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

The only active research performed by Jick and colleagues concerning the alleged causal relation between estrogens and endometrial cancer consisted of telephone interviews with 60 of 67 patients with endometrial cancer and a "control" group of 74 other women with intact uteri. In their case-control study, the authors describe no effort to deal with problems in surveillance or detection bis or to avoid bias in ascertainment of exposure to estrogens. The suggestion that 18,000 women were investigated is based on a statistical tour through secular trends in computerized accounts of estrogen prescriptions and separately reported diagnoses of endometrial cancer. Except for data in the small group selected for the case-control study, none of this information was checked or verified. On the basis of the statistical trends, the authors conclude that estrogens increase the risk of endometrial cancer to "even higher" than 20 times than that in nonusers but that the changes are stopped or reversed shortly after discontinuation of the estrogens. This capacity for de-carcinogenesis is explained by the conjecture that estrogen is a "promotor" rather than an "inducer" of endometrial cancer. An alternative hypothesis is that many uterine cancers are asymptomatic, never detected during life and 1st found (if at all) at necropsy.
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PMID:Estrogens and endometrial cancer. 44 Mar 41

Three cases of clear cell carcinoma of the endometrium are here reported. Clear cell carcinoma is a rare and aggressive type of endometrial adenocarcinoma. Patients are older and are in the menopause much longer than are patients with typical endometrial carcinoma. This fact may reflect the presence of counterbalanced sex hormones in the process of carcinogenesis.
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PMID:Clear cell carcinoma of endometrium. 46 71

Three topics are briefly reviewed relating to carcinogenesis of estrogen responsive tissues: (a) enzymology of benzo(a)pyrene activation by human tissues, (b) microsomal activation of estrogens to estrogen arene oxides and (c) estrogen and progesterone receptor studies in endometrial carcinoma. The following working hypothesis is stated on the etiology of gynecologic tumors: "Environmental chemicals, such as cigarette smoke, polycyclic and polyhalogenated hydrocarbons, etc., induce special forms of cytochrome P-450 monooxygenase and related enzyme systems which can activate endogenous or prescribed estrogens and non-steroid antiestrogens to act as initiators and/or promoters of neoplasia in estrogen-dependent organs." The role of estrogen receptors is perceived as a homing device or cellular "Trojan Horse" for these activated estrogens.
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PMID:Carcinogen activation by human uterine enzymes. 46 42

The spectrum of progestin therapy has changed and expanded during the last few years. 1. The drug-therapy of choice in endometriosis is the medication of progestins for at least six months, for instance ethinyl-testosterone. If a patient wants additional children the "more gentle" dydrogesterone should be considered. 2. In the treatment of dysmenorrhea combination pills should be given, sequentials should be avoided. In the case of incompatibility of estrogens or in danger of oversuppression syndrome dydrogesterone should be applicated. 3. Dysfunctional bleedings should lead to an intense search for their cause. The treatment consists in an estrogen-progestin combination for 9 days and in cyclic continuation of this therapy for at least a further three months. In the case of hemorrhagic diathesis progestin treatment should be continued. 4. Cyclic adequate progestins have proofed to be successful in handling of hirsutism. The choice of the preparation depends on the patient's wish for children. 5. The progestin test is still the first step in diagnosis of amenorrhea. 6. Progestin therapy is indicated in progressive endometrial carcinoma. Some medical centres treat carcinoma of the mamma successfully with progestins. 7. Nowadays fast and early hormonal pregnancy tests are available. The progestin-pregnancy-test is limited to cases of premenopause. 8. The so-called short luteum phase has received considerable attention as a possible cause of infertility. In these cases a substitutional therapy of progestins should follow. Clomiphene or HCG-therapy is advisable. In short luteum phase and premenstrual spottings potent progestins should be given. 9. High dosage of progestins are in common use in the treatment of abortus imminens. 10. Combination pills and sequentials are widely used, the possible methods of a pure progestin contraception are: minipills, three-month-injections, implanted silastic capsules with progestional compounds, progestin impregnated intrauterine devices, vaginal silastic rings impregnated with progestional compounds. 11. Carcinogenesis of progestins was not detectable. 12. Some progestins are teratogenic.
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PMID:[Current status of gestagen administration. 2. Gestagen therapy in the area of reproduction]. 55 11

The problem of a relationship between nutrition and cancer has to be approached from two different points of view: 1. Direct effect of carcinogens present in foods or in food additives (direct carcinogenesis), 2. In-vivo synthesis of carcinogens caused by changes in metabolism due to altered dietary habits (indirect carcinogenesis). For the second mechanism, we have to make a distinction between the effects of nutritional deficiency and of nutritional excess. Some examples from animal experiments are presented. In man, possible relationships between nutrition and cancer are postulated mainly for tumors of the gastrointestinal tract and recently also for hormone-dependent cancers. Epidemiological evidence points to the major importance of the indirect way of carcinogenesis caused by specific nutritional deficiencies and excesses. Experimental studies in man are difficult to perform. Therefore, most hypotheses are based on statistical associations, and great caution is required in drawing inferences on causal relationships. Cancers of the upper and lower gastrointestinal tract epidemiologically behave in a different way, the former showing a marked decrease in most western countries, the latter a slight increase. The etiology of the cancers of the esophagus and stomach has still to be determined in spite of many hypotheses. Migrant studies show a major effect of environmental rather than genetic factors. Substantial differences in dietary habits between countries with high and low incidence of stomach cancer (Japan and United States) point to the importance of nutrition as an etiological factor with a high probability, but no specific dietary components have been identified so far. The same is true for cancer of the large bowel. Recent hypotheses suggest that dietary factors may relate to cancer of the colon by their effect on bile production and on the bacterial makeup of faeces which in turn might be transforming bile acids into active carcinogens. There is, however, disagreement about the specific dietary component responsible for this model of carcinogenesis. BURKITT stresses the importance of the lower consumption of dietary fiber, resulting in retarded bowel function and additional time for bacterial proliferation and degradation by bacteria of bile acids. WYNDER, on the other hand, explains the increased bile acid and neutral sterol excretion and microbial modification of these compounds with the high content of animal fat in the western diet. With hormone-dependent cancers (breast, endometrium, ovary, prostate), a correlation has been shown between body weight and height and breast cancer as well as between overweight and cancer of the endometrium. Which aspect of diet, if any, is responsible for changes in hormone metabolism, resulting in an increased risk of these cancers, is still to be proved. On the basis of current knowledge, it is extremely difficult to draw inferences for preventive action. Certainly, a cancer-preventing diet cannot be established...
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PMID:[Nutrition and cancer (author's transl)]. 101 38

The effect of oral contraceptives on the development of cancer indirectly is explored with regard to cancer of the female genital tract and the breast. No correlation between oral contraception and squamous cell carcinomas of the vulva and vagina and tumors of the ovary is known. As yet no statistics are available on the incidence of carcinoma of the endometrium in women who took oral contraceptives during their reproductive life span. Because of the direct hormonal suppression of the endometrial growth by oral contraception, a protective effect against endometrial hyperplasia and endometrial cancer must be expected. For cancer of the female breast no protective and no enhancing cancer risk due to progestational agents can be postulated. The known fragmentary data suggest rather a protective effect. Regarding dysplasia and carcinoma in situ of the uterine cervix, large investigations with great numbers of patients are available. An increase of the risk of developing cancer of the cervix by using oral contraception cannot be shown with sufficient accuracy at our present state of knowledge by statistical means. Some observations suggest that oral contraception increases the relevant exogenous factors for carcinogenesis of the uterine cervix such as sexual behavior and hygiene.
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PMID:[Does oral contraception cause cancer? (author's transl)]. 126 87

We compared the hormonal and epidemiological aspects of ovarian cancer patients in search of the etiology of this neoplasia. Case-control studies of Japanese women with and without cancer were conducted in parallel, with regard to both the excretion of 14 urinary steroids and the pertinent physical and physiological parameters. The results obtained are as follows: 1) premenopausal ovarian cancer patients before and after radical ovariectomy and postmenopausal-postoperative patients were associated with a specified steroid deviation profile characterized by a combination of general depression of androgens, progestins and corticosteroids with sole rescue of tetrahydrocortisol (THF) in urine. 2) The deviation profile of postmenopausal-preoperative cancer patients was distinguished from the 3 partner profiles by its preservation of normalcy in the excretions of androgen and progestin in urine. 3) Ovarian cancer patients were associated with growth retardation, when compared with urban healthy controls and patients with either breast cancer or endometrial cancer by the age-matching method. Ovarian cancer patients were also less fertile than age-matched normal controls, and were as infertile as age-matched patients with either breast cancer or endometrial cancer. 4) Epidemiological evidence was presented to suggest that the incidence of ovarian cancer in Japan was increasing in parallel with the recent increase of social tension in Japan. The possible relevance of the hormonal characteristics of ovarian cancer patients to both the epidemiological characteristics of the same cancer patients and the genesis of this neoplasia is discussed in the light of the 2-step carcinogenesis theory.
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PMID:Relation between the hormonal and epidemiological aspects of ovarian cancer patients in Japan. 144 27

The present study investigated comparatively the relation between host age and age-specific incidence rate (ASIR) of breast cancer in the United Kingdom and Japan. Comparison was also made between breast cancer and 5 non-mammary neoplasias as regards the cancer incidence/age profile. The results obtained are as follows: 1) the ASIR profile of breast cancer in the age range of 22.5 years to 47.5 years was characterized by a rapid rise versus age which was common between the United Kingdom and Japan. By use of the log-log plot, the growth of breast cancer risk was found to be quasi-exponential, and the above time range was termed the stage of exponential growth. 2) From 47.5 years of age on, the stage of stagnation ensued: the ASIR for the United Kingdom kept on rising with a much reduced inclination, whereas that for Japan followed the way of gradual decline. In the log-log plot, the junction between the 2 stages was recognized as a distinct break point. 3) A similar two-stage structure was found in the ASIR profiles of cancers of the stomach, lung, cervix uteri, and corpus uteri. The break points for the first 2 neoplasias were located at senescent ages, and those for cervical cancer and endometrial cancer were located at the pre- and peri-menopausal ages respectively (27.5-32.5 and 52.5 years). The profile of lymphoid leukemia gave 2 distinct surges at the ages of infancy and senescence, regardless of the country. The significance of the break point in the ASIR profile of breast cancer was discussed in relation to the two-step carcinogenesis theory.
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PMID:The genesis of breast cancer is a two-step phenomenon. I. Differential effects of aging on the cancer incidence in the United Kingdom and Japan. 156 61

This study compares the clinicopathologic features of 13 pure uterine papillary serous carcinomas (UPSC) with 19 tumors consisting of UPSC admixed with other types of endometrial carcinoma and nine UPSC associated with endometrial polyps. The mean patient age, frequency of preoperative clinical understaging, postoperative pathologic stage, and survival of patients was similar for the three groups. Surprisingly, widespread metastasis, recurrence, and death occurred even in those cases where myometrial invasion amounted to less than 1 mm or where tumor was confined to an endometrial polyp. Poor prognosis appeared to be related to a propensity for vascular invasion and multifocal carcinogenesis. The latter was manifested by the presence of cytologically malignant cells closely resembling the invasive serous carcinoma in the surface endometrium adjacent to the tumor in 89% of cases and in multiple sites in the genital tract and abdomen. This lesion, designated "intraepithelial carcinoma," was present in the endocervix in nine (22%) of the 41 cases, in the fallopian tube in two cases (5%), on the surface of the ovary in four cases (10%), and on peritoneal surfaces or omentum in 10 cases (25%). In addition, we found that UPSC display considerable morphologic heterogeneity. Foci of clear-cell carcinoma were identified in 13 (32%) of the 41 tumors. In five (12%) neoplasms, the invasive component was composed primarily of glands; and in 22 (54%) tumors, thin as opposed to thick papillae predominated. Accordingly, UPSC may be broadly defined as a carcinoma that displays foci of well-differentiated papillae lined by cells that are markedly atypical cytologically. UPSC frequently contain areas of clear cells. Glands with papillary infoldings sometimes predominate in the invasive component. Because the behavior of endometrial neoplasms, in which at least 25% of the carcinoma exhibits a glandular or papillary architecture with serous differentiation, is similar, the term "uterine serous carcinoma" is an appropriate designation for these tumors, regardless of whether other patterns of differentiation are present or whether the tumor is associated with a polyp.
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PMID:Uterine serous carcinoma. A morphologically diverse neoplasm with unifying clinicopathologic features. 159 38

We have constructed deletion maps of chromosome 3p for cancers of the female genital tract (uterine endometrium, uterine cervix and ovary). The tumours were tested for loss of heterozygosity using CA-repeat polymorphisms. The high degree of informativeness of these markers allowed the construction of detailed deletion maps from a relatively small number of samples. A common region of deletion was identified at chromosome 3p13-21.1 in endometrial cancer and at 3p13-14.3 in cervical cancer; 5 out of 13 (38%) endometrial cancers and six out of eight (75%) cervical cancers showed loss of heterozygosity at these regions. In ovarian cancer a separate common region of deletion was identified at 3p21.1-22; two out of four (50%) ovarian cancers had alleles deleted at this region. These data suggest the presence of a tumour-suppressor gene(s) for endometrial and cervical cancer at 3p13-21.3 and a separate gene at 3p21.1-22 that is involved in the carcinogenesis of ovarian cancer.
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PMID:Deletion mapping of chromosome 3p in female genital tract malignancies using microsatellite polymorphisms. 163 Aug 22


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