identified on chr omosome 13 that centred around 13q13, and two commonly deleted regions were identified on chromosome 3 that mapped to 3p24-pter and 3p12-p14 .1. Our findings suggest the presence of at least one tumor suppressor gene on chromosome 13 and two tumor suppressor genes on chromosome 3p that may be involved in the progression of these neoplasms, Deletions within the Fragile Histidine Triad gene, located at 3p14.2, have been reported in several tumors, leading to the suggestion that this gene is involved in tumor development, To evaluate the role of the Fragile Histidine Triad gene in nonmelanoma skin cancer, we have used reverse transcriptase polymerase chain reaction analysis to screen for deletio ns in 16 tumors (five basal cell carcinomas, five squamous cell carcin omas, five actinic keratoses, and one case of Bowen's disease) and HaC aT and A431 cell lines, A normal transcript was found to be expressed in 14 of 16 tumors and both cell lines, This suggests that the Fragile Histidine Triad gene is not a common target for deletion in Bowen's d isease and the cell lines HaCaT and A431.