Author(s): Jens Pfeiffer | Wolfgang Maier | Gerd J Ridder | Karim Zaoui | Ralf Birkenhäger
Journal: World Journal of Clinical Oncology
ISSN 2218-4333
Volume: 3;
Issue: 2;
Start page: 24;
Date: 2012;
Original page
Keywords: Genome-wide analysis | Head and neck cancer | Loss of heterozygosity | Multifocal cancer | Single nucleotide polymorphism microarray | Squamous cell carcinoma
ABSTRACT
AIM: To introduce an approach for the detection of putative genetic host factors that predispose patients to develop head and neck squamous cell carcinomas (HNSCC). METHODS: HNSCC most often result from the accumulation of somatic gene alterations found in tumor cells. A cancer-predisposing genetic background must be expected in individuals who develop multiple cancers, starting at an unexpectedly young age or with little carcinogen exposure. Genome-wide loss of heterozygosity (LOH) profiling by single nucleotide polymorphism microarray mapping was performed in a patient with a remarkable history of multifocal HNSCC. RESULTS: Regions of genomic deletions in germline DNA were identified on several chromosomes with a remarkable size between 1.6 Mb and 8.1 Mb (mega base-pair). No LOH was detected at the genomic location of the tumor suppressor gene P53. CONCLUSION: Specific patterns of germline DNA deletions may be responsible for susceptibility to HNSCC and should be further analyzed.
Journal: World Journal of Clinical Oncology
ISSN 2218-4333
Volume: 3;
Issue: 2;
Start page: 24;
Date: 2012;
Original page
Keywords: Genome-wide analysis | Head and neck cancer | Loss of heterozygosity | Multifocal cancer | Single nucleotide polymorphism microarray | Squamous cell carcinoma
ABSTRACT
AIM: To introduce an approach for the detection of putative genetic host factors that predispose patients to develop head and neck squamous cell carcinomas (HNSCC). METHODS: HNSCC most often result from the accumulation of somatic gene alterations found in tumor cells. A cancer-predisposing genetic background must be expected in individuals who develop multiple cancers, starting at an unexpectedly young age or with little carcinogen exposure. Genome-wide loss of heterozygosity (LOH) profiling by single nucleotide polymorphism microarray mapping was performed in a patient with a remarkable history of multifocal HNSCC. RESULTS: Regions of genomic deletions in germline DNA were identified on several chromosomes with a remarkable size between 1.6 Mb and 8.1 Mb (mega base-pair). No LOH was detected at the genomic location of the tumor suppressor gene P53. CONCLUSION: Specific patterns of germline DNA deletions may be responsible for susceptibility to HNSCC and should be further analyzed.
