Cell transformation by animal papillomaviruses

Ms, Campo

doi:10.1099/0022-1317-73-2-217

Cited by 24 publications

(12 citation statements)

References 28 publications

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“…E6 stimulates telomerase activity, which prevents ordinary replicative senescence. 37 E7 neutralizes the retinoblastoma pathway, 38 inhibiting both replicative and stress-induced senescence. 10 Despite such immortalization, agents that damage DNA can still induce senescence in some cancer cells, including HeLa, provided they have active p53 and Rb.…”

Section: Resultsmentioning

confidence: 99%

High NaCl Promotes Cellular Senescence

Dmitrieva¹,

Burg²

2007

Cell Cycle

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High extracellular NaCl was previously shown to increase the number of DNA breaks in mammalian cells in tissue culture, renal medullary cells in vivo, C. elegans and marine invertebrates. It was also shown to increase reactive oxygen species in renal cells, resulting in oxidation of proteins and DNA. Cellular senescence is a common response to such damage. Therefore, in the present studies we looked for signs of senescence in cells exposed to high NaCl. We find that (1) the rate of proliferation of HeLa cells exposed to high NaCl decreases gradually to the point of arrest, and the cells display signs of senescence, including hypertrophy and increased auto fluorescence. (2) High NaCl accelerates the appearance of senescence in primary mouse embryonic fibroblasts, as measured by senescence-associated beta-galactosidase activity (SA-beta-gal). (3) High NaCl retards growth and markedly decreases the life span of C. elegans, accompanied by features of accelerated aging, such as decreased locomotion and increased number of SA-beta-gal positive cells. (4) Mouse renal medullary cells, which are normally continuously exposed to high NaCl, express increased p16(INK4) (another indicator of senescence) much earlier than do cells in the renal cortex, which has the same level of NaCl as peripheral blood. We conclude that high NaCl accelerates cellular senescence and aging, most likely secondary to the DNA breaks and oxidative damage that it causes.

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Section: Resultsmentioning

confidence: 99%

High NaCl Promotes Cellular Senescence

Dmitrieva¹,

Burg²

2007

Cell Cycle

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“…BPV 4 DNA and antigens can be found in high copy numbers in the premalignant oesophageal papillomas, but not in the carcinomas. Cattle infected with BPV 4, which feed on bracken fern, have a high risk of oesophageal cancer, but the BPV 4 viral genome is not present in frank cancers or fully transformed cells (Campo, 1992). If this phenomenon holds true for human oesophageal carcinoma, we should predict a high seroprevalence for antibody against HPV.…”

Section: Oesophageal Carcinomamentioning

confidence: 99%

Reactivity to human papillomavirus type 16 L1 virus-like particles in sera from patients with genital cancer and patients with carcinomas at five different extragenital sites

et al. 2003

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A retrospective seroepidemiologic study was performed to examine the association between human papillomaviruses (HPV) 16 infection and carcinomas of the oropharynx, the oesophagus, penis and vagina. Sera were selected from the serum bank from the Antoni van Leeuwenhoek Hospital (Netherlands Cancer Institute) and the Slotervaart Hospital in Amsterdam, the Netherlands. Presence of HPV 16 specific antibody was assessed using HPV 16 L1 capsids. Sera positive for HPV 16 capsid antibody were further tested for antibody against HPV 16 E7 peptides. Prevalence of antibody against HPV 16 L1 capsids among both the negative control group without cancer and the negative control group with gastric cancer was 18%, while seroprevalence among the control group of patients with HPV-associated cervical squamous cell carcinoma was 47% (Po0.001). Among the patients with penile squamous cell carcinoma seroprevalence was 38% (Po0.001), among patients with oropharyngeal carcinoma 33% (P ¼ 0.04) and among patients with oesophageal squamous cell carcinoma 14% (P ¼ 0.7). The serological evidence for association between HPV 16 infection and both oropharyngeal carcinoma and penile carcinoma was established. The conclusion that no association was found between the presence of antibody against HPV 16 L1 capsids and oesophageal squamous cell carcinoma was in accordance with results of other studies carried out in the Netherlands using HPV DNA technology. In the subjects with HPV 16 L1 capsid antibody, no association was found between the antibody against HPV 16 E7 and clinical outcome.

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“…The prevalence of certain types of human pap illomavirus (HPV) in anogenital lesions has suggested a close association between viral infection and cervical can cer [1,2], The most common model used to study papillo mavirus has been bovine papillomavirus (BPV) type 1 infection in rodent cells [3], Despite the similar genomic organization of BPV and HPV, a number of functional differences in some genes suggest caution in extrapolating data from BPV to HPV and confirm the need for an in vitro system for HPV [4], The development of an experimental model to study HPV has been limited by the lack of a permissive cell cul ture and by difficulties in obtaining viral particles. Viral DNA transfection in primary and established cell lines has provided the only convenient method to investigate the molecular biology of HPV [5], However, this method cannot reproduce the natural history of virus infection because it forces the cells to receive abnormal quantities , HPV 11 productive infection in a nude mouse xenograft system [7], production of HPV 16 viral particles from a cell line derived from a human dysplastic lesion in a varia tion of the HPV 11 xenograft system [8], and HPV 31 pro duction in organotypic cultures of a cell line derived from a cervical intraepithelial lesion [9], Nevertheless, clear data on virion isolation of potential oncogenic HPVs from pathological lesions are still lacking.…”

Section: Sum M Arymentioning

confidence: 99%

Primary Keratinocytes Can Be Infected by Natural Isolates of Genital Human Papillomavirus

Venuti¹,

Lonardo

Standoli

et al. 1995

Intervirology

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Viral particles of human papillomavirus (HPV) types 11 and 16 were isolated from fiat condylomas and biopsies of dysplastic lesions and used to infect human keratinocytes. The presence of HPV DNA in infected cells was determined by molecular hybridization and the polymerase chain reaction. Late transcripts were detected shortly after infection. The persistence of HPV was limited to early passages after infection and the loss of viral DNA preceded cell culture senescence. Our experimental evidence supports the idea that pooling of several lesions can lead to the isolation of infectious HPV 16 virions.

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Cell transformation by animal papillomaviruses

Cited by 24 publications

References 28 publications

High NaCl Promotes Cellular Senescence

High NaCl Promotes Cellular Senescence

Reactivity to human papillomavirus type 16 L1 virus-like particles in sera from patients with genital cancer and patients with carcinomas at five different extragenital sites

Primary Keratinocytes Can Be Infected by Natural Isolates of Genital Human Papillomavirus

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