Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CA 125 and steroid production is compared in a group of 48 women with ovarian epithelial carcinoma. The histologic types were I C (n = 20), II C (n = 5), III C (n = 11), or V (n = 12). The number of patients in Stage I was six; Stage II, 11; Stage III, 16; and Stage IV, 15. All patients were naturally or surgically postmenopausal. Blood samples were taken at the first admission to the hospital and 14 cases with large tumors were followed with monthly sampling during chemotherapy, and in 13 cases until a recurrence of the tumor. CA 125 and steroid production were analyzed using radioimmunoassay. The results show a high correlation between initial CA 125 and especially progesterone plasma concentration. Both decreases during chemotherapy parallel the shrinkage of the tumor and increase 1 to 4 months before recurrence. Progesterone and CA 125 together predicted all recurrences but none of the factors alone. The prognostic value for 5-year survival was somewhat higher for progesterone than CA 125. CA 125 correlated highly with sex hormone binding globulin (SHBG) and negatively with albumin. The correlation may be due to the intercorrelation with tumor burden.
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PMID:Relationship between CA 125 and progesterone production in women with ovarian carcinoma. 237 70

The growth of the C3H mouse mammary tumor (MMT) is considered to be hormone independent. Medroxyprogesterone acetate (MPA) had no effect on the growth of transplanted autochthonous MMT or the colony-formation of MMT cells. The tumor angiogenesis factor (TAF) activity of tumor-extract prepared from C3H mouse with transplanted autochthonous MMT and injected with 0.67 mg of MPA (in vivo MPA group) and that prepared from the colony of MMT cells treated with 10(-6) M MPA (in vitro MPA group) was lower (100.0% and 9.8%) than those of the in vivo and in vitro cortisol groups (325.5% and 44.3%), and the in vivo and in vitro groups without treatment (393.5% and 46.8%), respectively. The fibroblast growth factor (FGF) activity of the in vivo and in vitro MPA groups was lower (23.7% and 2.7%) than those of the in vivo and in vitro cortisol groups (54.7% and 11.3%), and the in vivo and in vitro groups without treatment (49.6% and 11.3%), respectively. Therefore, MPA may reduce neovascularization induced by TAF and FGF, although it had no effect on the growth of this MMT, and it had a glucocorticoid action similar to that of cortisol.
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PMID:Inhibition of tumor angiogenesis activity in C3H mouse mammary tumor by medroxyprogesterone acetate. 246 26

The early discrimination of clinically aggressive breast cancer from indolent disease would be clinically useful. Some human breast cancers express haptoglobin-related protein (Hpr), the HPR gene product, or a substance that shares epitopes with it. We retrospectively examined the association between the expression of Hpr and the recurrence of cancer in 70 patients with early breast cancer (Stage I or II) treated by mastectomy from 1977 through 1985, using immunohistochemical analysis of routinely processed paraffin-embedded tissue and evaluating it without knowledge of the patients' status. The expression of Hpr epitopes was associated with earlier recurrence according to life-table analysis (P less than 0.0002). Progesterone-receptor status (determined in 64 patients), tumor size, clinical stage, axillary-lymphnode status, mitotic index, and tumor necrosis also predicted recurrence, but multivariate analysis showed that Hpr-epitope expression was an independent prognostic factor. Since both Hpr status and progesterone-receptor status were independent predictors of recurrence, they could be combined to stratify the cases further: breast cancer was found to have recurred in 11 of 12 patients (92 percent) who were positive for Hpr and negative for progesterone receptors, in 5 of 11 (45 percent) who were positive for Hpr and positive for progesterone receptors, and in 9 of 41 (22 percent) who were negative for Hpr, in whom progesterone-receptor status had little effect. We conclude that Hpr-epitope expression is a clinically important predictor of the recurrence of cancer in patients with early breast cancer, especially in combination with progesterone-receptor status.
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PMID:Haptoglobin-related protein (Hpr) epitopes in breast cancer as a predictor of recurrence of the disease. 247 78

Progesterone receptors (PR) were measured in 18 cases of endometrial carcinoma using the dextran-coated charcoal assay. The histological changes and PR levels of the endometrial carcinoma after the medroxyprogesterone acetate (MPA) treatment were studied. A higher PR levels were observed in well-differentiated tumors. After treatment with MPA, the PR content was reduced and histological appearance similar to normal endometrium was noticed. The histological changes of the tumor was closely related to the receptor levels.
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PMID:[Progesterone receptors in endometrial carcinoma and their response to medroxyprogesterone acetate]. 253 67

A variety of tumor characteristics can provide prognostic information useful in managing the patient with primary breast cancer. Some of these characteristics are firmly established, whereas others are observer dependent or require prospective validation. No single characteristic, however, is likely to fully define which patient with primary breast cancer is destined to relapse. This clinical dilemma--recognition of the high-risk patient--is particularly important in the management of women with node-negative breast cancer. Because most women with this early stage of disease will be cured by surgery alone, the use of adjuvant chemotherapy must be limited to high-risk subsets. Tumor size and ER status are established prognostic factors. Histologic and nuclear grade may be important, but problems of interobserver variability remain. Some studies have shown that aneuploidy or a high S-phase fraction may be independent, high-risk characteristics. Flow cytometric DNA content analysis must be applied with caution, however, because the calculation of S-phase fraction has not been standardized and because the prognostic utility of this approach has not been prospectively confirmed. For now, a prudent approach might be to gather as much prognostic information about each patient's tumor as possible. Those with several of the high-risk characteristics listed in Table 2 should receive strongest consideration for adjuvant treatment. Some of these same prognostic factors, along with several others, can be used to characterize the high-risk node-positive patient. The number of involved axillary nodes is the most important established predictor. Progesterone-receptor status is associated with both disease-free and overall survival, whereas ER status is independently related only to overall survival. Histologic grade, DNA ploidy, and S-phase fraction can also be used to help define the high-risk patient. Finally, tumors that amplify or overexpress the HER-2 gene may have a higher risk of relapse, although this finding has been questioned. Management of patients with breast cancer requires an individualized approach that is based on a careful weighing of a variety of prognostic considerations. The relative importance of these factors will require further large-scale, prospective, multiparameter studies. Although results from such studies are awaited, an understanding of the clinical heterogeneity of breast cancer must be based on a multiplicity of observations, each of which characterizes, in a limited way, the biology of this disease.
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PMID:Prognostic factors in breast cancer. 255 4

In order to clarify the minute reactions of endometrial adenocarcinoma to sex steroid hormones, especially Progesterone (P), two kinds of in vivo models with differing sex steroid hormone receptor content were transplanted into nude mice. Subsequently, Estrogen (E2) and P were administered alone or together. Sequential histopathological changes, tumor growth curve and volume doubling time were investigated as compared to the castrated control group. Growth rate was increased by E2 administration compared to controls for the model positive for the E2 receptor (ER) and negative for the P receptor (PR), with PR production confirmed in 1 of 3 mice. P produced a slight inhibition of growth, and the inhibitory effect of P was additive with E2. The histological findings consisted of dense solid masses of cells in the tumor in mice treated with E2. The cells decreased in number and in some foci, the tubular glands were cystic in P-treated mice. The number of tumor cells in mice treated with E2 and P was less than in mice given P alone because of a secretive function seen in the appearance of PAS positive granules in the glandular epithelium and degenerative change such as swelling. With the tumor negative for both ER and PR, on the other hand, there was little difference in tumor cell growth between the treated and control groups, and no inhibitory effect was observed after administration of P or coadministration of E2 and P. Histologically, findings with increased nuclear division of tumor cells suggestive of tumor cell growth were obtained after administration of E2 alone and coadministration of E2 and P. E2 exhibited cell growth promoting action in endometrial adenocarcinoma, whether or not ER was present, and P appeared to inhibit tumor cell growth in the presence of ER even when PR was absent. In short, it was suggested that P acted by some mechanism independent of PR. After coadministration of E2 and P, tumor cells were affected in a direction toward functional differentiation in the ER positive tumor. The inhibitory effect of P was obviously additive with E2 in this tumor, while it was suggested that in ER negative tumor, E2 alone promotes tumor cell growth.
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PMID:[Effects of female sex steroid hormones on human endometrial adenocarcinoma transplanted into nude mice]. 261 95

A monoclonal antibody against an Estrogen Receptor Related Protein (EG-D5 AG by Amersham) was analyzed in evaluating hormone dependence in 188 breast cancers, in addition to current index of steroid receptors. The Authors observed that the concentration of this new Antigen is not related with PgR but with ER concentration. In fact, increasing the ER values, increases the concentration of ER-D5 Ag, showing a good correlation between these two tumoral markers. In regard to Progesterone Receptor ranges, the ER-D5+ves were equally distributed between PgR-ves and PgR+ves Our experience suggests the application of ER-D5 Ag as R-ves tumor screening marker and emphasizes the importance of a second level in determining therapy and prognosis in breast cancer.
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PMID:A cytoplasmatic estrogen receptor related protein (ER-D5 Ag) in breast cancer. 272 21

Using an in vitro tritiated thymidine (3H-dThd) nuclear labeling followed by autoradiography, the effects of 17-beta-estradiol (E2) or progesterone (Pg) on cell proliferation were studied in 22 human benign breast tumors, i.e. 7 fibroadenomas 8 fibrocystic dysplasias 4 gynecomastias and 3 phyllodas. Small tumor fragments were incubated in a chemically-defined medium without serum and were hormonally stimulated in vitro. The procedure used allowed discrimination between weak labeling, suggestive of DNA repair mechanism, and strong labelling, suggesting a true DNA synthesis (S phase). Taking this into account, our results have shown that both estradiol and progesterone can induce in vitro cell replication of both ER+PgR+ and ER-PgR- human breast fibroadenoma, without affecting those of fibrocystic dysplasia, gynecomastia and phylloda. Progesterone, but not estradiol, might significantly decrease DNA repair mechanism in fibrocystic dysplasia, according to the Pg-induced decrease of nuclear incorporation of small amounts of 3H-dThd. We have thus characterized a dynamic test of hormone dependence which permits in vitro study of the hormonal sensitivity of human benign breast tumors, as well as that of any other human neoplasm. This test could be of great value to help clinicians to diagnose and treat hormone-dependent neoplasms properly. Its clinical relevance is now under study.
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PMID:In vitro influence of estradiol or progesterone on the thymidine labeling indices of human benign breast tumors. 275 Dec 71

The aim of this study was to investigate the effects of estradiol and tamoxifen (TAM) on the growth of human endometrial carcinomas in athymic mice. Tissues from primary tumors were implanted into estradiol-treated mice. In passage 2, animals were treated with (a) placebo, (b) estradiol, (c) estradiol plus TAM, and (d) TAM alone. The size of the tumors was measured weekly. Estrogen receptors (ER) were determined with the dextran-coated charcoal method and/or ER enzyme-linked immunoassay. Progesterone receptors were measured with the dextran-coated charcoal technique. Of 16 primary tumors, 2 grew in the athymic mice and were studied further. Tumor EL was positive for ER (145 fmol/mg protein) and progesterone receptors (993 fmol/mg protein). Tumor EL in passage 2 was not significantly stimulated by estradiol, but was stimulated by a combination of estradiol and TAM. Treatments (estradiol, estradiol plus TAM, or TAM) all increased tumor growth in passage 3. Tumor BR and a metastasis BR-MET were ER and progesterone receptor negative, applying dextran-coated charcoal, ER enzyme-linked immunoassay, and immunocytochemistry. The BR and BR-MET cells contain the complete ER gene but do not express any measurable amounts of ER mRNA as quantitated by Northern blot analysis, using a complete ER complementary DNA probe. In all animal passages the growth rate was significantly higher in estradiol-treated mice compared with the control. TAM alone had some growth stimulatory effect, but much smaller than observed in the estradiol group. TAM inhibited estradiol-stimulated growth. These results suggest that estradiol and possibly TAM are capable of stimulating tumor growth in the athymic mice independently from ER, potentially through a host-mediated mechanism.
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PMID:Enhanced growth of an estrogen receptor-negative endometrial adenocarcinoma by estradiol in athymic mice. 275 9

An altered pattern of cytochrome P-450-dependent microsomal steroid metabolism was identified in female mouse liver tumors induced by 5,9-dimethyldibenzo[c,g]carbazole, a potent organo-specific liver carcinogen. These tumor tissues were compared to extratumoral liver parenchyme, to normal, fetal and neonatal livers and to spontaneous liver tumors, the frequency of which is very low in the highly hybridized mouse strain (XVIInc/Z) used for liver tumorigenesis. Cytochrome P-450-dependent steroid hydroxylase activities were measured by the identification and quantification of four monohydroxyprogesterone and eight monohydroxytestosterone metabolites. In contrast to a general decrease (50%) of total P-450 in tumor microsomes, the individual steroid hydroxylases were regulated differently. Progesterone 16 alpha- and testosterone 6 alpha-, 6 beta-, 7 alpha- and 16 alpha-hydroxylase activities were decreased 50%, and more, whereas progesterone and testosterone 15 alpha-hydroxylase activities were raised 3-4 times with regard to microsomal protein content and 6-7 times with regard to total P-450. Consequently the most prominent feature of the steroid metabolism by tumor-borne microsomes is the hydroxylation at the 15 alpha-position. Furthermore, minor testosterone 2- and 15 beta-hydroxylase activities showed equally an increase of approximately 4 times (8 times with regard to total P-450). The observed new tumoral pattern of P-450-dependent microsomal steroid metabolism appearing characteristically in spontaneous and chemically induced liver tumors indicates that particular P-450 enzymes are strongly expressed in mouse liver tumors. These enzymes may be used as markers for early stages in liver tumorigenesis.
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PMID:Particular cytochrome P-450-dependent steroid metabolism: a new class of mouse liver tumor markers. 279 Dec 5


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