Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The R3327 HI experimental prostatic carcinoma was serially transplanted through six generations of castrated host rats to examine changes in the capacity to synthesize progesterone receptor (PgR) in response to diethylstilbestrol (DES) stimulation during progression from a well-differentiated state containing a significant stromal component to a poorly differentiated state with virtually no stroma. During progression, changes in growth rate and histopathology occurred in stepwise fashion, the most marked changes being observed between the first and second and between the fourth and fifth generations. The capacity for PgR synthesis in response to DES treatment fell progressively, but did not reach statistical significance during the first four generations. By the sixth generation, the stromal component had virtually disappeared, and no estrogen receptor (ER) or PgR was detectable. During the course of the investigation, a monoclonal antibody that reacts with rat PgR became available, and immunohistochemistry with this antibody confirmed that DES-induced PgR was present in stromal cells. We conclude that this work supports the hypothesis that prostatic stroma is a target tissue for estrogen and that this model may be useful for the investigation of other events associated with progression.
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PMID:Changes in tumor characteristics during progression of the R3327 HI experimental prostatic carcinoma. 169 Aug 81

Cytosolic and nuclear androgen, estrogen and progesterone receptor content was measured in the groups of 11 prostatic carcinoma (PCA) and 32 benign prostatic hypertrophy (BPH) samples. All BPH cases were positive for the cytosolic progesterone (PRc) and estrogen receptor (ERc), whereas only 85% of cases (23/27) contained the androgen receptor (ARc). Only those five patients who received estrogen treatment in the PCA group had detectable ARc. PRc was present in all of the PCA cases, whereas ERc could be detected in only 82% (9/11) of cases. Cytosolic contents of all three steroid receptors, however, were higher in the PCA group. The level of nuclear steroid receptors, although present in fewer cases in both groups, was higher than the cytoplasmic receptors. The serum profile of estradiol, cortisol, and prolactin was normal in both groups, whereas LH, FSH, and progesterone levels were higher than in normal adults. Serum testosterone level was within normal range in the BPH group, but it was significantly below normal (P less than 0.005) in PCA patients.
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PMID:Androgen, estrogen, and progesterone receptor contents and serum hormone profiles in patients with benign hypertrophy and carcinoma of the prostate. 169 95

Monoclonal antibody to human estrogen receptor (ER) provides a useful immunohistochemical tool for the evaluation of ER content in breast carcinoma, but visual interpretation is subjective. Computer-assisted image analysis has proved effective in immunohistochemical quantitation of ER in fresh tumor imprints and cryostat sections. We examined the usefulness of this technique in 5-microns-thick formalin-fixed paraffin-embedded tissue sections of 66 cases of primary breast carcinoma previously assayed by dextran-coated charcoal (DCC) analysis. Immunohistochemistry was automated and performed on a Code-on slide stainer (Instrumentation Laboratories, Lexington, MA) using Pronase predigestion, a monoclonal antibody (ER-ICA; Abbott, Chicago, IL), and a biotin-labeled secondary antibody. Detection was achieved with an avidin-alkaline phosphatase conjugate and nitroblue tetrazolium (NBT) bromochloroindoyl phosphate (BCIP) substrate. The immunohistochemical ER staining was analyzed visually and with the CAS/200 image analyzer (Elmhurst, IL). The visual semiquantitative histologic scores (HSCORE), the automated quantitative assays including the percentage of positive nuclear areas (PNA), and the quantitative immunocytochemical scores (QIC SCORE = PNA x % of positive stain/10) were compared with the corresponding DCC results. Linear correlations were demonstrated between all immunohistochemical assays and the logarithm of DCC, the strongest correlation seen with PNA (r = 0.91). Threshold points for positive HSCORE, QIC SCORE, and PNA assays were extrapolated using DCC as the reference. ER immunodetection by PNA as compared with visual examination alone was enhanced by 18% (up to 88%) in sensitivity and 34% (up to 94%) in specificity, and the DCC concordance rate increased by 26% (up to 91%). A comparative chart extrapolating DCC from PNA was thus established.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Image analysis for quantitation of estrogen receptor in formalin-fixed paraffin-embedded sections of breast carcinoma. 170 2

Microglandular adenosis (MA) of the breast is a benign, disorganized proliferation of glands lined by a single layer of cells. As such, differential diagnosis between MA and tubular carcinoma may be challenging in selected cases. A panel of antibodies was applied to 10 cases of MA and 10 of tubular carcinoma to investigate the potential benefit of immunohistochemistry in the separation of these lesions and the possible role of myoepithelial cells in MA. The luminal cells in nine cases of MA were surrounded by a cuff of muscle-specific actin-reactive cells, which also coexpressed cytokeratin and vimentin. The immunophenotype of these cells is characteristic of myoepithelial differentiation, which was heretofore thought to be lacking in MA. This finding demonstrates that myoepithelial cells are indeed present in MA subjacent to luminal epithelial cells; moreover, it distinghuishes MA from tubular carcinoma, all examples of which were actin negative in this analysis. In addition, circumferential type IV collagen deposition was observed around constituent glands of MA in nine cases but was lacking in all tubular carcinomas. Other markers included in this evaluation (S100 protein, gross cystic disease fluid protein 15, carcinoembryonic antigen, estrogen receptor protein) were of no differential diagnostic value.
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PMID:Microglandular adenosis of the breast. An immunohistochemical comparison with tubular carcinoma. 171 Jan 1

DNA content and estrogen-receptor status were studied in 54 consecutive patients with primary breast carcinoma. Estrogen-receptor determinations were performed by immunohistochemical assay on frozen sections with a monoclonal antibody against the estrogen-receptor molecule and by biochemical analysis with a dextran-coated charcoal method. Nuclear DNA content was measured by flow cytometry performed on formalin-fixed, paraffin-embedded sections. Seventy-two percent of tumours were positive for estrogen receptors by immunohistochemical assay and 67% by biochemical assay. Comparison of the qualitative results of immunohistochemical and biochemical estrogen-receptor determinations revealed a strong correlation between the two assays, with agreement in 90% of the cases (p less than 0.001). Regression analysis showed only a weak relationship between the quantitative results of the two assays. DNA analysis was performed in 51 cases, and 54% demonstrated aneuploid stemlines by flow cytometry. An association was demonstrated between aneuploidy and low levels of estrogen receptor. The association was highly significant with the immunohistochemical assay but not with the biochemical assay. The authors' results suggest that immunohistologic determinations of estrogen receptor status may better reflect the biologic features of the tumour cells. However, improved standardization in reporting the results is necessary if the test is to have widespread use.
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PMID:DNA content and estrogen receptors in primary carcinoma of the breast. 171 40

Within human carcinomas, there is often an infiltration of lymphocytes and other cells of the immune system. A variety of cytokines are produced by such cells that could have a paracrine influence on the growth of tumor epithelium. The effect of one of these cytokines, interleukin-4 (IL-4), on human breast and colon cancer cell lines was therefore examined. IL-4 inhibited the growth of human colon (HT 29) and breast [MCF-7 wild type (MCF-7 WT), MCF-7 Adriamycin-resistant (MCF-7r), MDA-MB-231, and MDA-MB-468] carcinoma cells in culture. Competitive binding of 125I-IL-4 demonstrated the presence of 2000 high affinity IL-4-binding sites on HT 29 cells. The Kd for specific binding of 125I-IL-4 to HT 29 cells was 77 pM. Further studies were conducted on the estrogen-dependent MCF-7 WT and estrogen-independent MDA-MB-231 breast carcinoma lines. Concentrations of IL-4 of 10-100 nM were required to significantly inhibit growth of these carcinoma cell lines; e.g., with MCF-7 WT cells, half-maximal inhibition of growth occurred at 20 nM IL-4. Specific binding of 125I-IL-4 was detected to MCF-7 WT and MDA-MB-231 cells, but the low level of binding precluded Scatchard analysis. IL-4 inhibited 90% of the 17 beta-estradiol-stimulated growth of MCF-7 WT cells in a dose-dependent manner but without a change in estrogen receptor expression. Inhibition of growth by IL-4 was less in the absence of estrogens. Combined treatment with IL-4 and other known inhibitors of breast carcinoma cell growth [transforming growth factor-beta 1 (TGF-beta 1) and the antiestrogen tamoxifen] showed additive inhibition. The hormone-independent cell lines MCF-7r and MDA-MB-231 were additively inhibited by IL-4 and TGF-beta 1. This was not the case with MDA-MB-468 cells in which inhibition by IL-4 and TGF-beta 1 was of similar magnitude but no significantly greater effect was observed on combined treatment. No secretion of IL-4 was detected from these cell lines either basally or on treatment with TGF-beta 1 or tamoxifen, and we conclude that IL-4 is a nonautocrine inhibitor of breast carcinoma cell growth.
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PMID:Inhibition of colon and breast carcinoma cell growth by interleukin-4. 172 1

The literature concerning the uncommon findings of bladder involvement of breast carcinoma is suggestive of a recent increase in reported cases. We report on 3 additional women with vesical deposits of metastatic breast carcinoma. The clinical presentation and dire significance of such cases, and their relationship to progesterone and estrogen receptor expression are discussed. We also postulate on the possible increase in the numbers of reported cases.
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PMID:Bladder involvement in metastatic breast carcinoma. 172 7

Although estrogen receptor (ER) content and its clinical significance have been extensively evaluated in invasive breast cancer, ER expression in carcinoma in situ (CIS) of the breast and its correlates are less well understood. Thus, using an indirect immunoperoxidase technique and paraffin-embedded tissue, the authors studied ER expression in 100 breast tumors containing CIS with or without invasive carcinoma. The percentages of positive and of strongly positive nuclei were compared among histologic categories of CIS and between CIS and invasive carcinoma. The relationships between histologic features of CIS (cell size, nuclear pleomorphism, necrosis, extent of CIS) the patient's age, and the ER status of CIS also were evaluated. ER expression in pure CIS was compared with that of CIS with adjacent invasive carcinoma. Significant differences were observed between comedo CIS, which was frequently ER negative, and non-comedo and lobular CIS, which usually were positive. A predominance of large cells, independently from other features, was the best morphologic predictor of ER negative status in CIS. ER in CIS correlated with ER in invasive carcinoma in 98% of cases (r2 = 0.677). CIS without invasive carcinoma was more frequently ER weak or negative than CIS associated with invasive carcinoma. There was no difference in the overall percentage of nuclear staining in CIS of women of premenopausal versus postmenopausal age; however, a higher proportion of strongly positive cells occurred in the postmenopausal group. The authors conclude that the ER expression in CIS correlates with pathologic features of differentiation and is similar to that of invasive carcinoma.
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PMID:Estrogen receptor immunohistochemistry in carcinoma in situ of the breast. 173 17

The optimal demonstration of estrogen receptor binding in thyroid tissues was made under conditions of 10% protease in 50 mM Tris-HCl buffer (pH 7.6) for 10 min as the pretreatment digestion step, incubation of primary antibody (ER-ICA monoclonal kit; Abbott Laboratories) at 37 degrees C for 2 h and incubation of secondary antibody (ABC kit; Vector) at 37 degrees C for 40 min. Thyroid tissues used for assessing the reaction were 17 cases of goiter, 25 adenoma cases, 27 cases of papillary carcinoma, 14 cases of follicular carcinoma and 10 latent cancer cases. Incidences of positive estrogen receptor reaction were 22% (11/51) for all thyroid cancers, 20% (5/25) for the thyroid adenomas and 59% (10/17) for goiters. 15% (4/27) of papillary carcinomas, 21% (3/14) of follicular carcinomas and 40% (4/10) of latent cancers proved positive, the estrogen receptor reaction being limited to the nuclei of thyroid follicular/papillary type cells.
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PMID:Immunohistochemical detection of estrogen receptors in paraffin sections of human thyroid tissues. 174 91

We have established a novel human breast carcinoma cell line, HMA-1, derived from ascites of a female breast cancer patient. HMA-1 was shown to be an epithelial cell line with intracytoplasmic duct-like vacuoles, microvilli, desmosomes and tonofibrils in accordance with human breast cancer. The cell line demonstrated a good cell growth ability in monolayer fashion with a doubling time of 46 hr. Based on a whole cell binding assay the cell line contained estrogen receptor (1.45 x 10(-4) sites/cell). Tamoxifen, an anti-estrogen agent induced a dose-dependent decrease in the cell growth rate, but estradiol stimulated the cell growth. HMA-1 could be transplanted subcutaneously into BALB/c nude mice, and was able to cause tumors approximately two months after heteroinoculation. These results indicate that HMA-1 cell line may serve as a new human breast carcinoma cell line which could be utilized in the breast cancer research.
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PMID:Establishment of an estrogen receptor-positive cell line (HMA-1) derived from human breast carcinoma. 175 37


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