Does human papillomavirus cause cervical cancer? The state of the epidemiological evidence

Muñóz, Núbia; Bosch, Xavier; Kaldor, John

doi:10.1038/bjc.1988.1

Cited by 188 publications

(56 citation statements)

References 33 publications

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“…38,39 Briefly, 2 ± 5.10 8 cells were harvested by trypsinization (0.15% trypsin, 0.015%. EDTA), washed once with cold PBS, and centrifuged for 5 min at 16006g.…”

Section: Isolated Nucleimentioning

confidence: 99%

“…30,38 Briefly, cells were collected after treatment with trypsin-EDTA (0.15%, 0.015% respectively), washed once with cold PBS, once with extraction buffer (EB) (50 mM PIPES pH 7.4, 50 mM KCl, 5 mM EGTA, 100 mM PMSF, 2 mM MgCl 2 , 1 mM DTT, 20 mM cytochalasin B, COMPLETE 1 ), resuspended in 1 vol of EB, and pelleted at 20006g for 5 min directly into a dounce homogenizer. The cell pellet was resuspended in 1 vol of 94% (v/v) ethanol and quickly frozen at 7808C.…”

Section: Cytoplasmic Extractsmentioning

confidence: 99%

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Staurosporine-induced apoptosis of HPV positive and negative human cervical cancer cells from different points in the cell cycle

et al. 2001

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In the present study, we compare the sensitivity of CaSki and HeLa cells (HPV positive, wild-type p53) and C33A cells (HPV negative, mutated p53) to a protein kinase inhibitor, the staurosporine (ST). We show that ST can reversibly arrest the three cervical-derived cell lines, either in G1 or in G2/M. Beyond certain ST concentrations or/and over 24 h exposure, the cells underwent apoptosis. This process took place in G1 and G2/M for C33A and CaSki plus HeLa cell lines, respectively. By using an in vitro cell-free system, we demonstrated that cytoplasmic extracts from apoptotic cells were sufficient to induce hallmarks of programmed cell death on isolated nuclei. Moreover, we found that only G2/M cytoplasmic extracts from viable CaSki and HeLa cells supplemented with ST, triggered apoptosis while exclusively G1 cytoplasmic fractions from C33A cells were efficient. Our study describes a possible involvement of the HPV infection or/and p53 status in this different ST-induced apoptosis susceptibility. Cell Death and Differentiation (2001) 8, 234 ± 244.

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“…38,39 Briefly, 2 ± 5.10 8 cells were harvested by trypsinization (0.15% trypsin, 0.015%. EDTA), washed once with cold PBS, and centrifuged for 5 min at 16006g.…”

Section: Isolated Nucleimentioning

confidence: 99%

Section: Cytoplasmic Extractsmentioning

confidence: 99%

Staurosporine-induced apoptosis of HPV positive and negative human cervical cancer cells from different points in the cell cycle

et al. 2001

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“…Approximately 25 HPV types have been detected in the anogenital tract, and epidemiological and biological evidence has pointed to a role for some of these viruses in the pathogenesis of cervical cancer (Munoz, 1988;zur Hausen, 1991).…”

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confidence: 99%

Detection and typing of human papillomaviruses present in fixed and stained archival cervical smears by a consensus polymerase chain reaction and direct sequence analysis allow the identification of a broad spectrum of human papillomavirus types

Smits¹,

Tieben

Tjong-A-Hung³

et al. 1992

Journal of General Virology

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“…However, some of these studies are difficult to interpret because of methodological flaws in study design (Munoz et al, 1988) or because of the inaccuracy of the hybridisation techniques used to detect HPV DNA (Schiffman, 1992). Recently a reliable and sensitive HPV detection strategy based on the polymerase chain reaction (PCR) has been developed in several laboratories (Manos et al., 1989;van den Brule et al, 1990) and is now considered the technique of choice for epidemiological studies (Schiffman, 1992).…”

mentioning

confidence: 99%

Human papillomavirus and invasive cervical cancer in Brazil

Eluf-Neto

Booth²,

Muñóz³

et al. 1994

Br J Cancer

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217

109

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Summary A hospital-based case-control study was undertaken to examine the role of human papillomavirus (HPV) (e.g. HPV 6, 11, 42, 43, 44) have been associated with condylomata acuminata and CIN I (Howley, 1991;Lorincz et al., 1992).Epidemiological studies investigating the relation between HPV and cervical neoplasia have found strong associations . However, some of these studies are difficult to interpret because of methodological flaws in study design (Munoz et al., 1988) or because of the inaccuracy of the hybridisation techniques used to detect HPV DNA (Schiffman, 1992). Recently a reliable and sensitive HPV detection strategy based on the polymerase chain reaction (PCR) has been developed in several laboratories (Manos et al., 1989;van den Brule et al., 1990) and is now considered the technique of choice for epidemiological studies (Schiffman, 1992). Employing this technique, two recent studies have found high risks of cervical cancer associated with HPV (Peng et al., 1991;Munoz et al., 1992).In developing countries cancer of the cervix is the leading cancer even when sites common to both sexes are combined (Parkin et al., 1988). This hospital-based case-control study using PCR was undertaken to examine the role of HPV in the development of invasive cervical cancer in Sao Paulo, Brazil, a city with one of the highest incidence rates of this disease worldwide (Muir et al., 1987). Patients and methods Study populationBetween June 1990 and June 1991 women with a diagnosis of invasive cervical cancer and women selected as controls were recruited from seven hospitals in Sao Paulo City. Five of these are general hospitals, and two are hospitals for the treatment of cancer. The cases were women between 25 and 79 years of age, whose diagnosis was confirmed by histopathology and who had had no previous treatment for the disease. Controls were enrolled from the same five general hospitals from which the cases were recruited. For cases from the hospitals in which only cancer patients are treated (n = 48), controls were selected from the largest general hospital included in the study. This was because had the cancer cases had another disease it is likely that they would have been treated there as it is the most commonly used referral hospital in the city. Controls were frequency matched to cases in 5-year age groups. Those with diseases associated with known risk factors for cervical neoplasia were excluded (sexually transmitted diseases, coronary heart disease, cerebrovascular disease, arterial thromboembolism, thrombophlebitis, chronic bronchitis, emphysema, neoplasia of the breast, reproductive and respiratory organs, anus, oral cavity, oesophagus, bladder and liver). Women who were admitted for treatment of a gynaecological condition or who had had a hysterectomy or conisation were ineligible as controls. Women with a psychiatric illness were ineligible as cases or as controls. Evidence of a gynaecological or cytological abnormality detected on examination after recruitment was not a criterion for exclusion.A ...

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Does human papillomavirus cause cervical cancer? The state of the epidemiological evidence

Cited by 188 publications

References 33 publications

Staurosporine-induced apoptosis of HPV positive and negative human cervical cancer cells from different points in the cell cycle

Staurosporine-induced apoptosis of HPV positive and negative human cervical cancer cells from different points in the cell cycle

Detection and typing of human papillomaviruses present in fixed and stained archival cervical smears by a consensus polymerase chain reaction and direct sequence analysis allow the identification of a broad spectrum of human papillomavirus types

Human papillomavirus and invasive cervical cancer in Brazil

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