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

Sera from cancer patients and healthy individuals, obtained from two independent sources, were examined for their abilities to react with herpes simplex virus-associated tumor antigens, AG-4 and NVA-TAA (nonvirion antigen-tumor-associated antigen). Both antigens were prepared by infection of HEp-2 cells with herpes simplex virus type 2, and all antigen-antibody interactions were measured by the micro-complement fixation test. Of sera from 16 patients with cancer of the uterine cervix, 81% (P less than 0.01) reacted with NVA-TAA, whereas 78% (P less than 0.001) of 18 sera examined reacted with AG-4. These values differed significantly from those for normal sera, of which 14% reacted with NVA-TAA and 13% with AG-4. Of sera for 8 patients with squamous cell carcinoma of head and neck or vulva, 75% (P less than 0.02) reacted with NVA-TAA, whereas 63% (P less than 0.05) reacted with AG-4. As a group, other cancers (including adenocarcinoma of lung, breast, ovary, and cervix; liposarcoma; sarcoma; melanoma; and carcinoma of the endometrium) did not differ significantly from controls in reactive patterns with AG-4 or NVA-TAA. These studies partly supported the reported preferential reactivity of AG-4 and NVA-TAA with sera of patients with squamous cell carcinoma, especially of the uterine cervix.
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PMID:Comparative diagnostic aspects of herpes simplex virus tumor-associated antigens. 18 98

Six patients who took oral contraceptive agents for 5 to 18 years developed endometrial neoplasia. Endometrial adenocarcinoma occurred in 4 of these patients and severe adenomatous hyperplasia occured in 2. Five of the 6 patients took sequential agents; 1 patient used a combined agent. An additional patient who took Premarin and Provera sequentially developed adenocarcinoma of the endometrium. Eighteen cases of endometrial adenocarcinoma and 7 cases of adenomatous hyperplasia in patients with long-term sequential oral contraceptive use have previously been reported by others. Progestogens may not be completely protective against the endometrial cancer-causing potential of the estrogens, especially in the sequential regimens.
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PMID:Endometrial carcinoma and oral contraceptive agents. 19 73

At the Wilford Hall U.S. Air Force Base Medical Center, Texas, about 4000 postmenopausal women received estrogen replacement therapy during 1975. Of these, 2700 took estrogens only and 1240 were given a progestogen along with estrogen. Hysterectomy had been done previously on 1700 patients (42%), leaving 2300 with intact uteri and a risk of endometrial cancer. Adenocarcinoma of the endometrium was diagnosed in 7 patients. Of these, 6 had received estrogen therapy. There was 1 endometrial malignancy in a patient also receiving a progestogen. Among 510 untreated postmenopausal women with intact uteri, 1 adenocarcinoma of the endometrium was found. Type and dosage of estrogen were unrelated to endometrial malignancy. In addition to the 7 endometrial cancers from the clinic, 22 cases were diagnosed elsewhere and referred for treatment, 11 of these had received no hormones. 10 were taking estrogens and 1 was receiving Oracon for birth control. The incidence of endometrial malignancy in the U.S. is reported to be 21/100,000 women/year. There is a 3-fold to 9-fold increased risk of endometrial cancer associated with obesity alone. The probability that untreated postmenopausal women with intact uteri will develop carcinoma of the endometrium is 1/1000/year. With estrogen users, it is reported to be increased -7.6/1000 women/year. In the author's clinic during 1975, the incidence among those receiving only estrogen was 4.7/1000. Among those also receiving a progestogen the incidence was .8/1000. Unopposed estrogens apparently have a role in the etiology of endometria hyperplasia and neoplasia through incomplete shedding of the endometrium. Progesterone produces more complete sloughing of the endometrium and also converts all degrees of hyperplasia into secretory endometrium. Nulliparity, infertility, and anovulation are predisoposing factors to endometrial carcinoma. Progestogens are palliative therapy for endometrial cancer.
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PMID:Estrogens, progestogens and endometrial cancer. 19 79

The effects of long-term estrogen replacement therapy upon neoplastic diseases were studied in 301 treated patients and 309 untreated patients. 207 women of each group had uteri in situ. Incidence figures for neoplasia were compared between the 2 groups and with the Third National Cancer Survey, yielding a risk ratio for the development of adenocarcinoma of the endometrium among estrogen-treated women of 3.8 (p .05) and 9.3, respectively. The addition of synthetic progestin to estrogen therapy provided significant (p .001) protection against the likelihood of developing endometrial cancer and did not reduce previously reported metabolic benefits of estrogen treatment. The data did not show an increased incidence of breast cancer among estrogen treated women, even with higher dosages or long-term therapy. It is recommended that estrogen therapy should be instituted whenever appropriate indications are present and no major contraindications exist; estrogen should be administered in the lowest dosage and duration that can adequately treat the indication for its use. Estrogens should probably be administered in cyclic fashion, especially if the uterus is in place, with sequentially added progestin.
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PMID:Effects of long-term estrogen replacement therapy. II. Neoplasia. 22 Aug 75

Despite many years of extensive investigation, there has been neither a clear-cut pattern of hormonal production nor milieu found in women with breast cancer. Estrogen replacement therapy for menopause does not significantly increase the risk of breast cancer and one study indicated that estrogen users have a lower incidence of breast cancer than that observed in untreated women. Some studies have shown that the mortality rate from breast cancer is lower in estrogen-treated postmenopausal women. Only one investigator has found any significantly increased risk of breast cancer in oral contraceptive users. In that report, increased duration of birth control pill use decreased the risk of breast carcinoma. Several studies were unable to find an increased risk of breast cancer from oral contraceptives while one investigation observed a lower incidence in birth control pill users than that expected. The mortality from carcinoma of the breast in oral contraceptive users was lower than in non-users, most likely due to earlier detection. Although some retrospective studies have indicated that estrogen use increases the risk of endometrial cancer, a prospective investigation found only an insignificant increase. Progestogens afford some protection from cancer in estrogen-treated postmenopausal women. The incidence of endometrial adenocarcinoma is lower than that observed in untreated postmenopausal women. Combination oral contraceptives are protective against developing adenocarcinoma of the endometrium but sequential birth control pills may afford less protection.
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PMID:The role of hormones in the etiology of breast and endometrial cancer. 29 15

Metabolic effects of long-term (at least 5 years) estrogen replacement therapy were studied. 301 patients were treated with replacement estrogen and 309 patients were untreated. Incidence figures for various metabolic diseases present at entry, and both during and after estrogen therapy were compared by statistical adjustments for certain group differences (Mantel-Haenszel statistics) and by statistical analysis. Long-term administration of estrogen to these women with hypoestrogenism was associated with significantly lower rates of development of cardiovascular disease (p .001), hypertension (p .001), osteoporosis (p .001), and fractures (p .01). The detrimental effects included a higher rate of abnormal uterine bleeding (47% of 207 women with uteri in situ) and an increase in the likelihood of developing adenocarcinoma of the endometrium. Cyclic adminsitration of estrogen did not seem to protect from the risk of endometrial carcinoma, however the addition of progesterone to sequential estrogen treatment did. It is believed that long-term estrogen therapy is of benefit for the woman deprived of estrogen function, particularly if this loss occurs at a relatively young age.
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PMID:Effects of long-term estrogen replacement therapy. I. Metabolic effects. 44 93

Office endometrial biopsy with the Kevorkian curette was performed in 400 patients presenting with abnormal uterine bleeding or other endometrial cancer-risk indicators. The use of this instrument has proved to be a safe, simple, inexpensive, and highly reliable outpatient procedure with excellent patient acceptance. It has provided tissue for adequate diagnosis in 91.8% of the cases, and the diagnostic accuracy when controlled by D&C and/or total abdominal hysterectomy (TAH) was 96.2%. As a result, 73.5% of the women required no further surgical procedures for either diagnostic or therapeutic purposes. In the postmenopausal age group, adenocarcinoma was diagnosed in 7 of 177 (3.9%) women. This procedure is highly recommended for early office diagnosis of uterine pathology and, in particular, endometrial adenocarcinoma and its presumed precursor lesion, adenomatous hyperplasia.
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PMID:The Kevorkian curette. An appraisal of its effectiveness in endometrial evaluation. 46 Jul 66

Psammoma bodies were found in less than 9% of 235 cases of endometrial carcinoma, considering both biopsies and surgical specimens. They may originate in papillary adenocarcinoma and do not indicate a slightly infiltrating or a well-differentiated tumor. The clinical profile of patients closely resembles that of women with endometrial carcinoma, but survival appears worse.
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PMID:Endometrial adenocarcinoma with psammoma bodies. 46 85

Because of adverse publicity regarding increased risk of endometrial cancer in women receiving estrogen therapy, a 2-year prospective study was conducted in 1976 to determine the incidence of endometrial cancer in postmenopausal women. A retrospective study for the year 1975 was also added. A postmenopausal survey card for each patient recorded the patient's visit and clinical data, as well as hormone therapies (estrogen, progestogen, androgen). Postmenopausal women never treated with hormones were also provided survey cards. A total of 2088 patient-years of estrogen use was recorded during the combined 3-year study period (1975-77). 8 of the estrogen users had a diagnosis of adenocarcinoma of the endometrium for an annual incidence rate of 3.8/1000 women. 2 endometrial cancers were detected in the estrogen-progestogen users for a cancer incidence rate of 0.5/1000 (3792 patient-years of observation); this finding suggests that progestogen provides better protection against endometrial cancer compared to estrogens. This difference between estrogen users and estrogen-progestogen users was statistically significant (p ? 0.01). 1 endometrial malignancy occurred among estrogen vaginal cream users, giving an incidence of 1.7/1000. The patient used Premarin vaginal cream (1 gm thrice weekly) for 7 months before the cancer was diagnosed. No endometrial cancer was diagnosed in both the progestogen and androgen groups. Overall, 14 endometrial cancers out of 8170 years of observation were diagnosed in this clinic; annual incidence rate for the study period was 1.7/1000. 199 women with endometrial hyperplasia (a precancerous lesion) were treated with progestogens for 3 to 6 months. The hyperplastic endometrium returned to normal in 96.5%. It was suggested that all postmenopausal women with intact uterus be given the Progestogen Challenge Test and that progestogens be given to the women each month as long as bleeding follows. This should prevent the development of endometrial cancer in most women.
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PMID:Reduced incidence of endometrial cancer among postmenopausal women treated with progestogens. 46 50

A study was undertaken to investigate changing trends in the microscopic patterns of endometrial carcinoma and to compare the biologic characteristics of those cases associated with and without estrogen usage. After each case was reviewed independently and in a random order by at least 2 pathologists, a diagnosis of cancer was agreed on in 274 patients who had been treated by 5 gynecologists at the Masachusetts General Hospital between 1940 and 1971. Six microscopic patterns were identified (adenocarcinoma, adenoacanthoma, atypical adenoacanthoma, adenosquamous carcinoma, clear-cell adenocarcinoma, and undifferentiated carcinoma). The frequency of each pattern relative to the other 5 changed only slightly during the 30-year interval. The tumors that developed in estrogen users were more highly differentiated than those that developed in nonusers (P less than 0.005) and were found at an earlier average age (P less than 0.02). That the adenoacanthoma was associated with estrogen usage more frequently (51%) than any other tumor type (P less than 0.02) may reflect, in part, a similar and lower mean age of estrogen users (56 years) and patients with adenoacanthoma (55 years) compared with that of nonusers with the other forms of tumors (60--67 years). Although the overall 5- and 10-year survival rates of the estrogen users were higher than those of the nonusers, the differences between the 2 groups disappeared when the grade of the neoplasm was considered.
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PMID:Changing trends and prognostic features in endometrial cancer associated with exogenous estrogen therapy. 47 66


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