Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Xanthomatous changes are unusual lesions of the corpus endometrium that may mask endometrial carcinoma. The term "xanthomatous endometritis" refers to morphological changes frequently induced by estrogen stimulation. We report for the first time a case of uterine metastasis of balloon-cell melanoma mimicking xanthomatous endometritis. Light microscopic, immunohistological, and ultrastructural results are presented and discussed in connection with our ideas on the pathogenesis of this peculiar tumor. The findings favor the hypothesis of a regressive phenomenon in the balloon-cell transformation of melanoma cells. The melan-A immunohistology seems to be more important in the diagnosis of balloon cell melanoma than the classic melanoma antibody HMB 45.
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PMID:[Endometrial metastasis of a "balloon" cell melanoma mimicking a "xanthomatous endometritis"]. 1132 31

A new method of survival analysis, denoted period analysis, has recently been developed, which has been shown to provide more up-to-date estimates of long-term survival rates than traditional methods of survival analysis. We applied period analysis to data from the nationwide Finnish cancer registry to provide up-to-date estimates of 5-, 10-, 15- and 20-year relative survival rates (RSR) achieved by the end of the 20th century. For most forms of cancer, period estimates of long-term survival are much higher than corresponding traditional survival estimates which suggests that for these cancers there has been ongoing major progress in survival rates in recent years which so far has remained undisclosed by traditional methods of survival analysis. For example, period analysis reveals that 10 year RSR have come close to (or even exceed) 80% for cancer of the corpus uteri and melanoma, 75% for breast cancer, 70% for bladder cancer, 65% for cancer of the cervix uteri, and 55% for cancer of the colon and prostate. Period analysis further reveals that 20 year RSR have now come close to (or even exceed) 75% for endometrial cancer and melanoma, 60% for breast cancer and cervical cancer, 55% for colon cancer and bladder cancer, and 40%-50% for cancer of the rectum, the ovaries, kidneys and nervous system.
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PMID:Long-term cancer patient survival achieved by the end of the 20th century: most up-to-date estimates from the nationwide Finnish cancer registry. 1148 67

Endometriosis, like cancer, is characterized by cell invasion and unrestrained growth. Furthermore, endometriosis and cancer are similar in other aspects, such as the development of new blood vessels and a decrease in the number of cells undergoing apoptosis. In spite of these similarities, endometriosis is not considered a malignant disorder. The possibility that endometriosis could, however, transform and become cancer has been debated in the literature since 1925. Mutations in the genes that encode for metabolic and detoxification enzymes, such as GALT and GSTM, have been implicated in the pathogenesis of endometriosis and in the progression to carcinoma of the ovary. PTEN, a tumor suppressor commonly mutated (50%) in endometrial carcinoma, is found mutated in endometrioid carcinoma of the ovary, but not in other forms of ovarian cancer. A recent study has shown that somatic mutations in the PTEN gene were identified in 20% of endometrioid carcinomas and 20.6% of solitary endometrial cysts, suggesting that inactivation of the PTEN tumor suppressor gene is an early event in the development of ovarian endometrioid carcinoma. In addition to cancerous transformation at the site of endometriosis, there is recent evidence to indicate that having endometriosis itself may increase a woman's risk of developing non-Hodgkin's lymphoma, malignant melanoma, and breast cancer.
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PMID:Role of endometriosis in cancer and tumor development. 1194 55

Germline mutations in the tumor-suppressor gene PTEN (MMAC1, TEP1) are found in Cowden syndrome, which predisposes to hamartomas, breast cancer, trichilemmomas, and thyroid tumors of follicular epithelium. PTEN has also been found to be somatically deleted, mutated, and/or silenced in various sporadically occurring cancers such as glioblastoma, breast cancer, kidney cancer, malignant melanoma, and endometrial cancer. Loss or reduction of PTEN protein expression as well as inappropriate subcellular compartmentalization is seen in non-medullary thyroid cancers. However, although allelic loss of the PTEN locus in 10q23.3 is frequently seen, this is not coupled with mutations in the PTEN gene. To approach further the frequency and mechanism behind PTEN silencing, we screened a panel of 87 sporadic thyroid tumors for PTEN mRNA expression, including 14 anaplastic carcinomas, 37 follicular carcinomas, 21 atypical adenomas, and 15 ordinary adenomas. Complete loss of PTEN mRNA expression was evident in six of the tumors, including four anaplastic carcinomas, one widely invasive carcinoma, and one ordinary adenoma. The transcriptional silencing of PTEN was significantly associated with the anaplastic subtype, suggesting that PTEN is involved in the carcinogenesis of highly malignant or late-stage thyroid cancers, whereas this particular mechanism appears to be of minor importance in differentiated follicular thyroid tumors. No association was observed between the expression, loss of heterozygosity, and mutation status in the 33 cases in which these parameters were compared. This indicates that PTEN silencing is a result of a wide variety of epigenetic and/or structural silencing mechanisms rather than a consequence of structural biallelic inactivation of the classical type. Furthermore, the high rate of alterations in the 10q23 region might indicate the presence of an as-yet unknown tumor-suppressor gene with an important role in the development of thyroid tumors.
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PMID:Silencing of the PTEN tumor-suppressor gene in anaplastic thyroid cancer. 1220 92

Ever since a gradual but significant reduction in the estrogenic and progestogenic components of oral contraceptives (OCs) was made, there has been a corresponding decrease in adverse effects associated with the pill. The beneficial effects include prevention of pregnancy, reduction in pelvic inflammatory disease, protection against ovarian/endometrial cancer and benign breast tumors and ovarian cysts, reduction in the occurrence of rheumatoid arthritis among OC users, and regulation of the menstrual cycle. The adverse effects include diseases of the circulatory system (myocardial infarction, venous thromboembolism, subarachnoid hemorrhage, hypertension), possible carcinogenicity (breast, cervix, melanoma), pituitary adenomas, liver disorders, glucose metabolix effects (diabetes), vitamin status alteration, delay in return of menstruation and fertility, and a number of minor side effects (nausea, vomiting). Contraindications to OC use include history of malignancy of the breast or genital tract, venous thromboembolism, cerebrovascular accident, undiagnosed abnormal vaginal bleeding, focal migraine, or familial hyperlipidemia. The following situations require medical assessment before OCs are prescribed, and medical supervision if OCs are prescribed: age 40+, smoking and age over 35, mild hypertension or a history of hypertensive disease of pregnancy (toxemia), epilepsy, diabetes mellitus, history of bouts of depression, history of oligomenorrhea or amenorrhea in nulliparous women, and gallbladder disease. Problems could occur with OC use in the following situations: 1) lactation (ideally, OCs should be withheld until the child is weaned but if not possible, OCs should not be given until lactation is established); 2) drug interaction (other contraceptive form should be used when the patient is taking antibiotics or anticonvulsants); 3) tropical diseases (studies are still underway); 4) adolescence (very young girls should use other contraceptive method until regular menstruation is established); 5) postcoital contraception (limited use of steroids in emergency situation); and 6) hormonal pregnancy tests (use of oral steroids for pregnancy testing is not recommended). The 3 main types of OCs currently used are the combined estrogen and progestagen, the progestagen-only OC, and the triphasic OC. The lowest effective dose of a compound should be used, and healthy women may continue to use OCs for many years.
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PMID:Statement on steroidal oral contraceptives. 1226 73

Findings of several recent epidemiological studies of the relationship between oral contraceptives (OC) and the development of cancer were summarized. Enough time has now elapsed since the introduction of OCs to enable investigators to examine the latent and longterm effects of OC use on the development of cancer. In general recent findings indicated that OC use was not associated with the development of breast cancer breast cancer and was negatively associated with endometrial ovarian cancer. Findings in regard to cervical and liver cancer cases and melanoma were unclear. In reference to breast cancer, in a study of 1191 breast cancer cases and 5026 controls, conduct Rosenberg and others, the relative risk of breast cancer for women who ever used OCs as compared with women who never used OC was 1.0. No increased risk was observes for women who 1) used OCs for more than 5 years, even 10 years following OC discontinuance; 2) took OCs while they were nulliparous or premenopausal; 3) had a family history of benign or 1st degree breast cancer. 4735 breast cancer patients and 4685 controls were included in the recent Cancer and Steroid Hormone Study (cash) conducted by the Centers for Disease Control. Results indicated that the relative risk of breast cancer for every users of OCs compared to never users was 0.9. No increased risk was observed for women who took OCs for 10 or more or 20 or more years. No increased risk was associated with any of the OC formulations commonly available in the US. The cash data were also used to assess issues raised in 2 other studies. A Los Angeles study of 314 cases and 314 controls found that women who used high progestin OCs for 2 or more years had s significantly increased risk of developing breast cancer by age 37, and a Britidh study found that OC use of 4 or more years prior ro 1st pregnancy was associated with an increase risk of cancer by age 45. In terms of the cash data no increased risk of breast cancer by the ages specified above was observed for these 2 identically defined subgroups of OC users. Several studies found that the risk of developing ovarian cancer was reduced by 50% for OC users. Furthermore, the risk decreased as duration of OC use increased, and the protevtive effect continued for at least 10 years following discontinuation of OC use. An initial analysis of CASH data revealed that the reduced risk was associated with all types of OC formulations currently marketed in the US. Several studies found a similar reduction in the risk of endometrial cancer among OC users. According to the CASH data, the relative risk of endometrial cancer was 0.5 for women who used OC for 12 or more months compared to never users, the protective effect lasted for at least 10 years, and the reduced risk was observed for the 7 most common OCs used in US. Most studies which included OC users detected a positive relattionship between OC use and the development of cervical neoplasms however, the data in these studies is subject to selective and misclassification biases and confounding effects. Despite these problems, there is a possibility that OC use enhances the risk of cevical neoplasms and speeds up the transition from cervical dyplasia to invasive cancer. The results of studies. Taking into account the role of sun exposure, need to be undertaken. The relationship between OC use and liver tumors has not be examined epidemiologically, and this deficit should be corrected.
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PMID:Researchers can now investigate long-term effects of OCs on cancer. 1227 18

The PTEN tumor suppressor gene encodes a phosphatidylinositol 3'-phosphatase that is inactivated in a high percentage of human tumors, particularly glioblastoma, melanoma, and prostate and endometrial carcinoma. Previous studies showed that PTEN is a seryl phosphoprotein and a substrate of protein kinase CK2 (CK2). However, the sites in PTEN that are phosphorylated in vivo have not been identified directly, nor has the effect of phosphorylation on PTEN catalytic activity been reported. We used mass spectrometric methods to identify Ser(370) and Ser(385) as in vivo phosphorylation sites of PTEN. These sites also are phosphorylated by CK2 in vitro, and phosphorylation inhibits PTEN activity towards its substrate, PIP3. We also identify a novel in vivo phosphorylation site, Thr(366). Following transient over-expression, a fraction of CK2 and PTEN co-immunoprecipitate. Moreover, pharmacological inhibition of CK2 activity leads to decreased Akt activation in PTEN+/+ but not PTEN-/- fibroblasts. Our results contrast with previous assignments of PTEN phosphorylation sites based solely on mutagenesis approaches, suggest that CK2 is a physiologically relevant PTEN kinase, and raise the possibility that CK2-mediated inhibition of PTEN plays a role in oncogenesis.
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PMID:Direct identification of PTEN phosphorylation sites. 1229 95

Recent studies have demonstrated new benefits of pill use, reduced risks associated with the minipill, and the possibility of screening out high risk women. The minipill is as effective as other formulations except in cases of chronic malnutrition or concomitant use of antibiotics or anticonvulsives. Oral contraceptives (OCs) frequently lessen menstrual problems. They prevent functional cysts in the ovaries, and reduce the incidence of benign breast tumors and the relative risk of developing ovarian cancer after 3 years of use. Combined OCs reduce the risk of endometrial cancer although sequentials increase it. OCs offer protection against salpingitis and other pelvic infections, against tubal pregnancies, and against chronic rheumatoid arthritis. Minipills appear to be less frequently associated with bothersome side effects than other OCs. The most significant risk of OCs is of death due to thrombo emboli of venous origin, myocardial ischemia, cerebrovascular accidents, and hypertension in women over 35, particularly those who smoke heavily. In 1981 the 2 British studies reported a reduced risk from these causes compared to results published in 1977. Estrogens are clearly responsible for some of the complications, apparently due to a weakening of the fibrinolytic systems, but progestagens or estrogen-progestagen combinations are also implicated. Arterial hypertension and cerebral and cardiac accidents appear to be due to the effect of progestagens on arterial tension, glucose metabolism, and the level of high density lipoprotein cholesterol. Risks of some liver diseases are elevated in pill users, but the question of tumors of the pituitary is not yet resolved. The incidence of uterine cancer appears to be elevated in pill users although the association is obscured by other factors. Some evidence exists of an association between estrogen-progestagen formulations and melanoma. No increase in abortion or fetal malformations except possibly an increase in twin pregnancies is noted after discontinuation of the pill. Pills should not be prescribed for smokers over 35 or any women over 45. Pills are possibly acceptable for women 35-44 in good health with no signs of diabetes, hypertension, or hyperlipoproteinemia. They should be followed up more frequently and should recognize the signs of complications.
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PMID:[Oral contraception in 1983 (author's transl)]. 1231 9

We used the nationwide Swedish Family-Cancer Database to analyse cancer risks in women who have had children with different men. Cancer cases were retrieved from the Swedish Cancer Registry for 1961-1998. A total of 3 million women and 316 497 cancer cases were covered. For women having children with more than one partner, an increased risk was shown for upper aerodigestive tract, anal, liver, pancreatic, lung, cervical, other female genital, kidney and urinary bladder cancers. A decreased risk was observed for breast and endometrial cancer, and melanoma. In women who had at least three or more children with three or more partners, the increased risks were even more pronounced for pancreatic, lung and cervical cancer. Conversely, the risk for breast and endometrial cancer, and melanoma was decreased. The present results indicated that women who had children with multiple partners showed an excess of smoking-related and sexually transmitted cancers. The decreased risks for breast and endometrial cancer and for melanoma were possibly related to lifestyle factors connected with economic deprivation. The magnitude of the effects was so large that failure to consider the number of partners may introduce bias.
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PMID:Cancer risks in women who had children with different partners from the Swedish Family-Cancer Database. 1239 40

Familial risk of pancreatic cancer has been mainly assessed through case-control studies based on reported but not medically verified cancers in family members. We used the nationwide Swedish Family-Cancer Database on 10.2 million individuals and 21,000 pancreatic cancers to calculate standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) for pancreatic cancer in 0- to 66-year-old offspring of parents with pancreatic or other specified tumors. Additionally, SIRs for second primary pancreatic cancers were analyzed after any first neoplasm. SIRs for pancreatic cancer (1.68, 95% CI 1.16-2.35) and pancreatic adenocarcinoma (1.73, 95% CI 1.13-2.54) were increased when a parent presented with pancreatic cancer. The risk was not dependent on diagnostic age of offspring or parents. Pancreatic cancer was associated with parental lung, rectal or endometrial cancer and with melanoma. SIRs for pancreatic cancer were 10.01 and 7.96 among offspring who were diagnosed before age 50 years when parents were diagnosed with squamous cell and adenocarcinoma of the lung, respectively, before age 60 years. The population-attributable proportion of familial pancreatic cancer was 1.1%. Risks for second pancreatic cancers were increased in men and women after small intestinal, colon and bladder cancer. The degree of familial clustering for pancreatic cancer and its population-attributable proportion were lower than the data cited in the literature. Clustering of pancreatic cancer with sites presenting in hereditary nonpolyposis colorectal cancer was noted. The strong association of pancreatic and lung cancers is puzzling, and it remains unclear to what extent this represents familial sharing of smoking habits.
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PMID:Familial and second primary pancreatic cancers: a nationwide epidemiologic study from Sweden. 1247 70


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