Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of a woman who died from cerebral metastasis of adenocarcinoma of the uterine corpus, clinical stage IA at the time of first referral, is described. Three months after preoperative endocavitary radiotherapy followed by radical surgery followed by postoperative radiotherapy, the 59-year-old patient developed neurological symptoms. A cerebral tumor was diagnosed and subsequently excised. Histology showed metastasis of an adenocarcinoma. The patient died 3 weeks after cranial surgery. Meticulous postmortem examination failed to reveal any other tumor besides the endometrial neoplasm. Comparative immunohistochemical examination of the primary tumor and the cerebral process supported the assertion that the brain metastasis derived from the adenocarcinoma of the endometrium. Literature reports on cerebral metastasis of endometrial carcinoma are discussed.
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PMID:Cerebral metastasis of endometrial carcinoma. 169 19

Recently, hematopoietic growth factors have been implicated in protean nonhematopoietic processes. In the current study, expression of macrophage colony-stimulating factor (M-CSF) and its receptor (the c-fms proto-oncogene) was investigated in 42 samples of gynecologic tissues. There were 15 samples of normal ovarian and uterine tissue or benign conditions of these organs; 11 samples of primary ovarian cancer tissue; seven samples of metastatic ovarian cancer tissue; and nine samples of primary endometrial cancer tissue. Steady state transcript levels were assessed by Northern Blot analysis. Macrophage colony-stimulating factor (M-CSF) expression was not observed in any of the specimens of benign abnormalities or of normal organs; c-fms expression was detected in two of 15 (13%) of these specimens, albeit at very low levels. In contrast, 14 (78%) of 18 ovarian tumor specimens, and five (55%) of nine endometrial tumor specimens expressed M-CSF. Similarly, 16 (89%) of 18 ovarian tumor specimens and six (67%) of nine endometrial tumor specimens expressed c-fms. Most positive malignant tissues (19 [86%] of 22) showed coexpression of M-CSF and c-fms. Of interest, M-CSF and c-fms mRNA were detected in tumor, but not in adjacent normal tissue. Furthermore, M-CSF and c-fms transcripts were produced by all metastatic tumors, including two cases in which the corresponding primary tumor from the same patient was negative. Because M-CSF mediates its effects by binding to its receptor, the increased levels of both these gene products in gynecologic malignancies suggest that an interaction between M-CSF and c-fms may participate in the development of ovarian and endometrial carcinomas and especially in progression to the metastatic state.
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PMID:Expression of the macrophage colony-stimulating factor and its receptor in gynecologic malignancies. 182 26

A distinct type of cervical involvement by endometrial cancer is reported and termed cervical implantation metastasis. It is believed to result from implantation of endometrial cancer on the denuded endocervix after fractional dilatation and curettage (D & C). The histologic criteria for diagnosis are: (1) the cervical implantation metastasis must be imbedded in the endocervical epithelium or superficial stroma surrounded by an implantation site of inflammatory cells and granulation tissue (free-floating cancer cells above the cervical mucosa are not acceptable as implantation tissue), (2) the histologic findings of the cervical implantation metastasis must be similar to those of the endometrial adenocarcinoma in the uterine corpus, (3) the cervical implantation metastasis must be separate from the primary tumor with no evidence of direct extension, and (4) the cervical implantation metastasis should be surrounded by nonneoplastic endocervical glands with no transition between the two. Of the 176 patients who underwent fractional D & C before hysterectomy, nine (5%) were found to have cervical implantation metastasis. No patients had cervical implantation metastasis who did not undergo fractional D & C before hysterectomy. When stratified according to stage, grade, and myometrial invasion, there was no statistically significant difference in the recurrence rate between patients with or without cervical implantation metastasis. It appears that cervical implantation metastasis does not alter prognosis or require specific treatment.
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PMID:Cervical implantation metastasis by endometrial adenocarcinoma. 187 85

The rationale for endocrine therapy in patients with advanced endometrial carcinoma may be based on the presence of estrogen or progesterone receptors in the primary tumor. A study was designed to evaluate tumor cell heterogeneity of steroid hormone receptors in the primary and metastatic sites in endometrial cancer. Primary endometrial cancer tissue samples from 10 patients and 16 metastatic tumor sites were simultaneously analyzed for estrogen and progesterone receptors, using a radioligand biochemical assay. The primary tumor was estrogen receptor (ER) and progesterone receptor (PR) positive in 70 and 60% of the patients, respectively. The metastatic sites were ER positive in 63% and PR positive in 25%. The primary tumor tissue and the metastatic disease showed an identical ER and PR status in only 25 and 19%, respectively. Four patients had multiple metastatic sites analyzed. In two of four patients the PR values, and in three of four patients the ER values, in these metastatic sites were discordant. These data support the concept of tumor cell heterogeneity for steroid hormone receptors in endometrial cancer. To optimize treatment planning, it may be important to biopsy primary, metastatic, and recurrent tumor sites for individual analysis of receptor activity.
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PMID:Heterogeneity in hormone receptor status in primary and metastatic endometrial cancer. 222 58

UM-EC-2 was established from a patient with poorly differentiated stage IB endometrial carcinoma. This cell line produces tumors in nude mice that have the same histological features as the patient's tumor. UM-EC-2 cells express b2-microglobulin, the epidermal growth factor receptor (EGF), and the H blood group antigen. This membrane antigen phenotype is consistent with cells of human endometrial origin. The karyotype of UM-EC-2 is fairly complex, with rearrangements affecting all chromosomes except 3, 10, 14, 19, and 20. There were two populations of cells, a hyperdiploid population with a modal number of 53-55 and a hypertetraploid population with a modal number of 109. A postulated sequence of events before and after tetraploidization is suggested based on the number of copies of individual chromosomes and rearrangements. Comparison of the UM-EC-2 karyotype to that of UM-EC-1 (a previously described line from a different patient with endometrial carcinoma) revealed that the two lines share eight very similar chromosome changes, which include loss of most of chromosome 4, breakpoints affecting proximal bands on 8p, loss of most of 9q, a breakpoint at 12q22, loss of 13q, breakpoints in proximal bands on 18q, and a breakpoint at 22p11. These changes may represent nonrandom chromosome abnormalities in poorly differentiated endometrial cancer. Estrogen (ER) and progesterone (PgR) receptors were not detected in either the primary tumor or the cell line. Nevertheless, UM-EC-2 cells were very sensitive to growth inhibition by tamoxifen (TAM) in vitro. One micromolar TAM caused 50% inhibition of cell growth, 2.5 microM caused cytostasis, and 5 microM TAM was cytotoxic, killing all cells after 5-7 days of exposure to the drug. Paradoxically, 100 nM estradiol (E2) caused a moderate increase in the growth of the cells but it did not prevent or reverse growth inhibitory effects of TAM. These findings support the concept that in some tumors TAM causes growth inhibition by an ER-independent mechanism. UM-EC-2 cells were also sensitive to growth regulation by EGF. Thus, these cells provide a new in vitro model of human endometrial cancer in which the roles of both TAM and EGF as growth regulatory substances can be investigated.
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PMID:Establishment and characterization of UM-EC-2, a tamoxifen-sensitive, estrogen receptor-negative human endometrial carcinoma cell line. 234 64

A prosthesis was designed to protect the intestinal loop from external beam radiation therapy when post-operative radiation is indicated. It is a silicone inflatable balloon, which, when implanted displaces the intestinal loops out of the pelvic irradiation field. The prosthesis can be deflated between each course of irradiation, without surgery. The device has been used in 8 patients: 6 patients with recurrent pelvic tumor (2 rectal cancers, 1 anal cancer, 1 cancer of the endometrium, 1 cervical carcinoma, 1 ovarian carcinoma), 2 patients with primary tumor (1 malignant paraganglioma, 1 cervical carcinoma). Radiotherapy was administered by means of high power appliances. After radiotherapy, the prosthesis was deflated, then removed through a 3 cm incision under local or peridural anesthesia. The tolerance of the small intestine to the radiation therapy has been satisfactory in each case with no bowel injury due to radiation. Therefore, this simple device might be useful to prevent bowel injury during postoperative radiation in the treatment of abdominal and retroperitoneal tumor masses.
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PMID:[New surgical procedure for the protection of the small intestine before postoperative pelvic irradiation]. 237 97

The number of patients with uterine endometrial cancer has increased in recent years in Japan. The studies on the prognostic factors of endometrial cancer, however, have not been made in detail as compared with those on the prognostic factors of cervical cancers. We have therefore investigated retrospectively the prognoses of 94 cases with endometrial cancer treated in our clinic from 1973 to 1984. Out of 31 cases (32.9%) with recurrence, 13 cases were at the Stage I and II, and the recurrence ratios were 11.4% for Stage Ia, 18.2% for Stage Ib and 31.3% for Stage II. The prognosis of endometrial carcinoma appears to depend on the endocervical involvement of the cancer. Five prognostic factors for Stage I and II endometrial cancers analyzed here are as follows; (1) histologic differentiation (grade), (2) size (diameter) of the primary tumor, (3) myometrial invasion, (4) vascular invasion, (5) lymphnode metastasis. (1) The recurrence ratio was 15.0% in the well differentiated (Grade 1) group, 25.0% in the moderately differentiated (Grade 2) group, 27.3% in the poorly differentiated (Grade 3) group, and 12.5% in adenoacanthoma. (2) The ratio of recurrence was 2.9% with less than 3 cm diameter, 24% with 3-6 cm diameter, and 30% with greater than 6 cm diameter in tumor size. (3) The ratio of recurrence was 2.9% with less than 1/3, 24% with 1/3-2/3, and 30% with greater than 2/3 myometrial invasion. (4) The ratio of recurrence was 43.8% with vascular invasion, and 5.6% without it. (5) The ratio of recurrence was 75% with lymphnode metastasis, and 8.8% without it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Recurrence of endometrial cancer and its pathological factors]. 239 96

The records of 16 patients with an obstructed, fluid-filled uterus due to carcinoma of the uterus or to its treatment by radiation therapy were analysed. In 12 uteri the presence of malignant tumor was simultaneously established, e.g. primary cervical carcinoma (1), recurrence of cervical (4), endometrial Stage II or III carcinoma (2), second primary tumors, MMT (2), and endometrial carcinoma (3). The uterine fluid consisted of blood (8), pus (3) or was serous (3). Twice the fluid could not be analysed. In our series the prognosis of patients with recurrent cervical cancer or a second primary tumor was poor. Improvement of the prognosis can result by intensifying the follow-up examinations with CT and/or ultrasound in the first 2 years, and not by prolongation of the follow-up period. Estrogen therapy was believed to be the causal factor in three cases of hemotometra. In the near future an increase of this complication is possible as a consequence of hormonal replacement therapy given to prevent osteoporosis after pelvic irradiation.
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PMID:Fluid detection in the uterus during and after irradiation for carcinoma of the cervix--clinical implications. 240 60

Forty-two cases of recurrent and 14 cases of advanced clinical stage (III and IV) endometrial carcinoma are presented, in which progesterone and estrogen receptors from the metastatic sites were measured. Mean survival time (time from recurrence or, in advanced stages, from the time of diagnosis to death or last follow-up), mean total survival time (time from diagnosis to death or last follow-up), and mean time to recurrence (time from diagnosis of primary tumor to the time of recurrence) were positively correlated with positive progesterone and estrogen receptor status and with histologic grade of tumor. No correlation was found with age, clinical stage, depth of myometrial invasion, or site of metastasis. However, when multiple variables were considered with the Cox regression model, the combination most highly correlated with survival included progesterone receptor, grade of tumor, and site of metastasis (pelvis vs. other sites). All differences were statistically significant (p less than 0.05). We conclude that measurement of progesterone and estrogen receptors in metastatic or recurrent endometrial tumors may be used as an additional prognostic variable.
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PMID:Prognostic significance of steroid receptors measured in primary metastatic and recurrent endometrial carcinoma. 258 47

Monoclonal antibodies were used to investigate progesterone receptor structure (isoforms) in 33 primary human endometrial tumors. The monoclonal antibodies recognized on protein blots two progesterone receptor proteins with molecular weights of 116,000 and 81,000. The Mr 116,000 protein appeared as a triplet, while a single band was found for the Mr 81,000 protein. The triplet/singlet structure was found in all progesterone receptor-positive tumors, regardless of the degree of tumor differentiation. Protease activity, which gave rise to a false-negative pattern on protein blots, was found in approximately one-half of the tumors in which it was investigated. Inclusion of a cocktail of protease inhibitors during sample preparation resulted in the maintenance of the triplet/singlet progesterone receptor structure. Mixing experiments using a progesterone receptor-rich human endometrial carcinoma (EnCa 101), which lacks protease activity, and protease-containing primary tumor homogenates indicated that the protease was leupeptin sensitive. Interestingly, while the proteolytic activity reduced or eliminated the triplet/singlet progesterone receptor structure seen on protein blot analysis, it did not affect progesterone receptor concentration measured by Scatchard analysis. Sample preparation in the presence of protease inhibitors is therefore a requisite for structural analysis of the progesterone receptor in endometrial tumors.
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PMID:Progesterone receptor structure and protease activity in primary human endometrial carcinoma. 327 7


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