PMID- 15188450
OWN - NLM
STAT- MEDLINE
DCOM- 20040903
LR  - 20211203
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 40
IP  - 4
DP  - 2004 Aug
TI  - Loss of heterozygosity on chromosome 6 in HPV-16 positive cervical carcinomas 
      carrying the DRB1*1501-DQB1*0602 haplotype.
PG  - 277-84
AB  - High-risk human papillomaviruses (HPVs), specifically HPV-16 and -18, have been 
      associated with the development of carcinoma in situ (CIS) and of invasive 
      cervical cancer (CC). However, only a small fraction of HPV-infected women will 
      show signs of disease progression, suggesting that other factors in the 
      carcinogenic pathway are needed. We previously demonstrated that human leukocyte 
      antigen (HLA) DRB1*1501-DQB1*0602 (high risk) was associated with the development 
      of CIS and CC tumors in HPV-16-positive patients. To characterize the molecular 
      changes that could be relevant to tumor progression, we compared the extent of 
      loss of heterozygosity (LOH) on chromosome 6 in HPV-16-positive CIS patients who 
      were carriers of high-risk and neutral HLA haplotypes. CIS and CC cases 
      demonstrated similar LOH patterns. A wide range of LOH frequencies was found at 
      6p (10-53%) and 6q (5-28%) in CIS cases, suggesting that LOH is an early event in 
      the carcinogenic process. A comparative analysis of LOH frequencies in the 
      high-risk versus the neutral HLA haplotypes showed a statistically significant 
      difference in the extent of LOH at 6p24-p25 (58.6% versus 25.8%; P = 0.018) and 
      at 6p21.3 (79.3% versus 35.5%; P = 0.001), a region that contains the HLA 
      complex. LOH at this region could affect genes encoding HLA class I-II molecules, 
      as well as factors responsible for the assembly, transport, and stable expression 
      of HLA molecules. These losses may be a reflection of both an abnormal immune 
      response and a general genome-wide instability resulting from virus persistence.
CI  - Copyright 2004 Wiley-Liss, Inc.
FAU - Arias-Pulido, Hugo
AU  - Arias-Pulido H
AD  - Department of Molecular Genetics and Microbiology, University of New Mexico, 
      Health Sciences Center, School of Medicine, Albuquerque, New Mexico 87131, USA.
FAU - Joste, Nancy
AU  - Joste N
FAU - Wheeler, Cosette M
AU  - Wheeler CM
LA  - eng
GR  - R01AI32917/AI/NIAID NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (CBX5 protein, human)
RN  - 0 (Genetic Markers)
RN  - 0 (HLA-DQ Antigens)
RN  - 0 (HLA-DQ beta-Chains)
RN  - 0 (HLA-DQB1 antigen)
RN  - 0 (Membrane Glycoproteins)
RN  - 107283-02-3 (Chromobox Protein Homolog 5)
SB  - IM
MH  - Carcinoma/*genetics/*pathology
MH  - Carcinoma in Situ/*genetics
MH  - Chromobox Protein Homolog 5
MH  - Chromosome Deletion
MH  - Chromosome Mapping
MH  - Chromosomes, Human, Pair 6/*genetics
MH  - Female
MH  - Genetic Markers/genetics
MH  - HLA-DQ Antigens/*genetics
MH  - HLA-DQ beta-Chains
MH  - Haplotypes/*genetics
MH  - Humans
MH  - Loss of Heterozygosity/*genetics
MH  - Membrane Glycoproteins/*genetics
MH  - Neoplasm Invasiveness
MH  - Papillomaviridae/genetics/*isolation & purification
MH  - Papillomavirus Infections/*genetics
MH  - Uterine Cervical Neoplasms/*genetics/*virology
EDAT- 2004/06/10 05:00
MHDA- 2004/09/04 05:00
CRDT- 2004/06/10 05:00
PHST- 2004/06/10 05:00 [pubmed]
PHST- 2004/09/04 05:00 [medline]
PHST- 2004/06/10 05:00 [entrez]
AID - 10.1002/gcc.20048 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2004 Aug;40(4):277-84. doi: 10.1002/gcc.20048.