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

Incident cases of large bowel cancer from the Swiss canton of Vaud over the period 1974-88 were analyzed in relation to the distribution of site by sex, age, marital status and detailed subsite. A total of 1,968 cases were registered in males and 1,958 in females, corresponding to overall age-standardized (world) rates of 32.2/100,000 males and 22.4/100,000 females. The frequency of ascending and transverse colon cancer was lower in males (18.2% and 9.3%) than in females (23.1% and 10.0%, respectively), but cancers of the sigmoid colon and rectum were proportionally more frequent in males (34.0 and 30.0% versus 29.9 and 24.6% in females). Anal cancer accounted for 4.0% of large bowel cancers in females, but only 1.2% in males. Analysis of age-specific rates showed comparable values for ascending colon cancer in both sexes and in relation to each subsequent age group, as well as in sigmoid and rectal cancers up to middle age, while a male excess for the latter cancers became evident after age 55. A female excess for anal cancer was apparent in any subsequent age group. Information on marital status was available on 2,398 decreased subjects. Never married cases accounted for 12.2% of women and 8.1% of males. The excess of unmarried women was somewhat larger in the colon than in the sigma and rectum groups, but there was no evidence of excess of never married females for anal cancer. These data confirm that there are appreciable intersex heterogeneities in the descriptive epidemiology of various subsites of large bowel cancer, as well as complex interactions between sex and age, which may be related to female hormone correlates of intestinal carcinogenesis. Whatever the main biological mechanism(s), these data show noticeable similarities for both sexes in the descriptive epidemiology of cancers arising in the left colon and rectum, but noticeable differences with the right colon. Even more substantial are the differences with anal cancer, which should be linked to its venereal correlates.
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PMID:Patterns of large bowel cancer by subsite, age, sex and marital status. 186 55

Women diagnosed during the period 1943-1990 and reported to the Danish Cancer Registry with invasive squamous-cell carcinomas of the uterine cervix, vulva, vagina or anus, together with those having pre-cancerous lesions (CIN III or carcinoma in situ) of the uterine cervix diagnosed in the period 1958-1990, were followed for the occurrence of subsequent lung cancer over 762,000 person-years. Overall, these patients developed 2 to 2 1/2 times more lung cancers than women in the general Danish population. Women in whom cervical cancer was diagnosed recently, and before the age of 45 years, had a 4.6 times elevated risk of developing lung cancer, while young women with vulvar or vaginal cancer were at a 4.0-fold elevated risk. Similarly, women in whom anal cancer was diagnosed before the age of 60 years were at a 3.5-fold increased risk of developing lung cancer. The present study supports the hypothesis that smoking is involved in the aetiology of ano-genital malignancies. The particularly high risk of developing subsequent lung cancers seen in women who were pre-menopausal (< 45 years) at the time of the ano-genital cancer diagnosis suggests that the effect of smoking in ano-genital carcinogenesis might be partly mediated through alterations in oestrogen metabolism. Alternatively, patients who developed their initial ano-genital cancer at a young age might harbour some genetic susceptibility which could explain their excess lung-cancer risk.
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PMID:Risk of lung cancer in pre- and post-menopausal women with ano-genital malignancies. 766 18

A central role in anal carcinogenesis of high-risk types of human papillomaviruses (hrHPV) was recently established, but the possible role of benign anal lesions has not been addressed in hrHPV-positive and -negative anal cancers. As part of a population-based case-control study in Denmark and Sweden, we interviewed 417 case patients (93 men and 324 women) diagnosed during the period 1991-94 with invasive or in situ anal cancer, 534 patients with adenocarcinoma of the rectum and 554 population controls. Anal cancer specimens (n = 388) were tested for HPV by the polymerase chain reaction. Excluding the 5 years immediately before diagnosis, men, but not women, with anal cancer reported a history of haemorrhoids [multivariate odds ratio (OR) 1.8; 95% confidence interval (CI) 1.04-3.2] and unspecific anal irritation (OR 4.5; CI 2.3-8.7) significantly more often than controls. Women with anal cancer did not report a history of benign anal lesions other than anal abscess to any greater extent than controls, but they had used anal suppositories more often (OR 1.5; CI 1.1-2.0). Patients with hrHPV in anal cancer tissue (84%) and those without (16%) reported similar histories of most benign anal lesions, but anal fissure or fistula was more common among hrHPV-positive cases. Ulcerative colitis and Crohn's disease, reported by <1% of study participants, were not associated with anal cancer risk. The higher proportion of hrHPV-positive anal cancers among case patients with anal fissure or fistula suggests that such mucosal lesions may provide direct viral access to basal epithelial layers. Since risk associations with benign anal lesions in men may be confounded by unreported sexual behaviour, and since risk associations in women were generally negative, it seems unlikely that benign anal lesions act as promoters in hrHPV-associated anal carcinogenesis. Moreover, benign anal lesions appear not to be linked to an alternative, hrHPV-unassociated causal pathway to anal cancer. Ulcerative colitis and Crohn's disease were not supported as causal factors for anal cancer.
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PMID:Benign anal lesions, inflammatory bowel disease and risk for high-risk human papillomavirus-positive and -negative anal carcinoma. 983 90

To investigate whether ESE-1 gene abnormalities are involved in alterations of epithelial cell differentiation in squamous anal cancer ESE-1 expression and structure were screened in six patients by reverse transcriptase-polymerase chain reaction (RT-PCR) and automated sequence analysis. The complete cDNA of isoform ESE-1b was always expressed and correctly spliced, with single nucleotide polymorphism being observed in two cases. Presence of ESE-1b point mutations was excluded. Expression of SPRR2A and ENDOA/CK8, two epithelium-specific ESE-1 target genes, were revealed by RT-PCR in all cases. This first report of expression of ESE-1, and of SPRR2A and ENDOA/CK8 (both related to terminal differentiation in different types of epithelia lining) in anal cancer excludes the hypothesis that these genes influenced carcinogenesis in our patients. Despite selecting of patients without clinical evidence of HPV infection, PCR consistently revealed HPV-16 DNA, highlighting the importance of HPV infection in anal cancer.
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PMID:Expression analysis and mutational screening of the epithelium-specific ets gene-1 (ESE-1) in patients with squamous anal cancer. 1089 34

The association of Helicobacter pylori (H. pylori) with gastric cancer is thus far the best understood model to comprehend the causal relationship between a microbial pathogen and cancer in the human gastrointestinal tract. Besides H. pylori, a variety of other pathogens are now being recognized as potential carcinogens in different settings of human cancer. In this context, viral causes of human cancers are central to the issue since these account for 10-20% of cancers worldwide. In the case of H. pylori and gastric cancer, as well as the human papillomavirus and anal cancer, the causal relationship between the infectious agent and the related cancer in the gastrointestinal tract has been clearly confirmed by epidemiological and experimental studies. Similarly, Epstein-Barr virus and the oncogenic JC virus are being suggested as possible causative agents for cancers in the upper and lower gastrointestinal tract. This review discusses various viral and microbial pathogens and their oncogenic properties in the evolution of gastrointestinal carcinogenesis and summarizes the available experimental data make a convincing agreement favoring the associations between infectious agents and specific human cancers.
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PMID:The role of viral and bacterial pathogens in gastrointestinal cancer. 1833 78

Non-cervical anogenital cancers (i.e. anal, vulvar, vaginal and penile cancers) associated with the human papillomavirus (HPV), for which HPV is known to be the necessary cause of carcinogenesis, are poorly documented due to their relatively low incidence rate. The aim of this study is to describe the incidence rates of these cancers between 1984 and 2001, and their relative survival probabilities, in Quebec (Canada) between 1984 and 1998. The incidence of these cancers is on the rise, particularly anal cancer in women and, more recently (since 1993-95), vulvar cancer. Between 1984-86 and 1993-95, the 5-year relative survival probability for men with anal cancer decreased from 57% to 46%, while that for penile cancer dropped from 75% to 59%. However, during the same period, the 5-year relative survival probability for women with anal cancer rose from 56% to 65%, and remained stable for cervical and vulvar cancers, at 74% and 82%, respectively.
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PMID:The evolution of HPV-related anogenital cancers reported in Quebec - incidence rates and survival probabilities. 1834 64

Infection with the human papillomavirus (HPV) is the most common sexually transmitted disease afflicting approximately 80% of the population. HPV infection is an essential factor in cervical carcinogenesis and cervical carcinoma is the second most common cause of cancer among women worldwide. In addition to cervical cancer, other malignancies in both men and women such as esophageal, oropharyngeal, and anal cancer have been causally associated with this virus. Other gender-specific HPV-related cancers include penile, vulvar and vaginal cancer. HPV-16 is the most common HPV type associated with a malignant phenotype regardless of organ of origin. HPV-16 together with HPV-18 accounts for approximately 70% of cervical cancers. Other non-oncogenic HPV types including HPV types 6 and 11 are associated with over 90% of benign HPV-related lesions such as genital warts and juvenile respiratory papillomatosis.
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PMID:The spectrum and clinical sequelae of human papillomavirus infection. 1849 14

Papillomaviruses are small DNA viruses that infect and multiply in cutaneous or mucosal epithelial tissue. Human papillomavirus (HPV) 16 and 18 cause more than 99% of cervical carcinomas. Simultaneous presence of HPV is found in cervical intraepithelial neoplasia, vaginal intraepithelial neoplasia, vaginal and anal cancer. Invasive vulvar squamous cell carcinoma in younger women under the age of 50 are also associated with HPV. Most of the penile lesions are subclinical and the high prevalence of high-risk HPV suggests that they constitute a reservoir for high-risk HPV. Bowens disease and Buschke-Lowenstein tumors are associated with particular low- and high-risk HPV types. The potential role of HPV infection in the carcinogenic steps of breast, prostate, colorectal and lung cancers should be further tested. HPV-DNA might be transported from the original site of infection to the breast tissue by the bloodstream, and therefore is possibly involved in the carcinogenesis of breast neoplasia in some patients. HPV-DNA is detected in 40-70% of head and neck squamous cell carcinomas and in only 1% in normal epithelial cells. In this paper we propose the hypothesis that many epithelial normal cells are susceptible to HPV infection, which are the most sexually transmitted viruses. Experimental and epidemiological data imply a causative role for HPVs and they appear to be the second most important risk factor for cancer development in humans, exceeded only by tobacco usage.
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PMID:Nature of cervical cancer and other HPV - associated cancers. 1981 Jan 28

Human anal cancers are associated with high-risk human papillomaviruses (HPV) that cause other anogenital cancers and head and neck cancers. As with other cancers, HPV16 is the most common high-risk HPV in anal cancers. We describe the generation and characterization of a mouse model for human anal cancer. This model makes use of K14E6 and K14E7 transgenic mice in which the HPV16 E6 and E7 genes are directed in their expression to stratified squamous epithelia. HPV16 E6 and E7 possess oncogenic properties including, but not limited to, their capacity to inactivate the cellular tumor suppressors p53 and pRb, respectively. Both E6 and E7 were found to be functionally expressed in the anal epithelia of K14E6/K14E7 transgenic mice. To assess the susceptibility of these mice to anal cancer, mice were treated topically with dimethylbenz[a]anthracene (DMBA), a chemical carcinogen that is known to induce squamous cell carcinomas in other sites. Nearly 50% of DMBA-treated HPV16 E6/E7 transgenic mice showed overt signs of tumors, whereas none of the like-treated nontransgenic mice showed tumors. Histopathologic analyses confirmed that the HPV16 transgenic mice were increased in their susceptibility to anal cancers and precancerous lesions. Biomarker analyses demonstrated that these mouse anal cancers exhibit properties that are similar to those observed in HPV-positive precursors to human anal cancer. This is the first mouse model for investigating the contributions of viral and cellular factors in anal carcinogenesis, and should provide a platform for assessing new therapeutic modalities for treating and/or preventing this type of cancer.
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PMID:A mouse model for human anal cancer. 2094 89

Anal cancer is common among people infected with human immunodeficiency virus (HIV). This cancer is caused by human papillomavirus, and immunosuppression likely contributes to its development. In this issue of the Journal, Bertisch et al. (Am J Epidemiol. 2013;178(6):877-884) present the results of a case-control study of anal cancer among HIV-infected people in Switzerland. They demonstrate that anal cancer risk is increased in association with a low CD4+ cell count (a clinical measurement of immune status). In particular, HIV-induced immunosuppression was most severe among cases approximately 6-7 years prior to the diagnosis of anal cancer. A plausible biological interpretation is that immunosuppression is important at an early stage of the development of anal cancer, but that the neoplastic process becomes irreversible over time with persistent human papillomavirus infection and genetic damage. With current efforts to provide earlier combination antiretroviral therapy to HIV-infected people, anal cancer incidence may start to decline. Bertisch et al. also demonstrate a strong association between serum antibodies against the human papillomavirus type 16 protein E6 and anal cancer risk, highlighting the role of this viral oncoprotein in carcinogenesis. Additional biomarkers could help refine clinical approaches to anal cancer screening and prevention for the HIV-infected population.
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PMID:Invited commentary: Biological and clinical insights from epidemiologic research into HIV, HPV, and anal cancer. 2390 May 53


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