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At least 19 recordsLinked to original sources
PubMed1992

Hormone replacement therapy and breast cancer, endometrial cancer and cardiovascular disease: risks and benefits.

The relatively restricted use of hormone replacement therapy in the United Kingdom has frequently been noted. It is possible that low prescribing rates may, in part, be due to the difficulty in interpreting the wealth of research evidence relating to the risks and benefits of hormone replacement therapy. Conflicting conclusions from research can cause considerable uncertainty and confusion. This paper reviews the evidence relating to hormone replacement therapy and the risks of breast cancer, endometrial cancer and cardiovascular disease and discusses the issues which require critical assessment. This should add to the information base available to general practitioners and thus assist in decision-making in the context of uncertainty.

Breast Neoplasms↗
PubMed1979

Case-control study of hair dye use by patients with breast cancer and endometrial cancer.

A case-control study was undertaken of use of permanent and semipermanent hair dyes by women with cancers of several sites, including breast and endometrium. In London, Ontario, 50 cases of of breast cancer and in Toronto 35 cases of breast cancer and 36 cases of endometrial cancer were identified in cancer treatment centers. In London, controls were selected from hospitalized women with diseases other than cancer; in Toronto, controls were selected from women living in the same neighborhood as the patients with cancer. The results did not suggest an increased risk of either breast or endometrial cancer in users of permanent or permanent and semipermanent dyes combined. Although the numbers of cases and controls were small, the consistency of the results for both sites, in both study centers, and the absence of any clear positive relationship between various measures of intensity of use and risk of cancer provided evidence that a large increase in risk was not missed.

Adult↗
PubMed1992

[Development of a new supplementary diagnostic method for endometrial cancer by flow cytometry employing anti-endometrial cancer antibody, MSN-1 and MSN-3].

In cytology, it is often difficult to make a definite diagnosis of endometrial cancer. In order to devise a new supplementary method, using flow cytometry we analyzed the reactivities of endometrial cells with two monoclonal antibodies (MSN-1 and MSN-3), both of which are strongly reactive to endometrial cancer cells. Employing either or both antibodies in flow cytometry, we investigated the usefulness of this analysis for distinguishing endometrial cancer cells from normal endometrial cells. Results revealed a low positive rate for normal endometrium: 9.2% with MSN-1 and 5.0% with MSN-3. In contrast, for endometrial cancer the positive rate was high: 81.2% with MSN-1 and 43.8% with MSN-3. Combined analysis with both antibodies increased the positive rate for endometrial cancer to 93.7%. These results suggest that analysis by flow cytometry employing MSN-1 and MSN-3 may have a diagnostic value for endometrial cancer. We are also investigating the usefulness of two-color analysis using these antibodies.

Antibodies, Monoclonal↗
PubMedDate not supplied

Interrelation between Western type cancers and non-Western type cancers as regards their risk variation in time and space. IV. Hormonal transition of Japanese women from the pro-cervical cancer age through the pro-endometrial cancer age to the pro-hypogonadism age.

Chronological trend of urinary steroid excretions in Japanese women was investigated during the period of June 1972 to August 1986 using healthy women of urban and rural origins, patients with breast cancer and patients with either cervical cancer or endometrial cancer. The excretions of 14 neutral steroids were estimated by gas liquid chromatography, and the obtained data were tentatively correlated with the epidemiological backgrounds. In the course of the chronological transition from the 1st stage (1972-1974) to the 2nd stage (1975-79), the urinary steroid pattern of Japanese women with and without cancer experienced a common change to produce specific deviations that were in agreement with the hormonal characteristics of a pill user or of an endometrial cancer patient. At the 3rd stage (1980-86), patients with either cervical cancer or endometrial cancer were distinguished from 1st stage controls by non-specific depression of all androgens, progestins and corticosteroids in urine. Throughout the whole period, both the risk for cervical cancer and the reproductive activity (birth rate) were found to decrease continuously in Japanese women. Evidence was presented to suggest that the above deterioration of the hormonal environment in Japanese women could be related to the stress of modern life rather than to defects in the diet. On the basis of the above findings, the 1st, 2nd and 3rd stages of our investigation were tentatively termed the pro-cervical cancer age, the pro-endometrial cancer age and the pro-hypogonadism age. The relation between the chronological change of urinary steroids and that of the epidemiological background was analyzed from the view point of population ecology.

Age Factors↗
PubMed2019

Estrogen-independent molecular actions of mutant estrogen receptor 1 in endometrial cancer.

Estrogen receptor 1 (ESR1) mutations have been identified in hormone therapy-resistant breast cancer and primary endometrial cancer. Analyses in breast cancer suggest that mutant ESR1 exhibits estrogen-independent activity. In endometrial cancer, ESR1 mutations are associated with worse outcomes and less obesity, however, experimental investigation of these mutations has not been performed. Using a unique CRISPR/Cas9 strategy, we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus. We discovered estrogen-independent mutant ESR1 genomic binding that is significantly altered from wild-type ESR1. The D538G mutation impacted expression, including a large set of nonestrogen-regulated genes, and chromatin accessibility, with most affected loci bound by mutant ESR1. Mutant ESR1 is distinct from constitutive ESR1 activity because mutant-specific changes are not recapitulated with prolonged estrogen exposure. Overall, the D538G mutant ESR1 confers estrogen-independent activity while causing additional regulatory changes in endometrial cancer cells that are distinct from breast cancer cells.

CRISPR-Cas Systems↗
PubMed1991

Initial experience with placental protein 4 (PP-4) as tumor marker in cervical and endometrial cancer.

PP-4, a recently characterized glycoprotein from human placenta was studied using a specific double-antibody radioimmunoassay in sera of 130 volunteers, 74 cervical cancer patients and 43 endometrial cancer patients. Elevated levels (greater than 3 micrograms/l) were found in 35 (47.3%) cervical cancer patients and in 18 (41.9%) endometrial cancer patients. Degree of elevation were not correlated with clinical stage, histology, and histological degree of differentiation. 36 patients with cervical cancer and 20 patients with endometrial cancer were monitored on two to seven occasions during four to 50 weeks. Rising, remaining unchanged of falling levels of PP-4 correlated with progression, stabilization or regression of disease 55.5% in patients with cervical and 65.0% in patients with endometrial cancer. During and some months after external telecobalt irradiation therapy wide range of PP-4 levels were observed in some patients. The study suggest that PP-4 can be regarded as a tumor associated protein which most likely can serve as tumor marker in cervical and endometrial cancer.

Annexin A5↗
PubMed1976

Endometrial cancer: not a benign disease.

Endometrial cancer is by no means a benign disease. While many adequate treatment plans now exist for early endometrial cancer, the best method of treadtment of this disease has yet to be defined. The prognostic factors need further study and definition. Pelvic and aortic nodes are of more than passing significance in certain subsets of Stage 1 endometrial cancer, and there is much to be learned about the biologic behavior of apparent early endometrial cancer. Prospective studies may yield sufficient data to provide a solid base for further clinical therapeutic trials.

Adenocarcinoma↗
PubMed1992

Recommendations regarding estrogen replacement therapy after treatment of endometrial cancer.

A history of endometrial cancer has long been considered a contraindication to estrogen replacement therapy. Yet women with such a history, like other women when postmenopausal, often suffer vasomotor symptoms that could easily be relieved with estrogen. In fact there is no good evidence that estrogen significantly increases the risk of recurrence after treatment for endometrial cancer. Some studies now suggest that estrogen plus a progestin may actually decrease the risk of cancer recurrence in these patients. The benefits of estrogen in preventing osteoporosis and cardiovascular disease in postmenopausal women is substantial.

Cardiovascular Diseases↗
PubMed1979

Replacement estrogens and endometrial cancer.

We examined the incidence of endometrial cancer in a large prepaid group practice in the Seattle area. From July, 1975, to July, 1977, there was a sharp downward trend in the incidence of endometrial cancer that paralleled a substantial reduction in prescriptions for replacement estrogens. Incidence rates were estimated for estrogen users and nonusers among women 50 to 64 years of age with intact uteri; current long-term users had an annual risk for endometrial cancer between 1 and 3 per cent, whereas nonusers had a risk less than 1/10th as great. These incidence rates remained fairly constant over time among users and nonusers; the drop in overall incidence soon after estrogen use declined suggests that the increased risk associated with estrogens falls quickly after discontinuation. The reduction in incidence of endometrial cancer in this group practice was part of a general decline in the United States after 1975.

Estrogens↗
PubMed1992

[Apud cells in endometrial cancer].

55 endometrial carcinomas containing apud cells are studied. Correlation between the endocrine-metabolic disturbances and mitotic index, on the one hand, and number of apud cells and their product on the other, is revealed. If the percentage of apud cells is above 20 of all parenchymal cells, low mitotic index in the tumour, marked production of serotonin, calcitonin and other hormones and high incidence of endocrine disturbances together with a relatively favourable prognosis are observed. Low number of apud cells associated with high mitotic index and high incidence of unfavourable outcomes while the hormone production and endocrine disturbances were rare or absent.

APUD Cells↗
PubMed1992

Risk of prostate, ovarian, and endometrial cancer among relatives of women with breast cancer.

OBJECTIVE: To investigate the risk of prostate, ovarian, and endometrial cancer among relatives of patients with breast cancer. DESIGN: Cohort study of 947 pedigrees in which the proband had breast cancer, linked with the Icelandic cancer registry. SETTING: Iceland. SUBJECTS: The 947 pedigrees included 29,725 people, of whom 1539 had breast cancer, 467 had prostate cancer, 135 ovarian cancer, and 105 endometrial cancer. MAIN OUTCOME MEASURES: Risk of prostate, ovarian, and endometrial cancer among blood relatives of women with breast cancer compared with risk in spouses. RESULTS: The risk of prostate cancer was significantly raised for all relatives (1.5), first degree relatives (1.4), and second degree relatives (1.3) of women with breast cancer. Risk of ovarian cancer was raised for all relatives (1.9) and first degree relatives (1.9) and risk of endometrial cancer was raised for all relatives only (1.9). The risk of prostate cancer was raised if the proband with breast cancer had a first degree relative with prostate cancer. CONCLUSIONS: Coaggregation exists between breast cancer and cancers of the prostate, ovaries, and endometrium. This risk relation is probably based on genes which act by increasing the risk for cancer at these sites. Environmental factors that are common among relatives may also play a part. Continued research is required into pathophysiological mechanisms that could explain these observations.

Aged↗
PubMed2025

The protective role of γδ T cells in endometrial cancer.

Γδ T cells are non-conventional T cells that are not MHC restricted and have T cell receptors (TCRs) that are stimulated by phosphoantigens, stress-induced proteins, lipids, and other antigens. These cells are prognostic across cancer types in The Cancer Genome Atlas (TCGA) but have not been well studied in endometrial cancer, which has a rising incidence and mortality rate. Endometrial cancer patients have variable responses to checkpoint inhibitors which are related to the molecular subtype of their cancer. As such, there is a pressing need to understand the immune microenvironment in endometrial cancer. This study addresses this gap in knowledge by investigating γδ T cell repertoires and transcriptomes in this disease site. γδ T cell repertoires were obtained for 543 endometrial cancer patients within the TCGA and from 5 endometrial cancer patients in the single cell dataset SRP349751 using TRUST4. GLIPH2 was used to identify TCRs predicted to bind the same antigen. Transcriptomes were investigated in the single cell dataset. DNA Polymerase Epsilon Exonuclease (POLE) and Microsatellite Instability High (MSI-H) endometrial cancer subtypes had the most γδ T cell infiltration. Vδ1 and Vδ3 γδ T cell infiltration was prognostic independent of stage and molecular subtype. GLIPH2 analysis revealed TCRδ motifs for TDK, YTD, and GEL were public across all four molecular subtypes and were present in the single cell data set. Vδ1 γδ T cell transcriptomes were associated with cytotoxicity and recent TCR stimulation. These data support further investigation of immunotherapies targeting γδ T cells in endometrial cancer.

Humans↗
PubMed1991

Specific binding sites for insulin and insulin-like growth factor I in human endometrial cancer.

Insulin and insulin-like growth factor I are known to be mitogenic and therefore may play a role in the development of endometrial cancer. We undertook this study to investigate whether human endometrial cancer tissue has receptors for these substances. Endometrial cancer tissue samples were obtained at hysterectomy from 10 women with endometrial cancer, and control endometrial tissue was collected from normal cycling women undergoing hysterectomy for nonendocrine problems. Binding studies with iodine 125-insulin and [125I]insulin-like growth factor I revealed the presence of specific binding sites for insulin and insulin-like growth factor I in both normal endometrium and endometrial cancer tissue. The percent binding of [125I]insulin in the endometrial cancer tissue (mean +/- SE 2.4% +/- 0.5%/100 micrograms protein) was not significantly different from that in normal endometrium (3.5% +/- 1%/100 micrograms protein). On the contrary, the percent total binding of [125]insulin-like growth factor I in the endometrial cancer (5.3% +/- 1.5%/100 micrograms protein) was significantly (p less than 0.04) higher than that observed in normal endometrium (2.1% +/- 0.4%/100 micrograms protein). There was a significant positive correlation between the histologic grade of the tumor and the insulin-like growth factor I binding (r = 0.865, p less than 0.02). The affinity constants for the high-affinity receptors were similar in the normal and neoplastic endometrium. These results indicate that insulin and insulin-like growth factor I may play a role in the growth and development of endometrial cancer.

Adult↗
PubMed1991

Upper-body fat distribution and endometrial cancer risk.

STUDY OBJECTIVE: --To determine if body fat distribution affected endometrial cancer risk. DESIGN: --Case-control study. SETTING: --This study was carried out at the H. Lee Moffitt Cancer Center at the University of South Florida, Tampa, where all patients in the case group received their diagnoses and histological confirmations. PATIENTS: --Forty consecutive women newly diagnosed with endometrial cancer and 40 controls matched for age and Quetelet index. MAIN OUTCOME MEASURES: --Anthropometric measurements were taken for the abdomen, thigh, suprailiac, subscapular, biceps, and triceps skin fold thicknesses; waist and hip circumferences, weight, and height. Relative risks for endometrial cancer were calculated according to these anthropometric measurements. RESULTS: --Case patients with endometrial cancer had significantly greater waist-to-hip circumference ratios (P less than .001), abdomen-to-thigh skin fold ratios (P less than .01), and suprailiac-to-thigh skin fold ratios (P = .02) compared with control subjects matched for age and Quetelet index. The relative risk for endometrial cancer increased with an increasing waist-to-hip circumference ratio (less than or equal to 1.14 = 1.0; greater than 1.14 = 15.0), with an increasing abdomen-to-thigh skin fold ratio (less than or equal to 0.82 = 1.0; greater than 0.82 = 5.0), and with an increasing suprailiac to-thigh skin fold thickness ratio (less than or equal to 0.67 = 1.0; greater than 0.67 = 3.50). CONCLUSION: --Upper-body fat localization is a significant risk factor for endometrial cancer in women matched for age and Quetelet index.

Adult↗
PubMed1979

Review of epidemiologic studies of endometrial cancer and exogenous estrogen.

Epidemiologic literature on the association of exogenous estrogen and endometrial cancer is reviewed. Descriptive studies have documented fluctuations in the incidence of endometrial cancer, mainly of localized disease, associated with estrogen use. Etiologic studies have established an association between estrogen use during menopause and the occurrence of endometrial cancer. Although the association appears to be a valid one, several biases may have falsely increased the magnitude of this association. The association also appears to be strongest for local disease and weakest for the most invasive disease, which implies that the etiology for the more invasive endometrial cancers is largely unaccounted for by estrogen use. A need for a prospective study to define other potential risks and benefits of estrogen therapy is clear. However, appreciation of factors known to modify the risk of endometrial cancer from exogenous estrogen can help the clinician to use these preparations judiciously.

Dose-Response Relationship, Drug↗
PubMed1992

[In vitro study on the effect of sex steroid and growth factor on growth and laminin, collagen IV, and tissue plasminogen activator production of normal endometrial cells and endometrial cancer cells in culture].

The mechanism of the invasion and proliferation of endometrial cancer is closely related to interactions between the endometrial glands and stroma. In this study, we examined the biological role of sex steroids (estradiol; E2, progesterone; P) and growth factors (epidermal growth factor; EGF, transforming growth factor-beta; TGF-beta) on cell growth and laminin, collagen IV and tissue plasminogen activator (t-PA) production of normal endometrial cells and endometrial cancer cells in culture. Normal endometrial gland cells and stromal cells, and endometrial cancer cell lines (Ishikawa, OMC-2) were used. E2, P, EGF and TGF-beta were added to the culture in physiological concentrations. The growth of normal endometrial gland cells was promoted by E2 and EGF, whereas that of Ishikawa cells and OMC-2 cells was promoted by EGF. E2 enhanced the effects of EGF in normal endometrial gland cells. The growth of normal endometrial stromal cells was not affected by them. OMC-2 was inhibited by anti-EGF receptor antibody. On the other hand, the production of laminin and collagen IV of these cultured cells was inhibited by EGF and promoted by TGF-beta, whereas that of t-PA was promoted by EGF and inhibited by TGF-beta. These results suggest that the growth of normal endometrial gland cells with estrogen receptor (ER) is controlled by both E2 and EGF, whereas that of endometrial cancer cells is affected only by EGF, and those cells without ER depend particularly on the autocrine growth mechanism of EGF.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Division↗