Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
2006-4-20
pubmed:abstractText
Oncogene-expressing human papillomavirus type 16 (HPV16) is found in a subset of head and neck squamous cell carcinomas (HNSCC). HPV16 drives carcinogenesis by inactivating p53 and pRb with the viral oncoproteins E6 and E7, paralleled by a low level of mutations in TP53 and allelic loss at 3p, 9p, and 17p, genetic changes frequently found in HNSCCs of nonviral etiology. We hypothesize that two pathways to HNSCC exist: one determined by HPV16 and the other by environmental carcinogens. To define the critical genetic events in these two pathways, we now present a detailed genome analysis of HNSCC with and without HPV16 involvement by employing high-resolution microarray comparative genomic hybridization. Four regions showed alterations in HPV-negative tumors that were absent in HPV-positive tumors: losses at 3p11.2-26.3, 5q11.2-35.2, and 9p21.1-24, and gains/amplifications at 11q12.1-13.4. Also, HPV16-negative tumors demonstrated loss at 18q12.1-23, in contrast to gain in HPV16-positive tumors. Seven regions were altered at high frequency (>33%) in both groups: gains at 3q22.2-qter, 5p15.2-pter, 8p11.2-qter, 9q22-34.1, and 20p-20q, and losses at 11q14.1-qter and 13q11-33. These data show that HNSCC arising by environmental carcinogens are characterized by genetic alterations that differ from those observed in HPV16-induced HNSCC, and most likely occur early in carcinogenesis. A number of genetic changes are shared in both tumor groups and can be considered crucial in the later stages of HNSCC progression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2558-64
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:16314836-Adult, pubmed-meshheading:16314836-Aged, pubmed-meshheading:16314836-Carcinoma, Squamous Cell, pubmed-meshheading:16314836-Female, pubmed-meshheading:16314836-Gene Dosage, pubmed-meshheading:16314836-Gene Expression Regulation, Neoplastic, pubmed-meshheading:16314836-Genome, pubmed-meshheading:16314836-Head and Neck Neoplasms, pubmed-meshheading:16314836-Humans, pubmed-meshheading:16314836-Male, pubmed-meshheading:16314836-Microarray Analysis, pubmed-meshheading:16314836-Middle Aged, pubmed-meshheading:16314836-Nucleic Acid Hybridization, pubmed-meshheading:16314836-Oncogene Proteins, Viral, pubmed-meshheading:16314836-Papillomaviridae, pubmed-meshheading:16314836-Papillomavirus E7 Proteins, pubmed-meshheading:16314836-Papillomavirus Infections, pubmed-meshheading:16314836-Repressor Proteins, pubmed-meshheading:16314836-Signal Transduction, pubmed-meshheading:16314836-Tumor Suppressor Protein p53
pubmed:year
2006
pubmed:articleTitle
Genome-wide DNA copy number alterations in head and neck squamous cell carcinomas with or without oncogene-expressing human papillomavirus.
pubmed:affiliation
Department of Otolaryngology/Head-Neck Surgery, VU University Medical Center, Amsterdam, The Netherlands.
pubmed:publicationType
Journal Article, Comparative Study