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

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

To date, nine case-control studies conducted in developed countries have identified an association between oral contraceptives (OCs) and liver cancer. The most recent population-based data from both developed and developing countries failed to confirm such an association, however. A study conducted by the World Health Organization in eight developing countries (Chile, China, Colombia, Israel, Kenya, Nigeria, Philippines, and Thailand), in which 122 women with liver cancer were matched with 802 controls, found no elevated risk for OC users compared with never-users (relative risk, 0.7; 95% confidence interval, 0.4-1.2). This study is particularly significant since it was conducted in countries where hepatitis B virus infection, an important risk factor for primary liver cancer, is widespread. In addition, population mortality data from the US, UK, Japan, and Sweden have failed to document increases in liver cancer cases coincident with increases in OC use. Given that population statistics can detect changes on the magnitude of a 40-50% decrease in the risk of ovarian and endometrial cancer related to OC use, they should be able to detect increases of two to 20 times the risk of liver cancer. The increased risk of liver cancer found in the case-control studies may reflect bias resulting from the small size of these studies.
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PMID:Oral contraceptives and liver cancer. 1234 50

The pattern of transcriptional activation by 17beta-estradiol (E2) and 4-hydroxytamoxifen (4-OHT) was determined in ZR-75 and MDA-MB-231 breast, ECC1 and HEC1A endometrial and HepG2 liver cancer cell lines cotransfected with E2-responsive constructs and wild-type estrogen receptor alpha (ER alpha) or ER beta (ER beta) or variant forms of ER alpha expressing activation function 1, AF1 (ER alpha-AF1) or activation function 2, AF2 (ER alpha-AF2). The E2-responsive constructs contained promoter inserts from the human complement C3 (pC3), human cathepsin D (pCD) and rat creatine kinase B (pCKB) genes. Minimal ER beta-dependent transactivation (<2.5-fold induction) was observed for E2 only in ECC1 and MDA-MB-231 cells transfected with pCKB or pC3, whereas 4-OHT was inactive as an ER beta agonist for all promoters in the four cell lines. The ER alpha agonist and/or antagonist activities for E2 and 4-OHT were highly variable and the transactivation was dependent on ER subtype, ER alpha variant expressed, gene promoter, and cell context. For example, E2 did not activate pCD in HepG2 cells transfected with wild-type or variant ER alpha, whereas E2 activated reporter gene activity in the four endometrial and breast cancer cell lines transfected with ER alpha and pCD, pCKB or pC3. Hormone activation of these constructs by ER alpha-AF1 or ER alpha-AF2 was highly variable among the different cell lines and even in the same cell line transfected with the three E2-responsive constructs. Similar variability was observed for 4-OHT. For example, 4-OHT activates pC3 in HepG2 cells transfected with ER alpha or ER alpha-AF1, and pCKB in HEC1A cells. However, AF1-dependent activation by 4-OHT is not observed for pCKB in ECC1 cells or for pC3 and pCD in HEC1A or ECC1 endometrial cancer cells. The results of this study suggest that transcriptional activation by E2 and 4-OHT induces recruitment of different transcription factor complexes that are dependent on the cell type and also the gene promoter.
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PMID:17 beta-estradiol- and 4-hydroxytamoxifen-induced transactivation in breast, endometrial and liver cancer cells is dependent on ER-subtype, cell and promoter context. 1264 21

The objective of this study was to determine the site-specific cancer incidence of hypertensive patients and examine the effect of blood pressure-related variables on the risk of cancers with elevated incidence among the hypertensive patients. A record linkage study of Hypertension Register of the North Karelia Project and the Finnish Cancer Registry was conducted. The mean follow-up time was 16 years. A total of 20 529 hypertensive patients were studied. Main outcome measures were standardised incidence ratios and hazard ratios. The overall cancer incidence was close to that of the general population for both men and women. The incidence rate for the kidney cancer was significantly increased in hypertensive patients (standardised incidence ratio 1.34, 95% confidence interval (CI) 1.11-1.60), as well as incidence rates for cancers of pancreas (1.26, 1.02-1.54), and endometrium (1.22, 1.01-1.44) in hypertensive women. The incidence of lung cancer was significantly decreased (0.86, 0.77-0.95). The incidence of liver cancer was elevated with borderline significance (1.36, 0.99-1.82). In Cox regression models, the use of antihypertensive drugs at baseline was a significant predictor of kidney (hazard ratio for use of antihypertensive drugs 1.89, 95% CI 0.96-3.75) and pancreatic cancer (1.78, 0.99-3.22) in women but not in men. The incidence of endometrial cancer or liver cancer was not related to blood pressure levels or the use of antihypertensive drugs. In women, obesity was a significant predictor of cancers of the endometrium, kidney and liver. In conclusion, increased occurrence of some cancer types among hypertensive patients seem to be partly explained by obesity and the use of antihypertensive drugs.
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PMID:Cancer pattern among hypertensive patients in North Karelia, Finland. 1570 72

Chlamydial attachment and infectivity in vitro and ascending disease and sequelae in vivo have been reported to be enhanced/modulated by estrogen. Endometrial carcinoma cell lines Ishikawa and HEC-1B and the breast cancer lines MCF-7 and HCC-1806 were examined for Chlamydia trachomatis E infectivity. Estrogen receptor (ER) presence was confirmed by Western blot and qRT-PCR analyses. FACS analysis was used to determine the percent of plasma membrane-localized ERs (mERs), and their activity was tested by estrogen binding and competitive estrogen antagonists assays. Chlamydiae grew in all cell lines with HEC (90%) >> MCF-7 (57%)>Ishikawa (51%) >> HCC-1806 (20%). The cell line ER isoform composition was re-defined as: ERalpha + ERbeta + for MCF-7, HCC-1806 and Ishikawa; and ERbeta only for HEC-1B. HeLa cells were also tested and found to express ERbeta, but not ERalpha. A small percentage of both ERs were surface-exposed and functionally active. The endometrium-predominant ERbeta isoform was found in all cell lines, including those most representative of the common sites of C. trachomatis infection. Thus, the role of chlamydial attachment/infectivity will now be analyzed in ERbeta+and-isogenic HEC-1B cells.
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PMID:Characterization of estrogen-responsive epithelial cell lines and their infectivity by genital Chlamydia trachomatis. 1604 68

Melatonin is a phylogenetically well-preserved molecule with diverse physiological functions. In addition to its well-known regulatory control of the sleep/wake cycle, as well as circadian rhythms generally, melatonin is involved in immunomodulation, hematopoiesis, and antioxidative processes. Recent human and animal studies have now shown that melatonin also has important oncostatic properties. Both at physiological and pharmacological doses melatonin exerts growth inhibitory effects on breast cancer cell lines. In hepatomas, through its activation of MT1 and MT2 receptors, melatonin inhibits linoleic acid uptake, thereby preventing the formation of the mitogenic metabolite 1,3-hydroxyoctadecadienoic acid. In animal model studies, melatonin has been shown to have preventative action against nitrosodiethylamine (NDEA)-induced liver cancer. Melatonin also inhibits the growth of prostate tumors via activation of MT1 receptors thereby inducing translocation of the androgen receptor to the cytoplasm and inhibition of the effect of endogenous androgens. There is abundant evidence indicating that melatonin is involved in preventing tumor initiation, promotion, and progression. The anticarcinogenic effect of melatonin on neoplastic cells relies on its antioxidant, immunostimulating, and apoptotic properties. Melatonin's oncostatic actions include the direct augmentation of natural killer (NK) cell activity, which increases immunosurveillance, as well as the stimulation of cytokine production, for example, of interleukin (IL)-2, IL-6, IL-12, and interferon (IFN)-gamma. In addition to its direct oncostatic action, melatonin protects hematopoietic precursors from the toxic effect of anticancer chemotherapeutic drugs. Melatonin secretion is impaired in patients suffering from breast cancer, endometrial cancer, or colorectal cancer. The increased incidence of breast cancer and colorectal cancer seen in nurses and other night shift workers suggests a possible link between diminished secretion of melatonin and increased exposure to light during nighttime. The physiological surge of melatonin at night is thus considered a "natural restraint" on tumor initiation, promotion, and progression.
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PMID:Therapeutic actions of melatonin in cancer: possible mechanisms. 1881 50

Estrogen action is regulated at the receptor level by regulation of expression of estrogen receptors, and at the pre-receptor level by interconversions between the active hormone (estradiol) and its inactive counterparts (estrone, estrone-sulfate). In peripheral tissues, estrogens can be produced via the aromatase or the sulfatase pathways. Aromatase converts androstenedione and testosterone to estrone and estradiol, respectively, and sulfatase releases estrogens from inactive sulfates, while sulfotransferase catalyzes the reverse reaction. In both pathways, 17beta-hydroxysteroid dehydrogenases (17beta-HSDs) are of paramount importance as they catalyze activation of estrone to estradiol and inactivation of estradiol to estrone. These enzymes belong to either the short-chain dehydrogenase/reductase (SDR) or the aldo-keto reductase (AKR) protein superfamilies. Differential expression of these pre-receptor regulatory enzymes can lead to high estradiol concentrations, which have been implicated in the development of different diseases. Here, we have examined gene expression levels of estrogen-metabolizing enzymes, as six SDRs (17beta-HSD types 1, 2, 4, 7, 8, 12) and one AKR (17beta-HSD type 5; AKR1C3), of aromatase, steroid sulfatase (STS) and estrogen sulfotransferase (SULT1E1), and of the alpha and beta estrogen receptors (ERs), in breast cancer (MCF-7), endometrial cancer (Ishikawa), choriocarcinoma (JEG3) and liver cancer (HepG2) cell lines. After RNA isolation and cDNA synthesis, real-time PCR analyses were performed. The expression of AKR1C3 was examined also at the protein level. Our data show that in all four cancer cell lines, estradiol can be synthesized from estrone by the action of 17beta-HSD type 12, or from estrone-sulfate by sulfatase. In JEG3 and HepG2 cells, estradiol can be formed from androgens by aromatase and 17beta-HSD type 1. Also in HepG2 cells, AKR1C3, which converts androstenedione to testosterone, in concert with aromatase might be responsible for estradiol formation. In MCF7 and Ishikawa cells, estradiol exerts its actions through ERalpha, while in JEG3 and HepG2 cells, it may act through non-ER-mediated pathways.
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PMID:Expression of 17beta-hydroxysteroid dehydrogenases and other estrogen-metabolizing enzymes in different cancer cell lines. 1902 35

Cancer risks for a person who has inherited a MUTYH mutation from only one parent (monoallelic mutation carrier) are uncertain. Using the Colon Cancer Family Registry and Newfoundland Familial Colon Cancer Registry, we identified 2,179 first- and second-degree relatives of 144 incident colorectal cancer (CRC) cases who were monoallelic or biallelic mutation carriers ascertained by sampling population complete cancer registries in the United States, Canada and Australia. Using Cox regression weighted to adjust for sampling on family history, we estimated that the country-, age- and sex-specific standardized incidence ratios (SIRs) for monoallelic mutation carriers, compared to the general population, were: 2.04 (95% confidence interval, CI 1.56-2.70; p < 0.001) for CRC, 3.24 (95%CI 2.18-4.98; p < 0.001) for gastric cancer, 3.09 (95%CI 1.07-12.25; p = 0.07) for liver cancer and 2.33 (95%CI 1.18-5.08; p = 0.02) for endometrial cancer. Age-specific cumulative risks to age 70 years, estimated using the SIRs and US population incidences, were: for CRC, 6% (95%CI 5-8%) for men and 4% (95%CI 3-6%) for women; for gastric cancer, 2% (95%CI 1-3%) for men and 0.7% (95%CI 0.5-1%) for women; for liver cancer, 1% (95%CI 0.3-3%) for men and 0.3% (95%CI 0.1-1%) for women and for endometrial cancer, 4% (95%CI 2-8%). There was no evidence of increased risks for cancers of the brain, pancreas, kidney, lung, breast or prostate. Monoallelic MUTYH mutation carriers with a family history of CRC, such as those identified from screening multiple-case CRC families, are at increased risk of colorectal, gastric, endometrial and possibly liver cancers.
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PMID:Cancer risks for monoallelic MUTYH mutation carriers with a family history of colorectal cancer. 2117 Oct 15

We evaluated the local control of gamma knife stereotactic radiosurgery (GKSRS) in the treatment of cerebral metastases from primary tumors that rarely metastasize to the central nervous system (CNS). There is little published data on this subject with very few series on specific primary tumors. We present our experience treating these lesions with GKSRS combined with a review of the salient literature. A retrospective study of 36 patients who collectively underwent 44 GKSRS procedures for CNS metastatic disease was undertaken. Our series includes four patients with sarcoma, two with prostate cancer, three with thyroid cancer, five with endometrial cancer, seven with ovarian cancer, two with cervical cancer, six with esophageal cancer, two with bladder cancer, one with liver cancer, one with pancreatic cancer, and three with testicular cancer. With 44 gamma knife sessions treating 74 tumors, 63 tumors showed no radiographic evidence of progression, and 13 tumors demonstrated radiographic progression between one and 12 months after gamma knife treatment. In six patients in the population, further treatment with GKSRS was necessary due to enlargement of untreated lesions or new metastatic disease. GKSRS for uncommon CNS metastases is appears to be efficacious in controlling the treated tumor. The majority of tumors treated in our study did not progress post gamma knife.
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PMID:Stereotactic radiosurgical treatment of brain metastasis of primary tumors that rarely metastasize to the central nervous system. 2287 Aug 50

Competing endogenous RNAs (ceRNAs) refer to RNA transcripts, such as mRNAs, non-coding RNAs, pseudogene transcripts, and circular RNAs, that can regulate each other by competing for the same pool of miRNAs. ceRNAs involve in the pathogenesis of several common cancers such as prostate cancer, liver cancer, breast cancer, lung cancer, gastric cancer, endometrial cancer, and so on. ceRNA activity is determined by factors such as miRNA/ceRNA abundance, ceRNAs binding affinity to miRNAs, RNA editing, and RNA-binding proteins. The alteration of any of these factors may lead to ceRNA network imbalance and thus contribute to cancer initiation and progression. There are generally three steps in ceRNA research conductions: ceRNA prediction, ceRNA validation, and ceRNA functional investigation. Deciphering ceRNA interplay in cancer provides new insight into cancer pathogenesis and opportunities for therapy exploration. In this review, we try to give readers a concise and reliable illustration on the mechanism, functions, research approaches, and perspective of ceRNA in cancer.
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PMID:Competing endogenous RNA interplay in cancer: mechanism, methodology, and perspectives. 2560 44


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