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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate the association between seropositivity for herpes simplex virus (type 1 and type 2) and cervical intraepithelial neoplacia (CIN), we analysed data from a population-based case-control study of CIN grade II-III which included Norwegian women aged 20 to 44 years, 94 cases and 228 controls. Our objectives were to determine if HSV-1 and/or HSV-2 seropositivity were independent risk factors for CIN, taking human papillomavirus exposure into account, and to elucidate the combined effect of HPV positivity and seropositivity for HSV In logistic regression analyses, the association between HSV-2 or HSV-1 seropositivity and CIN II-III was not explained by HPV (adjusted OR 3.0; 95%, CI 1.3-7.2 and adjusted OR 3.3; 95% CI 1.3-8.4, respectively). In analyses restricted to HPV-16 DNA-positive individuals, seropositivity for HSV-2 increased the risk of CIN (OR 11.1; 95% CI 1.2-105.7), whereas HSV-1 seropositivity was not significantly associated with CIN. In women positive for other HPV types, only HSV-1 seropositivity was associated with CIN (OR 8.5; 95% CI 1.3-55.8). In analyses of the HPV-16-seropositive individuals, neither HSV-1 nor HSV-2 seropositivity was associated with CIN. Compared to the reference group of jointly unexposed subjects, the HPV-16 DNA-positive women who were anti-HSV-2 negative had an increased risk of CIN (OR 29; 95% CI 12-67), whereas the risk in women who were both HPV-16 DNA-positive and HSV-2 was OR=247 (95% CI 31-1996). The estimate of interaction was strong, but did not reach significance, and our findings may suggest that the combined effect of the two viruses is of aetiological importance in cervical carcinogenesis. Furthermore, the results indicate that HPV DNA positivity is not sufficient to explain the sexual behaviour-associated risk of cervical neoplasia and that further studies on the role of genital HSV (type 1 as well as type 2) and other STDs are warranted.
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PMID:Herpes simplex virus and human papillomavirus in a population-based case-control study of cervical intraepithelial neoplasia grade II-III. 954 32

A retroviral vector carrying both positive (neo) and negative (herpes simplex virus thymidine kinase or HSV-tk) selection markers was constructed as a substrate for mutational assay in mammalian cells. Using a population of rat fibroblast cells carrying a single copy per cell of retroviral DNA randomly integrated in their chromosomes, we examined the cytotoxic and mutagenic activities of ultraviolet light (UV) at four wavelengths (254, 290, 300, and 320 nm). The action spectra for these activities are similar to some of the previously reported spectra for photochemical DNA modifications, erythema, cell killing, and mouse skin carcinogenesis, except at 290 and 320 nm. At 290 nm, no significant mutagenicity was observed. At 320 nm, both cytotoxic and mutagenic activities were 10 times higher than the values expected from the absorption spectrum for DNA and the action spectrum for bacterial inactivation and mutagenesis. Structural comparison of some of the HSV-tk mutants obtained after irradiation with 300 and 320 nm UV revealed partially different patterns of mutation specificity, suggesting the involvement of multiple molecular mechanisms in the genotoxicity associated with this range of UV.
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PMID:Cytotoxicity and mutagenicity of UVB assessed using cultured rat fibroblast. 1070 53

Herpes simplex virus (HSV-2) and cytomegalovirus (CMV) infections produce brain damage in the newborn, and human papillomavirus (HPV) plays a role in cervical carcinogenesis. To assess the frequency of herpes virus and HPV in semen and its role in transmission, semen from 111 male partners of women with histologically-detected genital HPV infection was analysed for HSV, CMV and HPV infection. We used cell culture to detect HSV and CMV, and polymerase chain reaction (PCR) for HPV. Virological findings in the sperm were correlated to the presence or absence of HPV-associated genital lesions and to the viral type. Viral cultures yielded HSV-2 DNA in 9% and CMV DNA in 6.3% of cases. No correlation was established with a history of clinically apparent infection for HSV. HPV-DNA was detected in 23.4% of semen by PCR techniques: in 48% of subjects with urethral lesions, in 22% of patients with penile lesions, in 2% of patients without HPV-associated lesions. HPV-DNA type 16 was detected in 3.6% of cases. Patients with a positive HPV semen sample and penile or urethral lesions had the same HPV type detected in the two specimens. The study shows a high detection of clinically inapparent HSV and CMV, but does not confirm high HPV prevalence in semen from men without detectable lesions. Our study also suggests that the mechanism for semen contamination by HPV is the exfoliation of infected cells from urethral lesions during semen ejaculation, and probably, by abrasion from penile lesions. This could result in the contamination of semen used in assisted reproductive technology.
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PMID:Frequency of herpes simplex virus, cytomegalovirus and human papillomavirus DNA in semen. 1219 37

Human papillomaviruses (HPVs) play the major role in cervical carcinogenesis. The authors reevaluated the role of herpes simplex virus type 2 (HSV-2) in this multistage process by conducting a longitudinal, nested case-control study using 1974-1993 data and comparing the results with those from a meta-analysis of studies. A Nordic cohort of 550,000 women was followed up for an average of 5 years, after which 178 cervical carcinoma cases and 527 controls were identified. HSV-2; HPV-16, HPV-18, and HPV-33; and Chlamydia trachomatis antibodies were determined at baseline by HSV-2 glycoprotein gG-2 and HPV virus-like-particle enzyme immunoassays and by using the microimmunofluorescence method. The relative risk of cervical carcinoma was calculated by conditional logistic regression. Longitudinal studies on HSV-2 and cervical neoplasia were identified through MEDLINE (National Library of Medicine, Bethesda, Maryland), and weighted mean relative risks were calculated. Smoking (relative risk = 1.6, 95% confidence interval (CI): 1.1, 2.3) and HPV-16/HPV-18/HPV-33 (relative risk = 2.9, 95% CI: 1.9, 4.3) were both associated with cervical carcinoma. The smoking- and HPV-16/HPV-18/HPV-33-adjusted relative risks for HSV-2 were 1.0 (95% CI: 0.6, 1.7) and 0.7 (95% CI: 0.3, 1.6), respectively, for HPV seropositives. In the meta-analysis, the relative risk for HSV-2 was 0.9 (95% CI: 0.6, 1.3). In both sets of data, HSV-2 did not play a role in cervical carcinogenesis.
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PMID:Herpes simplex virus and risk of cervical cancer: a longitudinal, nested case-control study in the nordic countries. 1237 Jan 56

Clinical and subclinical human papillomavirus (HPV) infections are the most common sexually transmitted infections in the world, and most sexually-active individuals are likely to be exposed to HPV infection during their lifetimes. More than 40 genotypes of HPV infect the epithelial lining of the anogenital tract and other mucosal areas of the body; of these, 13-18 types are considered to be high-oncogenic risk HPV types (HR-HPV). Persistent infection with HR-HPVs is now unequivocally established as a necessary cause of cervical cancer and is likely to be responsible for a substantial proportion of other anogenital neoplasms and upper aero-digestive tract cancers. Low oncogenic risk HPV types (LR-HPV) are also responsible for considerable morbidity as the cause of genital warts. Youth and certain sexual characteristics are key risk factors for HPV acquisition and persistence of HPV infection, but other mediating factors include smoking, oral contraceptive (OC) use, other STIs (e.g. chlamydia, herpes simplex virus), chronic inflammation, immunosuppressive conditions including HIV infection, parity, dietary factors, and polymorphisms in the human leukocyte antigen system. Not surprisingly, these factors are also established or candidate cofactors identified in epidemiologic studies of cervical cancer. HPV transmissibility and molecular events in HPV-induced carcinogenesis have been the focus of recent multidisciplinary epidemiologic studies. This shift in research focus coincides with a shift in cancer prevention techniques towards immunization with HPV vaccines and HPV testing of precancerous lesions.
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PMID:The epidemiology of genital human papillomavirus infection. 1640 26

Routine cytological screening has been carried out in 27,062 asymptomatic women attending Gynaec and Family Planning O.P.D. of Queen Mary's Hospital, Lucknow, India (April 1971-December 2004). Incidence of squamous intraepithelial lesion (SIL) was found to be 5.9% in the series, while cervical malignancy was seen in 0.6% of cases. The study highlighted the immense utility of cytological screening in minimizing the incidence of carcinoma cervix in the segment of the urban population screened, as the incidence dropped down to 0.5% in the second half from 1.1% noticed in the first half of the screening period. The study also emphasized the utility of clinically downstaging the cervical cancer as 7,316 women showing clinical lesions of cervix were found to harbor SIL in 15.3% and carcinoma cervix in 1.3% of cases as against the incidence of 2.5% for SIL and 0.6% for frank cancer in women with normal cervix. The investigation into different risk factors involved in cervical carcinogenesis revealed that the incidence of SIL and cancer cervix showed a rise with increasing age and parity and prolonged sexual period. The incidences of both cervical cytopathologies were also higher in women of low socio-economic status while religion was found to have no bearing on the occurrence of the disease. Among the four sexually transmitted diseases (STDs) diagnosed in the cervical smears, Trichomonas vaginalis was found to be more prevalent (2.6%), while human papillomavirus (HPV) and Herpes simplex was seen in 0.4 and 0.2% of cases, respectively Herpes simplex was found to have strong affinity with both SIL and carcinoma cervix, while only SIL incidence was high with HPV infection. The study emphasizes need of proper education to women of low socio-economic class for creating awareness regarding hazards and risk factors of cervical cancer as well as management and cure of the disease.
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PMID:Results of longterm hospital based cytological screening in asymptomatic women. 1647 Aug 54

The interplay between human papillomavirus, notably type 16, and HIV in cervical carcinogenesis leads to persistent infection and cervical neoplasia by destruction of the afferent arm (Langerhans cells) of the host immune system. The joint effect takes place at the early stages of squamous intraepithelial lesions and has severe consequences if left untreated. The recent increase of cervical cancer mortality in young women in developed countries may well be a result of the HIV epidemic. Infection with Chlamydia trachomatis is associated with cervical squamous cell carcinoma but not with cervical adenocarcinoma, and the association remains after adjusting for human papillomavirus 16. Joint effects of C. trachomatis and the human papillomaviruses have not been studied at the population level but indirect evidence from epidemiological studies suggests that the interaction might be different (synergistic versus antagonistic) at different stages (cervical intraepithelial neoplasia versus invasive cervical cancer) of cervical carcino-genesis. Concomitant exposure to human papillomaviruses 6 or 11 and human papillomavirus type 16 has not been shown to result in excess risk of cervical squamous cell carcinoma. This antagonistic joint effect was also discovered between human papillomavirus types 18 and 16, as well as 33 and 16. Herpes simplex virus type 2 antibodies are associated with a modest risk of cervical cancer, which is not surprising since the presence of herpes simplex virus antibodies reflects risk-taking sexual behaviour. However, no excess risk remains after adjustment for human papillomavirus type 16, and no interaction between these two viruses has been found in epidemiological studies. Evidence of interaction between human papillomavirus type 16 and the other members of the herpesvirus family is still at an experimental level and difficult to judge. Little progress has been made in the most promising experimental association between the oncogenic human papillomaviruses and adeno-associated viruses. In addition to the well established interaction between human papillomaviruses and HIV, intriguing interactions are emerging between the human papillomaviruses and C. trachomatis, as well as between the different human papillomavirus types.
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PMID:Interactions between human papillomavirus and other sexually transmitted agents in the etiology of cervical cancer. 1703 63

The strong correlation between smoking and exposure to oncogenic human papillomaviruses (HPVs) has made it difficult to verify the independent role of smoking in cervical carcinogenesis. Thus, the authors evaluated this role. Five large Nordic serum banks containing samples from more than 1,000,000 subjects were linked with nationwide cancer registries (1973-2003). Serum samples were retrieved from 588 women who developed invasive cervical cancer and 2,861 matched controls. The samples were analyzed for cotinine (a biomarker of tobacco exposure) and antibodies to HPV types 16 and 18, herpes simplex virus type 2, and Chlamydia trachomatis. Smoking was associated with the risk of squamous cell carcinoma (SCC) among HPV16- and/or HPV18-seropositive heavy smokers (odds ratio=2.7, 95% confidence interval: 1.7, 4.3). A similar risk of SCC (odds ratio=3.2, 95% confidence interval: 2.6, 4.0) was found in heavy smokers after adjustment for HPV16/18 antibodies. The point estimates increased with increasing age at diagnosis and increasing cotinine level. This study confirms that smoking is an independent risk factor for cervical cancer/SCC in women infected with oncogenic HPVs. These findings emphasize the importance of cervical cancer prevention among women exposed to tobacco smoke.
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PMID:Is smoking an independent risk factor for invasive cervical cancer? A nested case-control study within Nordic biobanks. 1977 89

Future cancer therapies will be molecular cures. They will correct, block or destroy cancer cells by targeting molecular changes that lead to carcinogenesis. Destroying cancer cells can be done using oncolytic viruses. By blocking antibody mediated neutralization of oncolytic viruses, Herpes simplex virus type 1 glycoproteins E and I could be used in the adjuvant treatment of cancer for improving the chances of oncolytic viruses to kill cancer cells in vivo.
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PMID:Development of a selective biopharmaceutical from Herpes simplex virus type 1 glycoproteins E and I for blocking antibody mediated neutralization of oncolytic viruses. 2116 33

Congenital tumours are a group of distinct infrequent disorders whose exact aetiologies have not clearly been understood so far. Viral infection seems to be one of the key factors involved in the carcinogenesis of certain tumours. This study was performed to assess whether viral DNAs are present in the congenital tumours or not. Nucleic acid from 31 congenital tumours was extracted. Detection of Epstein-Barr virus, Cytomegalovirus (CMV), adenovirus, Herpes simplex virus 1 (HSV1) and 2, Human herpes virus 6 (HHV6), and BK virus was performed using polymerase chain reaction. Viral nucleic acid was detected in eight subjects (25.8%), mostly adenovirus, CMV, and HHV6. Despite their low frequencies, a possible role could be identified for viral infections in tumour development or progression.
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PMID:Contributory role of viral infection in congenital tumour development. 2410 42


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