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Results for “Cervical Cancer--etiology”

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At least 19 recordsLinked to original sources
PubMed1991

Biology of female sex hormone action in relation to contraceptive agents and neoplasia.

This article will present an overview of estrogen and progestin action at a cellular level, with emphasis on points that are relevant to neoplasia. In breast, endometrium and ovary, these two classes of hormone are clearly implicated in carcinogenesis, but their involvement with cancers of the liver, cervix and other tissues is more problematic. In the latter situations, I will highlight the major points to be considered if the hormones are involved without wishing to judge whether there actually is a causal involvement.

Animals↗
PubMed1991

Oral contraceptives and cervical neoplasia.

Although initial studies examining the relationship of oral contraceptives to risk of cervical neoplasia were reassuring, more recent studies provide some evidence of a positive relationship, particularly for long-term usage. Results, however, are difficult to interpret, because of a variety of methodologic complexities, including potential sources of confounding and bias. Sexual behavior and Pap smear screening have been identified as important confounders, but in several well-controlled studies residual excess risks of nearly 2-fold persist for users of 5 or more years. A possible promotional effect of oral contraceptives is suggested by higher risks associated with recent usage. There also is some suggestion of a stronger effect for adenocarcinomas than for squamous cell tumors. A relationship is biologically possible, given findings of hormone receptors in cervical tissue and the fact that oral contraceptives have been found to induce cervical hyperplasia. In addition, oral contraceptives may induce proliferation of the human papillomaviruses, the leading suspect agent for cervical cancer. Although a number of lines of evidence support a relationship of oral contraceptives to cervical cancer risk, firm conclusions await the results of additional studies that specifically address some of the methodologic shortcomings of previous investigations. In particular, additional follow-up studies are needed to define the effect of oral contraceptives on the natural history of cervical lesions.

Adenocarcinoma↗
PubMed1992

Human papillomavirus (HPV) infection, HIV infection and cervical cancer in Tanzania, east Africa.

The presence of HPV-DNA was determined in tumor biopsies of cervical-cancer patients and in cervical swabs of non-cancer patients from Tanzania, East Africa, by Southern blot hybridization and/or PCR. HPV types 16 and 18 were detected in 38% and 32%, respectively, of 50 cervical-carcinoma biopsies. A consensus primer PCR capable of detecting a broad spectrum of HPV types revealed the presence of HPV-DNA in 59% of 359 cervical swabs of non-cancer patients. Type-specific PCR showed that types 16 and 18 accounted for 13.2% and 17.5%, respectively, of all HPV infections. Therefore we concluded that HPV 18 is more prevalent in Tanzania than in any other geographical location so far reported. The strongest risk factors for the presence of any HPV-DNA in the 359 female non-cancer patients were young age and HIV infection. The epidemiology of HPV types 16 and 18 was found to differ from that of other HPV types, being associated in univariate analysis with trichomonas vaginalis infection, martial status (single/divorced), age at first intercourse, and young age at menarche. However, young age at menarche accounted for most of the effects of all other, variables in multivariate analysis. Of the non-cancer patients, 12.8% had antibodies against HIV I (no patient being severely symptomatic), and HIV infection was highly correlated with the presence of HPV-DNA, especially types 16 and 18. While HPV-DNA of any type was detectable 1.4-fold more often in HIV-positive patients than in HIV-negative patients, evidence of an infection with HPV types 16 or 18 was found 2.2-fold more often in the HIV-positive patients. The HIV-positive women did not show an increased rate of cervical cytological abnormalities as assessed by PAP staining of a single cervical smear, the overall rate of abnormalities being 2.8%. Furthermore, the age-adjusted prevalence of HIV antibodies was found to be considerably lower in 270 cervical-carcinoma patients (3% HIV-positive) in comparison with non-cancer patients. Thus there was no association observable between the prevalence of HIV infections and the frequency of cervical cytological abnormalities or cervical cancer in the setting of this cross-sectional study.

Cervix Uteri↗
PubMed1990

Oncogenic transformation by human papillomavirus type 16 deoxyribonucleic acid in the presence of progesterone or progestins from oral contraceptives.

Compelling evidence supports a role of certain types of human papillomaviruses as the cause of cervical cancer. In addition to human papillomaviruses, other agents, such as hormones, have been implicated as cofactors in this type of neoplasia. In this study we provide evidence for oncogenic transformation of primary baby rat kidney cells by human papillomavirus type 16 deoxyribonucleic acid plus ras oncogene in the presence of progesterone but not estrogen. Integrated and intact human papillomavirus type 16 deoxyribonucleic acid is present and expressed in all the five progesterone-transformed colonies that we examined. Moreover, all these cell lines are capable of anchorage-independent growth and induce tumors in syngeneic animals. We also observed oncogenic transformation with human papillomavirus type 16 deoxyribonucleic acid plus ras in the presence of ethanol-soluble extracts from two brands of commonly used oral contraceptive tablets. No transformation is achieved in the presence of ethanol-soluble extracts from the inert tablets, provided in packages of each brand of oral contraceptive. These results may have implications for a papillomavirus-hormone link to cervical neoplasia.

Administration, Oral↗
PubMed1978

Sperm basic proteins in cervical carcinogenesis: Correlation with socioeconomic class.

Two types of basic protein, a histone and a protamine, were separated from single ejaculates of human sperm and a ratio between their contents in a given number of sperm established. The ratio varied widely in different males and correlated with ranking by social class: the lower the social class, the greater the proportion of protamine. Statistically similar correlations link social class with the incidence of venereal disease and the incidence of in-situ carcinoma of the cervix, both of which are epidemiological variables in squamous cervical cancer. The basic proteins of the sperm head, especially the protamines, may thus also have a role in the aetiology of squamous cervical cancer.

Carcinogens↗
PubMed1990

Relative and attributable risk for cervical cancer: a comparative study in the United States and Italy.

The attributable risk for invasive cervical cancer in the US and Italian populations has been estimated in relation to main 'aetiological' factors (number of sexual partners, age at first intercourse, parity, oral contraceptive use and smoking) and history of Pap smear using data from two case-control studies conducted in the US (466 cases and 788 controls) and Italy (528 cases and 456 controls). The risk of cervical cancer increased in both studies with multiple sexual partners, decreasing age at first intercourse, higher parity, oral contraceptive use and smoking. Levels of exposure to various risk factors were markedly different in the two countries (ie number of sexual partners, frequency of oral contraceptive use and smoking were greater in the US). Multiple Pap smears and a short interval since last Pap smear strongly reduced risk of cervical cancer in both populations, although screening was much more widespread in the US study population, with only 9% of controls reporting no previous smear versus 38% of the Italian control series. The combined population attributable risk for the five 'aetiological' risk factors was slightly greater in the US study (76%) than in the Italian one (69%), chiefly because of a higher prevalence of exposure to sexual factors in US study women. A substantially larger proportion of Italian cases were due in part to deficiency in screening (46% in US and 84% in Italy). Thus, further inclusion of the effect of screening programmes (number of Pap smears and time since last Pap) led to an overall proportion of cases attributable to the examined risk factors of 87% in the US and 95% in Italy.

Adult↗
PubMed1991

Invasive cervical cancer and intrauterine device use.

Although the hypothesis that intrauterine device (IUD) use might promote cervical cancer has been considered since the introduction of IUDs in the early 1900s, previous studies are inconclusive. Data collected in interviews with 481 invasive cervical cancer cases and 801 general population controls from Birmingham, Chicago, Denver, Miami and Philadelphia were used to address this issue. These data were analysed to determine the relationship between IUD use and the risk of cervical cancer, with consideration of the type of IUD (copper and inert) and duration of use. A non-significant reduced risk of cervical cancer was associated with copper IUD use, indicated by an adjusted odds ratio (OR) of 0.6 (95% Cl: 0.3-1.2), but virtually no effect was found for inert IUD use (OR = 1.1, 95% Cl: 0.9-1.7). Decreased risk with increased duration of copper IUD use supports a possible protective effect of copper IUD use on the development of invasive cervical cancer.

Adult↗
PubMed1989

Invasive cervical cancer and smoking in Latin America.

A case-control study of 667 patients with invasive squamous cell carcinoma of the cervix and 1,430 controls from four Latin American countries showed an age-adjusted relative risk (RR) of 1.2 [95% confidence interval (CI) = 1.0-1.4] for women who had ever smoked, with risk rising to 1.7 (95% CI, 0.8-3.6) for women who smoked greater than or equal to 30 cigarettes per day. The associations were practically eliminated after adjustment for the number of sexual partners and alcohol consumption, probably a surrogate for an unidentified life-style risk factor. Some excess risk persisted among women who smoked for extended periods (RR = 1.5 for greater than or equal to 40 yr), as well as those who began smoking at older ages (RR = 1.7 for greater than 30 yr), which suggests a late-stage effect. In addition, among women who tested positive for human papillomavirus (HPV) type 16 or 18 by filter in situ hybridization, there was an increased risk for women who had ever smoked and a dose-response relationship with the number of cigarettes smoked (adjusted RRs compared with HPV-negative nonsmokers = 5.0 for HPV-positive nonsmokers, 5.5 for less than 10 cigarettes/day, and 8.4 for greater than or equal to 10 cigarettes/day). In contrast, HPV-negative women had no increased risk associated with smoking. These results, from a high-incidence area where intensive smoking among women is still relatively rare, suggest that smoking has a limited effect on cervical cancer risk, possibly only among women with specific types of HPV.

Age Factors↗
PubMed1991

Determinants of genital human papillomavirus infection in young women.

Carcinoma of the cervix has several well-established epidemiologic risk factors, including multiple sexual partners and early age at first intercourse. Human papillomavirus (HPV) infection appears to have an etiologic role in the development of cervical neoplasia, but evidence linking HPV infection to known risk factors for cervical cancer has been inconsistent. The lack of expected correlations may be due to the inaccuracy of HPV assays previously used. A polymerase chain reaction DNA amplification method for the detection of HPV was used to investigate the determinants of genital HPV infection in a cross-sectional sample of 467 women attending a university health service. In contrast to studies using less accurate detection methods, the risk factors for HPV infection found here were consistent with those for cervical neoplasia. The risk of HPV infection was strongly and independently associated with increasing numbers of sexual partners in a lifetime, use of oral contraceptives, younger age, and black race. Age at first intercourse, smoking, and history of a prior sexually transmitted disease were correlated with, but not independently predictive of, HPV infection. These results demonstrate that the key risk factors for cervical carcinoma are strongly associated with genital HPV infection. This correlation suggests that HPV has an etiologic role in cervical neoplasia and reaffirms the sexual route of HPV transmission.

Adolescent↗
PubMedDate not supplied

The spermicide nonoxynol-9 does not inactivate papillomavirus.

Vaginal spermicides are effective contraceptive, and are also capable of inactivating many sexually transmitted pathogens by their detergent effect on bacterial cell membranes and viral envelopes. A 5% concentration of nonoxynol-9, the most frequently used active ingredient of spermicides, was tested for its ability to reduce the transforming activity of bovine papillomavirus type 1 (BPV-1), and the infectivity of BK virus (BKV) and cytomegalovirus (CMV). Nonoxynol-9 markedly reduced the infectivity of CMV, an enveloped virus, but did not significantly affect the activity of the nonenveloped viruses BPV-1 and BKV. Papillomavirus infections are strongly implicated in the etiology of cervical cancer. The reported protective effect of vaginal spermicides against cervical cancer is very likely not mediated by direct inactivation of papillomaviruses by the spermicide.

Animals↗
PubMed1990

Human papillomavirus infection in sexually active adolescent females: prevalence and risk factors.

We examined the prevalence of human papillomavirus (HPV) infection, and associated risk factors for infection with HPV types 6, 11, 16, 18, 31, 33, and 35, in 661 sexually active adolescent females attending family planning clinics. Fifteen percent were positive for HPV DNA by RNA-DNA dot-blot hybridization. More than 60% of the HPV-positive subjects harbored at least one of the following cancer-related HPV types: 16, 18, 31, 33, or 35. Those with HPV had a mean range of four to 10 lifetime sexual partners compared with a mean range of one to three in those without HPV (p less than 0.001). After the analysis was adjusted for number of lifetime sexual partners, no other risk factor was associated with HPV infection. We conclude that oncogenic-related HPV types are common sexually transmitted organisms found in our population. The strong relationship with number of sexual partners suggests that acquisition of HPV infection is predominantly influenced by sexual behavior. However, in our population, confounders such as oral contraceptive use, past history of Chlamydia trachomatis infection, or substance abuse were not found to be significant independent risk factors.

Adolescent↗