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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the mortality and incidence of cervical cancer have been decreasing, those of uterine-body, or endometrial, cancer have been increasing. The proportion of endometrial cancer was reported to have become 33.6% of primary uterine cancers in 1995. Infection with certain types of human papilloma virus (HPV) is considered to be etiologically important for the occurrence of cervical cancer. Because HPV is sexually transmitted, some risk factors for cervical cancer are associated with certain kinds of sexual behavior such as a young age at first intercourse, multiple partners, and infrequent use of barrier-type contraceptives such as condoms. Frequent conceptions and deliveries and histories of sexually transmitted diseases like infection with herpes simplex virus type 2 or chlamydia also have been suggested to be associated with the risk of cervical cancer. Smoking habits and infrequent intake of vegetables and fruits may be related to the increased risk of cervical cancer by supporting persistent infection of HPV through impaired immunological function. Although host factors such as a variant of a tumor suppressor gene like p53 have been assessed in terms of the risk of cervical cancer, these are not yet clearly elucidated. Estrogen stimulation of the endometrium unopposed by progesterone stimulation, namely, unopposed estrogen stimulation, is thought to be involved in the etiology of endometrial cancer. Frequent intake of animal fat, obesity or being overweight, infertility, and histories of diabetes mellitus, hypertension, and polycystic ovary syndrome have been reported to be risk factors for endometrial cancer, and they are thought to increase unopposed estrogen stimulation. Estrogen replacement therapy for postmenopausal symptoms, tamoxifen therapy for breast cancer, and taking sequential-type oral contraceptives have been shown to be exogenous risk factors for endometrial cancer in that they increase unopposed estrogen stimulation to endometrium.
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PMID:[Recent progress in epidemiologic research of uterine cancer]. 1124 42

Obesity is associated with higher cervical cancer mortality, but its relationship with sexual behavioral risk factors that predispose women to human papilloma virus (HPV) and cervical cancer is unclear. We used data from 3,329 women participants, aged 20-59 years, of the 1999-2004 National Health and Nutrition Examination Survey, to analyze the relationship between BMI and age at first intercourse, number of sexual partners, condom use during sexual activity, history of sexually transmitted disease (STD), herpes simplex virus 2 (HSV-2) seropositivity, and HPV prevalence. BMI was not associated with the prevalence of HPV. Mildly obese women (BMI 30.0-34.9 kg/m(2)) were least likely to report a STD history (9% vs. 13% in normal weight) and >or=2 sexual partners in the previous year (8% vs. 13%) while overweight women (BMI 25.0-29.9 kg/m(2)) were least likely to report >or=10 lifetime partners; among those with multiple partners, BMI was not associated with sexual activity without condoms in the past month. After adjustment for age, race/ethnicity, and education, women with higher BMI were less likely to report sexual behavioral risk factors than normal-weight women; however, odds ratios were only significant for mildly obese women for reporting a STD history (0.74, 95% confidence interval 0.55-0.99) and having >or=2 sexual partners in the last year (0.57, 0.39-0.85). Higher BMI was not associated with HSV-2 seropositivity after adjustment. HPV and sexual behavioral risk factors for HPV and cervical cancer are not more prevalent in obese than normal-weight women and unlikely to account for higher-observed cervical cancer mortality in obese women.
Obesity (Silver Spring) 2008 Nov
PMID:Obesity and the likelihood of sexual behavioral risk factors for HPV and cervical cancer. 1871 77

Despite decreases in the cancer death rates in high-resource countries, such as the USA, the number of cancer cases and deaths is projected to more than double worldwide over the next 20-40 years. Cancer is now the third leading cause of death, with >12 million new cases and 7.6 million cancer deaths estimated to have occurred globally in 2007. By 2030, it is projected that there will be approximately 26 million new cancer cases and 17 million cancer deaths per year. The projected increase will be driven largely by growth and aging of populations and will be largest in low- and medium-resource countries. Under current trends, increased longevity in developing countries will nearly triple the number of people who survive to age 65 by 2050. This demographic shift is compounded by the entrenchment of modifiable risk factors such as smoking and obesity in many low-and medium-resource countries and by the slower decline in cancers related to chronic infections (especially stomach, liver and uterine cervix) in economically developing than in industrialized countries. This paper identifies several preventive measures that offer the most feasible approach to mitigate the anticipated global increase in cancer in countries that can least afford it. Foremost among these are the need to strengthen efforts in international tobacco control and to increase the availability of vaccines against hepatitis B and human papilloma virus in countries where they are most needed.
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PMID:The global burden of cancer: priorities for prevention. 1993 10

Cancer is one of the major causes of death in countries across the world. However, at least half of cancers could be prevented. This article reviews the relationship between cancer incidence and the major risk factors: tobacco use, exposure to infections, nutrition, obesity and physical activity. Several major current cancer prevention initiatives are presented, including the effort for global tobacco control, vaccination programs for human papilloma virus, chemoprevention, and cohort studies to identify and elucidate cancer causes. Two concerns that cross the cancer prevention research spectrum are the importance of social determinants of health, and the potential role of genetic factors in explaining cancer incidence and guiding intervention development. In the future, optimism is warranted regarding cancer prevention. If currently known criteria are applied and extended, significant reductions in cancer rates are possible.
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PMID:Cancer prevention: major initiatives and looking into the future. 2038 61

Cancer has many causes, some of which can, at least in part, be avoided through interventions known to reduce cancer risk. Healthy People 2020 objectives call for reducing colorectal cancer incidence to 38.6 per 100,000 persons, reducing late-stage breast cancer incidence to 41.0 per 100,000 women, and reducing cervical cancer incidence to 7.1 per 100,000 women. To assess progress toward reaching these Healthy People 2020 targets, CDC analyzed data from U.S. Cancer Statistics (USCS) for 2010. USCS includes incidence data from CDC's National Program of Cancer Registries and the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program and mortality data from the National Vital Statistics System. In 2010, a total of 1,456,496 invasive cancers were reported to cancer registries in the United States (excluding Arkansas and Minnesota), an annual incidence rate of 446 cases per 100,000 persons, compared with 459 in 2009. Cancer incidence rates were higher among men (503) than women (405), highest among blacks (455), and ranged by state from 380 to 511 per 100,000 persons. Many factors, including tobacco use, obesity, insufficient physical activity, and human papilloma virus (HPV) infection, contribute to the risk for developing cancer, and differences in cancer incidence indicate differences in the prevalence of these risk factors. These differences can be reduced through policy approaches such as the Affordable Care Act, which could increase access for millions of persons to appropriate and timely cancer preventive services, including help with smoking cessation, cancer screening, and vaccination against HPV.
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PMID:Invasive cancer incidence - United States, 2010. 2467 Sep 26

Cancers of the uterus correspond to cervical cancers and uterine corpus cancers. Cervical cancer is common among young women, especially in immunocompromised populations. Its carcinogenesis is induced by the human papilloma virus (HPV). All factors promoting the HPV contamination and/or limiting the clearance of HPV or promoting its progression are risk factors for cervical cancer: sex at an early age, multiple sexual partners, multiparty, smoking, hormonal contraceptives, immunosuppression or certain infections. Cancers of the uterine corpus, substantially represented by endometrial cancers, represent the fourth leading cause of cancer in women in France. Risk factors are related to hyperestrogenism with early age of menarche and late menopause, obesity, diabetes, inadequate hormone-replacement therapy for menopause. Endometrial cancers fall in the scope of familial cancers making evoke a Lynch syndrome/HNPCC.
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PMID:[Epidemiology and risk factors for cancer of the uterus]. 2509 Jul 59

Gynecologic cancers are the unregulated growth of neoplastic cells that arise in the cervix, ovaries, fallopian tubes, uterus, vagina, and vulva. Although gynecologic cancers are characterized by different signs and symptoms, studies have shown that they share common risk factors, such as smoking, obesity, age, exposure to certain chemicals, infection with human immunodeficiency virus (HIV), and infection with human papilloma virus (HPV). Despite recent advancements in the preventative, diagnostic, and therapeutic interventions for gynecologic cancers, many patients still die as a result of metastasis and recurrence. Since mounting evidence indicates that the epithelial-mesenchymal transition (EMT) process plays an essential role in metastatic relapse of cancer, understanding the molecular aberrations responsible for the EMT and its underlying signaling should be given high priority in order to reduce cancer morbidity and mortality.
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PMID:EMT-Inducing Molecular Factors in Gynecological Cancers. 2635 73

Cancer is now the leading cause of death in Japan. A rapid increase in cancer mortality is expected as Japan is facing a super-aged society. Many causes of cancer are known to be closely linked to life style factors, such as smoking, drinking, and diet. The oral environment is known to be involved in the pathogenesis and development of various diseases such as bronchitis, pneumonia, diabetes, heart disease, and dementia. Because the oral cavity acts as the bodily entrance for air and food, it is constantly exposed to foreign substances, including bacteria and viruses. A large number of bacteria are endemic to the oral cavity, and indigenous oral flora act to prevent the settlement of foreign bacteria. The oral environment is influenced by local factors, including dental plaque, tartar, teeth alignment, occlusion, an incompatible prosthesis, and bad lifestyle habits, and systemic factors, including smoking, consumption of alcohol, irregular lifestyle and eating habits, obesity, stress, hormones, and heredity. It has recently been revealed that the oral environment is associated with cancer. In particular, commensal bacteria in the oral cavity are involved in the development of cancer. Moreover, Candida, human papilloma virus and Epstein-Barr virus as well as commensal bacteria have been reported to be associated with the pathogenesis of cancer. In this review, we introduce recent findings of the correlation between the oral environment and cancer.
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PMID:Oral environment and cancer. 2748

Villitis of unknown etiology (VUE) and chronic deciduitis with plasma cells (CD) are supposed to be non infectious placental lesions caused by a pathologic immune reaction similar to a host versus graft mechanism. In some investigations, infection of human trophoblastic cells with human papilloma virus (HPV) has been described, and a relationship with miscarriage, preeclampsia, and chronic inflammatory placental lesions has been suspected. Infection with enterovirus, especially Coxsackievirus, has been observed in cases with spontaneous abortion and adverse perinatal outcome, respectively. We investigated 20 cases with VUE and 30 cases with chronic deciduitis with plasma cells. The placenta specimens were analyzed for expression of HPV capsid protein by immunohistochemistry, for presence of HPV DNA via polymerase chain reaction (PCR), and for presence of enterovirus mRNA using RT-PCR, respectively. VUE was associated with maternal diseases: atopic lesions in 21%, other autoimmune diseases in 15.5%, and obesity in 31.5%, respectively. Birth weight below the 10th percentile was detected in 63% of the cases with VUE. Chronic deciduitis was associated with preterm labor and preterm premature rupture of membranes (26%). Intrauterine fetal demise occurred in 5 cases with CD (18.5%). HPV DNA, HPV capsid protein, and enterovirus mRNA were not detected in all investigated VUE or CD cases. Our investigations show that a causal role for enterovirus and human papilloma virus in the development of VUE and CD is unlikely. Therefore, HPV vaccination is unlikely to reduce the incidence of VUE and CD in the future.
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PMID:Villitis of unknown etiology and chronic deciduitis are not associated with human papilloma virus and enterovirus infection. 3202 22

Metabolic syndrome (MetS) is a group of risk factors that causes cardiovascular and diabetic morbidity and mortality, which is diagnosed by central obesity, dyslipidemia, hyperglycemia, and hypertension. Increasing epidemiological data and experimental results indicate that the presence of MetS increases the incidence of common malignancies and related mortality. Epidemiological studies have previously reported an association of endometrial cancer occurrence with MetS. Aromatization of androstenedione to estrogen, insulin resistance, and diabetes can cause increased levels of free estrogen, and the detrimental effect of elevated estrogen as a carcinogen is well studied in endometrial cancer. Medications used to manage MetS such as metformin and statins are suggested to reduce endometrial cancer risk and improve survival. Some large population-based epidemiological studies have suggested that the MetS is related to an increased risk of cervical carcinoma. MetS may contribute to viral-host interactions, which lead to persistent human papilloma virus (HPV) infection, although limited epidemiological data are available. Specific effects of obesity and diabetes on the occurrence of ovarian cancer have been suggested. However, the direct correlation between MetS and ovarian cancer is still lacking. Previous retrospective studies reported that the use of metformin, statins, and beta-blockers could be associated with cancer prevention or better prognosis. Proper diagnosis and management of the MetS should be a part of the strategies undertaken to prevent and treat gynecologic cancer. So far, only limited data is available on this subject, and further clinical and fundamental research is required to further clarify the effect of these therapies on gynecologic cancer treatment.
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PMID:Associations between metabolic syndrome and gynecologic cancer. 3248 65


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