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

Of all cancers in the United States, 35% are estimated to be caused by dietary factors and may be preventable. Diets high in fat or calories, for example, are said to be associated with five of the six most common cancers: breast, colorectal, pancreatic, prostatic, and uterine. Conversely, some dietary components such as vitamin A, in fruits and vegetables, and fiber may help protect against certain cancers. Obesity may confer a small risk of breast cancer on a woman, but women with upper body fat localization are at significantly higher risk of developing breast cancer and endometrial cancer.
Prim Care 1992 Sep
PMID:Nutrition and cancer prevention. 132 28

The success of the Pap smear in screening for cervical cancer illustrates many of the tenets of screening for disease. Unfortunately, no other gynecologic malignancy shares this success. Detection of most gynecologic malignancies occurs once they have become symptomatic and on clinical examination at the interval cancer-related checkup as recommended by the ACS. These examinations, done yearly in women older than 40 and every 3 years in younger women, can go a long way in the detection of genital tract disease. In detecting vulvar neoplasms, visual inspection of the entire perineum coupled with palpation to include Bartholin's glands and early biopsy of suspicious vulvar lesions promotes earlier diagnosis. Self-examination similar to breast self-examination and increased patient awareness are potential education goals for physicians as well as cancer and medical societies. Vaginal examination at the cancer checkup should continue. The finding that most vaginal cancers are picked up by abnormal cytology while they are still asymptomatic argues strongly for Pap testing after menopause. The knowledge that women who are status posthysterectomy for benign disease are not protected from developing vaginal cancers mandates continued Pap testing in this population as well. Because endometrial cancer is common, primary care physicians should maintain a high index of suspicion. Aspiration biopsy is a simple office-based procedure with low risk and good yield, and any woman in the perimenopausal and postmenopausal period who presents with atypical bleeding patterns should be evaluated. Although not recommended as a general screening test, the ACS does advocate endometrial sampling in the high risk woman at the time of menopause. The greatest challenge to primary care physicians may be the early detection of ovarian cancer. No single test is available, nor is any advocated in screening for this lethal disease. Currently, only periodic physical examination is recommended at the cancer checkup interval. Ultrasound, both transabdominal and transvaginal, may help in detecting adnexal masses, but is not sensitive enough to differentiate benign from malignant lesions. In this setting, and in the patient with suspected ovarian cancer, CA 125 and AFP may be helpful in determining which patients require surgical exploration. Women with positive family histories for ovarian cancer require greater vigilance and close follow-up with serial ultrasound and CA 125 determinations. As the population ages, cancer, which is primarily a disease of age, will continue to increase in incidence.(ABSTRACT TRUNCATED AT 400 WORDS)
Prim Care 1992 Sep
PMID:Screening for gynecologic cancer. Vulvar, vaginal, endometrial, and ovarian neoplasms. 141 66

Several controversial areas have been reviewed. It would seem from the evidence at hand that progression from endometrial hyperplasia to endometrial carcinoma does occur in a significant percentage of women and that endometrial hyperplasia, particularly adenomatous hyperplasia and atypical hyperplasia, must be regarded as premalignant changes. Gambrell believes that all stages of hyperplasia should be regarded as premalignant. Previous and retrospective studies provide evidence implicating estrogens in the causation of both endometrial hyperplasia and endometrial carcinoma. Although some of these studies may have design flaws, the amount of data is substantial. Prospective studies have demonstrated an increased risk of hyperplasia in women treated with estrogens. An increased risk of endometrial carcinoma in estrogen users compared with nonusers has been suggested even more recently. Reviewed as a whole, the cumulative evidence provided by these studies clearly supports this association, and it would appear the only issue left to resolve may be the magnitude of the association. Cyclic administration of estrogens may decrease the risk of development of endometrial carcinoma. It would seem, however, that such administration does not totally eliminate risk under any circumstances, and in fact, a dose-related relationship appears to persist. It seems well established that progestogens do decrease the risk of both endometrial hyperplasia and endometrial carcinoma associated with the administration of estrogen to peri- and postmenopausal women. Such reduction in risk is significant and lower relative risks in estrogen/progestogen treated women have been reported compared to untreated women. This reduction in risk has been reported in a variety of studies. Whitehead and co-workers have provided a clear biochemical mechanism for progestogen protection of the endometrium in the antagonism of estrogen at the endometrial cellular level. The evidence at hand in the literature would suggest that progestogens should be administered for at least 10 days per cycle. In summary, there is good evidence that the addition of a progestin to estrogen therapy prescribed for the symptoms of menopause provides protection from endometrial hyperplasia and related carcinoma. The protection conferred is greater than that afforded by cyclical estrogen-alone therapy, and allows for continuous therapy, hereby providing greater symptomatic relief. There is little evidence for adverse effects caused by the added progestins, but further studies of women on combined therapy will undoubtedly be warranted.
Obstet Gynecol Surv 1992 Sep
PMID:Review of the endometrial effects of estrogens and progestins. 143 9

Tamoxifen, which is increasingly being used in breast cancer patients, has been associated with an elevated frequency of endometrial carcinoma. To our knowledge not a single case of uterine serous papillary carcinoma (USPC) has been documented during tamoxifen treatment. No conclusions as to a causal relationship are yet being made, but if it is due to tamoxifen, we should advise a strategy for prevention, because this subtype is not as curable as endometrioid carcinoma.
Eur J Obstet Gynecol Reprod Biol 1992 Sep 23
PMID:An unusual type of endometrial cancer, related to tamoxifen? 145 92

A bolus of carboplatin (CBDCA) 200-450mg/body (148-292mg/m2) with 500ml saline was administrated into the abdominal cavity (ip) of 4 patients with ovarian cancer and 2 patients with uterine endometrial cancer, and concentrations of free and total platinum (Pt) in the blood and ascites were measured with the passage of time. Moreover, the results were analyzed with a 2-compartment model and moment analyses in order to study in vivo kinetics of CBDCA at the time of the ip administration. 1) The shift of Pt to blood through ip administration depended on the peritoneal clearance. Cmax in blood was seen one hour after ip in patients with a normal peritoneum, and was seen between 4 and 6 hours after ip in patients with peritonitis carcinomatosa. The level was lower in the latter group. 2) The non-binding rate of Pt with protein in the ascites at the time of the ip administration was correlated with the CBDCA concentration in the ascites. 3) The non-binding rate was 80% or more both in the ascites and in the blood within 4 hours after ip. The high level of the nonbinding rate appeared to cause prolongation of the presence of the free-Pt in the ascites and blood, especially in patients with peritonitis carcinomatosa. 4) AUC level in blood was equal to or higher than that observed when the same dose was administered iv. The levels of free-Pt and AUC in the abdominal cavity were 2 to 5 times higher than those in blood in patients with a normal peritoneum, and 7 to 14 times higher in patients with peritonitis carcinomatosa.(ABSTRACT TRUNCATED AT 250 WORDS)
Nihon Sanka Fujinka Gakkai Zasshi 1992 Sep
PMID:[Usefulness of intraperitoneal carboplatin administration-- pharmacokinetic analysis]. 145 47

Tongue metastases are exceptional, with a frequency of 0.1% to 0.2% in autopsy series of patients with disseminated cancer. A case of secondary papillary endometrial carcinoma of the tongue is reported as the first sign of metastasis in a 78-year-old white woman treated 7 years before by complete hysterectomy and radiotherapy. The lesion presented as a 3 x 3-cm submucosal mass of the dorsum of the tongue. Fine-needle aspiration and excisional biopsy established the diagnosis. Metastases to the lungs, liver, and bone developed 3 months later, and she died 6.5 months after initial diagnosis. A review of reports of 77 lingual metastases showed that the mean age was 57 years, with a male predominance. The lung, kidney, and skin were the most common primary sites. The tongue was the first site of metastases in 61% and the first sign of the primary malignant neoplasm in 15% of the cases. Average survival was 10 months.
Arch Pathol Lab Med 1992 Sep
PMID:Metastatic papillary endometrial carcinoma of the tongue. Case report and review of the literature. 152 64

Marked changes in both growth factor and proto-oncogene expression occur due to treatment of hormonally-responsive human cancers with progestins and antiestrogens. In human endometrial cancer cell lines the antiproliferative effects of progestins and antiestrogens in a particular cell line appear to be associated with similar effects on growth factor and/or proto-oncogene expression. This suggests that although these compounds initially interact with different steroid hormone receptors, the molecular mechanisms of their growth inhibition may be essentially similar. In the case of human breast cancer cell lines, however, the effects of progestins and antiestrogens on gene regulation are often different, suggesting that the molecular mechanisms of progestin and antiestrogen growth inhibition may be essentially dissimilar.
J Steroid Biochem Mol Biol 1992 Sep
PMID:Mechanisms of growth inhibition by antiestrogens and progestins in human breast and endometrial cancer cells. 152 52

Uterine papillary serous carcinoma (UPSC) is an aggressive malignancy that accounts for a disproportionate number of intraabdominal failures among endometrial carcinoma patients. The histologic appearance and tendency toward intraabdominal spread resemble those of papillary serous adenocarcinoma of the ovary. Because approximately 70% of untreated ovarian carcinoma patients respond to platinum-based chemotherapy, it has been suggested that UPSC patients might respond to similar treatment regimens. Twenty patients with UPSC were treated with cisplatin, doxorubicin (Adriamycin), cyclophosphamide (PAC) chemotherapy between January 1982 and December 1989. They included 9 patients with advanced primary disease, 5 with recurrence, and 6 who received PAC as adjuvant therapy. Patients received a mean of five cycles of PAC. Only 2 of 11 patients with measurable disease greater than 2 cm achieved complete clinical responses of 12 and 31 months duration; there were no partial responses. Actuarial 5-year survival for all patients was 23%. The mean progression-free interval was 9 months. Patients with clinical stages I or II disease had a higher survival rate than those with stage III or IV disease (P = 0.003). Survival did not correlate with depth of myometrial invasion (P = 0.81) or size of residual tumor following initial surgery (P = 0.16). Estrogen or progesterone receptors were detected in 10 of 11 tumors tested. Seven of 9 patients tested had elevated serum levels of CA-125 (greater than 35 U/ml). Correlation between CA-125 value and clinical course was demonstrated in 3 of 5 patients who had serial measurements. Of all patients, 3 are currently alive; 1 has documented disease. Moderate to severe toxicity was seen in 14 patients (70%). There was one possible treatment-related death from cardiomyopathy. UPSC, despite its histologic and clinical similarities to ovarian carcinoma, was relatively resistant to PAC chemotherapy in this mixed group of patients.
Gynecol Oncol 1992 Sep
PMID:Uterine papillary serous carcinoma (UPSC) treated with cisplatin, doxorubicin, and cyclophosphamide (PAC). 152 8

Specific low-affinity high-capacity binding sites for gonadotropin-releasing hormone (GnRH) have recently been discovered in human breast and ovarian carcinomata. We checked whether similar binding sites are present in human endometrial cancer. Plasma membrane preparations were incubated with [125I,D-Ala6-desGly10]-GnRH-ethylamide in the presence or absence of unlabelled GnRH agonists or other peptides. GnRH-binding could be demonstrated in all 12 tumor samples tested. The mathematical analysis of the binding data was consistent with a single class of low affinity (Ka = (0.8-1.4) x 10(5) M-1) and high-capacity (Bmax = (134-142) x 10(-12) M/mg membrane protein) binding sites. Native GnRH had a similar affinity to the binding sites as the GnRH agonist used. Other peptides such as oxytocin, somatostatin and thyrotropin-releasing hormone did not crossreact with the binding sites. A photolabelled derivative of [D-Lys6]-GnRH was prepared with the bifunctional photolabile reagent (4-azidobenzyl)-N-hydroxysuccinimide. Photoaffinity labelling of endometrial carcinoma membranes and subsequent sodium dodecyl sulfate electrophoresis in 10% polyacrylamide gel revealed the presence of a single molecular mass component of 62 +/- 1.9 kDa. The appearance of this photolabelled binding site could be largely suppressed by the addition of unlabelled GnRH-agonist (10(-4) M) and thus represents the specific binding site for GnRH in endometrial cancer.
Eur J Obstet Gynecol Reprod Biol 1991 Sep 13
PMID:Specific low affinity binding sites for gonadotropin-releasing hormone in human endometrial carcinomata. 165 55

One hundred eighty-three patients with endometrial carcinoma had both immunohistochemical and biochemical analysis of estrogen receptor (ER) and progesterone receptor (PR) content of the tumor. Biochemical analysis was done on a homogenate of uterine curettings; immunohistochemical stainings were done on formalin-fixed, paraffin-embedded sections. The biochemical method was scored quantitatively and the immunohistochemical, in a semiquantitative way. There was a significant correlation between the immunohistochemical categories of the malignant component of the tumor and the biochemical levels of receptor content (P = 0.0001). The sensitivity of the immunohistochemical method for the ER content was 78.5% and the specificity was 58.2%. The sensitivity for the PR was 52.5% and the specificity was 92.8%. Changing cut-off levels for positivity of the biochemical analysis changed the sensitivity and specificity. Survival was predicted by the immunohistochemical status of the ER (P = 0.001) and PR (P = 0.01). Similarly, it was predicted by the biochemical receptor status. Multivariate analysis of the immunohistochemical receptor status and the biochemical receptor status showed that the immunohistochemically determined estrogen status was the most significant predictor of survival (P = 0.001). The immunohistochemical analysis of sex steroid receptor status on formalin-fixed, paraffin-embedded tissue is not only possible and practical, but also predicts survival.
Am J Clin Pathol 1990 Sep
PMID:Immunohistochemical evaluation of estrogen and progesterone receptor content in 183 patients with endometrial carcinoma. Part II: Correlation between biochemical and immunohistochemical methods and survival. 169 30


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