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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since hormones relate to the etiology of breast cancer, 40 studies have looked at the possible association of oral contraceptives (OCs) with breast cancer. Most research conducted through 1986 and including the largest related case control study and several after 1986 found no association between ever use of OCs and breast cancer. On the other hand, some studies conducted after 1986 with women 45 years old who had breast cancer and had taken OCs have suggested a dose response relationship, 2 fold increased risk of breast cancer, or increased risk with duration of OC use. These results motivated several organizations to review the literature and to issue guidelines. The US Food and Drug Administration, the UK Committee on the Safety of Medicines, and IPPF did not find a reason to change practices. The Committee on the Safety of Medicines did suggest, however, that health providers mention the possible increase in risk. At least 8 studies have revealed an increased risk of cervical cancer with duration of OC use, especially after 5 years of use. Yet experience has disclosed an obstacle to understanding the relationship between cervical cancer and OC use--cervical cancer may be caused by the human papilloma virus transmitted by sexual intercourse. Unlike results of breast and cervical cancer research, research results have clearly established that OC use lowers the risk of endometrial cancer by about 50% and the risk of ovarian cancer by about 40%. In fact, the US Cancer and Steroid Hormone [CASH] study showed a protective effect of OCs for endometrial and ovarian cancers at least 15 years after discontinuation. Even though some studies found a dose response effect with duration of use, a large international study did not find any relationship between OC us and liver cancer. Moreover studies did not reveal an association between OC use and malignant melanoma or pituitary adenoma.
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PMID:Neoplastic effects of oral contraceptives. 167 77

Recently some studies have shown an association between the pill and increased risk of breast cancer and cancer of the cervix. Several well- designed prospective studies indicated that there was an increased risk of breast cancer for women without children with menarche before 13 who took the pill for many years. A control case study of 407 breast cancer victims compared 424 controls found that the risk of women who had taken hormonal contraceptives was double, however, the duration of use, age, parity was not considered. Although there has been a slight increase of breast cancer incidence in Switzerland, it could be attributed to better diagnostic measures. The increase or dysplasia and carcinoma of the cervix has been linked to taking the pill for 5 years or more, but making a direct correlation is speculative. Among smokers cervical carcinoma is more frequent even without pill use. The pill has changed sexual habits allowing sexual intercourse at an earlier age with more partners and spreading sexually-transmitted carcinogens (human papilloma virus). Cytological cervix control, treatment of vaginal infections, and use of condoms or other barrier methods could minimize this risk. On the other hand, an analysis of data of 47,000 women observed since 1967 indicated that there were more carcinoma in situ findings and even more invasive cervical carcinomas after using the pill for 10 years or longer. The incidence of carcinoma of the endometrium is lower after longterm use of the pill due to the antiestrogenic effect of the gestagen component. Similarly, after taking a combination preparation for 6 months the incidence of ovarian carcinomas also dropped, especially among nulliparas. Medical advice should include careful explanation of risks and benefits of the pill, cytological examination when the pill os prescribed. The low-dose micropills seem to diminish the risks, but nonhormonal alternatives are also available.
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PMID:[Oral contraceptives and cancer]. 281 16

Physicians must understand the effects of oral contraceptives (OCs) on gynecologic cancers in order to properly address the fears and concerns of their patients. The largest study providing data on this topic was a case-control study of breast, ovarian, and endometrial cancer in US women 20-54 years old. When interpreting the results of such a study, the strengths and weaknesses of a retrospective case-control study must be considered and avoidance of subject and researcher bias must be addressed in the report. The statistical concept of relative risk quantifies the association between use of OCs and the risk of a cancer. A relative risk of 1.0 shows no difference, a risk of 0.5 shows a diminished risk, and one of 1.5 shows an increased risk. Current data show no increased risk of breast cancer associated with OC use, a beneficial effect on ovarian cancer (producing a 40% reduction in risk), a relative risk of 0.5 of endometrial cancer (another beneficial effect of OC use), and an unknown effect on cervical cancer because of all of the confounding variables (such as increased screening, the number of sexual partners, age at first coitus, and exposure to human papilloma virus).
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PMID:The pill and gynecologic cancer: controversy and mystery prevail. 756 39

The inactivation of the tumor suppressor gene p53 has been demonstrated in a variety of human tumors. Herein, we performed a p53 gene analysis of human gynecologic tumor cell lines and tumor tissues. In the SK-OV-3 cell line, Southern analysis suggested the presence of sequence deletions/rearrangements in at least one allele of p53 gene. Transcripts were not detectable by either Northern or PCR analysis. Sequencing analysis of the entire coding region revealed mutations changing the p53 amino acid composition in all six endometrial carcinoma cell lines tested (Ishikawa, Hec1-A, Hec1-B, KLE, RL95-2, and AN-3), and four cell lines in ovarian carcinoma cell lines (Caov-3, -4, OVCAR-3, and Kuramochi). Of the seven cervical carcinoma cell lines, two (HT-3 and C-33A) contained p53 codon changes. We were unable to detect the human papilloma virus (HPV) in these two cell lines. By contrast, five HPV-positive cervical carcinoma cell lines (HeLa S-3, Caski, SiHa, C-41, and ME-180) contained wild-type p53 gene sequences. Examination of loss of heterozygosity (LOH) by PCR revealed that about 30% of the human ovarian carcinoma tissues has LOH at the locus of p53 gene. We suggest that, in the HPV-positive cervical tumors, p53 inactivation occurred via the known mechanism of viral E6/cellular p53 protein association, whereas in all other tumors (ovarian carcinoma, endometrial carcinoma, HPV-negative cervical carcinoma) p53 function was compromised by changes in the amino acid sequence.
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PMID:[Analysis of p53 gene in gynecologic tumors]. 815 58

Although human papilloma virus (HPV) associated lesions constitute a well recognized clinical entity in the female lower genital tract, namely vulva, vagina and cervix, few studies have demonstrated HPV infection in other genital sites, particularly in the ovary and uterine corpus. Recently, with the highly sensitive polymerase chain reaction (PCR) technique, HPV infections were found in an ovarian tumour and adenocarcinoma of the cervix. This prompted a retrospective analysis of HPV DNA in 22 cases of endometrial adenocarcinoma in order to investigate the possible carcinogenesis of HPV in the uterine corpus. In this study DNA extraction was performed from paraffinized cancerous tissues and the normal cervical counterpart. HPV 6, 11, 16 and 18 primers specific oligonucleotides were used in PCR to detect the presence of this oncogenic virus. HPV 16 DNA was found in 1 endometrial adenocarcinoma and 4 cervical tissues. Our result did not support the aetiological role of HPV in the carcinogenesis of endometrial carcinoma.
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PMID:Detection of human papilloma virus (HPV) infection in paraffin-embedded tissues of endometrial carcinoma. 821 21

During the past decades, the expansion of molecular biology has had a pivotal role in understanding the basis of cancer development and progression. In addition, real advances have been made in the application of DNA recombinant technology to cancer therapy and patient management. In gynecologic oncologic fields, there are also many investigations to explore the basic pathogenesis of gynecologic cancer, such as cervical cancer, ovarian cancer, and endometrial cancer. It is now known that specific types of human papilloma virus (HPV) are the principal etiologic agents for both cervical cancer and its precursors. However, the various kinds of alterations in oncogenes and tumor suppressor genes may play additional roles in carcinogenesis of cervical cancer. Although ovarian carcinoma is the most frequent cause of death from gynecologic malignancies, the histogenesis and biological characteristics of these tumors are not well understood. During the last several years, many key observations have been made concerning the genetic alterations associated with ovarian cancer. Recent researches including some dominant oncogenes and tumor suppressor gene mutations common to these malignancies are providing bases to elucidate the mechanisms underlying this cancer. The most important basis of endometrial cancer is that K-ras and p53 mutations are also frequently observed.
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PMID:Molecular genetics of gynecologic cancer. 936 94

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

Endometrial cancer is one of the most prevalent neoplastic diseases in women, in the developed countries. In spite of hormonal dysfunction, no pivotal mechanism leading to this pathology is known. The study design was to evaluate the presence of human papilloma virus within the endometrium by in situ hybridization and its potential role in the occurrence of dysplastic and neoplastic endometrial lesions. Immunological antiviral and antitumour defense was investigated by cytometric measurement of selected lymphocyte subsets. Viral infection was present in nearly 25% of endometrial cancer patients and occasionally within endometrial hyperplasia with cellular atypia. The presence of human papilloma virus correlated with significant depletion of CD4 lymphocytes as well as activated T cells and NK.
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PMID:[Human papilloma virus (HPV) infection in the pathology of the endometrium. Role of immunological activation in antiviral and antineoplastic defense]. 1217 12

We report two cases of endometrial microglandular adenocarcinoma, a rare neoplasm, which, in its morphologic features, mimics cervical microglandular hyperplasia and mucinous proliferations of endometrium. The criteria for a correct pathological diagnosis, such as clinical, morphologic, and immunohistochemical data, are emphasized. For the first time, we probed to establish whether endometrial mucinous microglandular adenocarcinoma could be correlated to human papilloma virus (HPV) infection by using polymerase chain reaction amplification (PCR) of tumoral DNA. Similar to previous studies reported in the literature, the present lesions, occurring in postmenopausal women, immunohistochemically showed positivity for B72.3, Ca 125, CEA, Vimentin, estrogen and progesterone receptors, and negativity for p53. Molecular study by PCR amplification of tumor DNA showed no signal for HPV DNA in any of these cases; thus, this variant of endometrial carcinoma is not caused by the HPV infection, but probably by other pathogenetic mechanisms, such as an accumulation of the mutations, which arrive in old age or as the consequence of a peculiar hormonal situation.
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PMID:Endometrial mucinous microglandular adenocarcinoma: morphologic, immunohistochemical features, and emphasis in the human papillomavirus status. 1630 89

Squamous cell carcinoma (SCC) of the rectum is an extremely rare malignancy, accounting for 0.1-0.2% of rectal malignancies. It is associated with ulcerative colitis, prior radiation, schistosomiasis, ovarian cancer, endometrial cancer, human papilloma virus, colocutaneous fistulas and colonic duplication. Prior reported cases of SCC of the rectum have involved treatment with brachytherapy and external beam radiation. This case is particularly interesting because of the remote exposure of radiation (21 years previously) and the subsequent development of SCC of the rectum. Although extremely rare, SCC of the rectum can occur decades after radiation exposure.
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PMID:Squamous cell carcinoma of the rectum 21 years after radiotherapy for cervical carcinoma. 1963 83


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