Chromosomal characterizations of human nasal and nasopharyngeal cells immortalized by human papillomavirus type 16 DNA

Dębiec‐Rychter, Maria; Zukowski, Kim; Wang, Ching Yung; Wen, Wu-Nan

doi:10.1016/0165-4608(91)90053-w

Cited by 13 publications

(4 citation statements)

References 23 publications

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“…Analysis of our present findings and previously reported data suggest that gains at 1q31-q32 and 7p13-p14, as well as losses at 6q26-q27 are alterations that are unique for HPV18 positive cases. HPV integration at the 1q31-q32 has been found in nasal epithelial cells immortalized with HPV16 DNA and also contains the short tandem repeat region F13B [15]. The NEK7 (NIMA (never in mitosis gene a)-related kinase 7, 1q31.3) gene is located in this region and plays an important role in the control of mitosis initiation [16].…”

Section: Resultsmentioning

confidence: 99%

Chromosomal imbalances in four new uterine cervix carcinoma derived cell lines

Hidalgo

Monroy²,

Arana

et al. 2003

BMC Cancer

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Background: Uterine cervix carcinoma is the second most common female malignancy worldwide and a major health problem in Mexico, representing the primary cause of death among the Mexican female population. High risk human papillomavirus (HPV) infection is considered to be the most important risk factor for the development of this tumor and cervical carcinoma derived cell lines are very useful models for the study of viral carcinogenesis. Comparative Genomic Hybridization (CGH) experiments have detected a specific pattern of chromosomal imbalances during cervical cancer progression, indicating chromosomal regions that might contain genes that are important for cervical transformation.

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Section: Resultsmentioning

confidence: 99%

Chromosomal imbalances in four new uterine cervix carcinoma derived cell lines

Hidalgo

Monroy²,

Arana

et al. 2003

BMC Cancer

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“…We also noted breakpoints at lq44 and lq42, which are in close proximity to the TGFBZ locus. In addition, anomalies in the region lq32-qter may be involved in the process of cell immortalization (Paraskeva et al, 1989;Paraskeva, 1990;Sugarawa et al, 1990), mediated by, for example, human papillomavirus type 16, which may integrate at this location (Debiec-Rychter et al, 1991) and is a suspected aetiological agent of oral squamous cell carcinoma (Yeudall and Campo, 1991). Several putative suppressor genes are located on both the long and short arms of chromosome 1 (Olah et al, 1989), and the high frequency of breakpoints detected in this study may implicate a loss of function of one or more of these genes in cell transformation.…”

Section: Discussionmentioning

confidence: 99%

Consistent chromosomal anomalies in keratinocyte cell lines derived from untreated malignant lesions of the oral cavity

Patel

Yeudall

Gardner

et al. 1993

Genes Chromosomes & Cancer

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Cytogenetic analysis has been carried out on 8 early passage cell lines derived from 8 untreated human oral squamous cell carcinomas. Clonal aberrations were detected in the karyotypes of each cell line. A high frequency of breakpoints were noted on chromosomes 1, 7, 8, 9, 11, and X. An isochromosome 8 was present in 6 out of 8 cell lines; isochromosome 9 (3 cell lines) and isochromosome 11 (1 cell line) were also found. In 4 out of 8 cell lines X chromosome harboured breakpoints, a novel finding in oral squamous cell carcinomas. Breakpoints were common on chromosome 1, with 1p12-p13 most frequently involved. Tandem duplication of 11q13-q23, which contains a number of growth regulatory genes, was also noted in 2 cases. We correlate the sites of proto-oncogenes and other growth control genes with chromosomal breakpoints and suggest that several of these may play a role in the pathogenesis of oral cancer.

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“…(92)(93)(94) Analyses of several foreskin and cervical keratinocyte lines hybridized with radiolabeled HPV-16 DNA indicated that one or two in tegration sites were presen t in each cell line with the viral sequences at the junction of chromosome translocations within duplicated chromosomal regions, HSR, or diffusely stained regions. Furthermore, a comparison of the HPV data with those of literature regarding other DNA viruses has led to the conclusion that there is a clustering of viral integration sites within fragile chromosomal sites strongly indicating the existence of nonrandom viral integration in a human genome.…”

Section: Cyfogenetic Alterations In Cervical Neoplasiamentioning

confidence: 99%

“…Normal genital epithelial cells transfected with recombinant HPV became permanent cell lines only with oncogenic HPVs that exhibited transcriptionally active viral sequences with the HPV integrated into the cellular genome. (90,91) The most frequent alteration involved chromosome l. (92)(93)(94) The majority of these HPV-immortalized cell lines were nontumorigenic, independent of the origin of the target cells. The evidence suggests that alterations of chromosome 1 are important to escape from terminal cell differentiation and result in selective growth advantage.…”

Section: Cyfogenetic Alterations In Cervical Neoplasiamentioning

confidence: 99%