Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A proportion of cancers in endocrine target tissues can show the presence of specific receptors for either steroid or polypetide hormones. Manipulation of the controlling hormones does not guarantee regression. A third of cancers in endocrine target organs (breast, uterine endometrium, and prostate) show a 50% reduction in size of lesions after hormonal therapy. If regression resulting from an aggressive form of therapy lasts a short while and the tumor reactivates by the time the unpleasant effects of the therapy wear off, the treatment is not palliative. Endocrine therapy in prostatic cancer is palliative but there is no evidence that is increases survival. 11 different progestational agents in endometrial cancer therapy in the past 25 years resulted in a 30-35% response. Response must be maintained by continual treatment and may last from 12 months to 7-8 years. In breast cancer, tumors with a significant level of estrogen receptor (ER+) have about a 60% chance of regression vs. tumors without estrogen receptors (ER-), 10%. Advanced cancers of the thyroid of the papillary or follicular type regress when the patient is treated by thyroxine, .3 mg daily. Leukemia and lymphoma are frequently treated, with varying degrees of success with corticosteroid therapy, which may also predispose the patient to intercurrent infection. Renal cancer has been often treated by medroxyprogesterone acetate or testosterone propionate, with little success.
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PMID:Endocrine therapy in cancer. 8 86

This study was designed to detect either 5alpha-dihydrotestosterone (DHT) or 17beta-estradiol (E2)-binding protein in the testes of a 1-year-old patient with testicular feminization syndrome (TFS) and in the testes of patients with prostatic cancer. Sucrose gradient analyses revealed E27S protein binding (but no such 7S protein binding of DHT) in the testes of the patient with TFS, but both E2 and DHT 7 S protein binding was observed in normal senile testes. The dissociation constants (Kd) were measured by charcoal adsorption. The Kd of E2 protein binding in both testes of different status was approximately 1.3 x 10(-9) M, and the Kd of DHT protein binding was 2.0 x 10(-9) M in the senile testes. A ligand specificty study indicated characteristics of both E2 and DHT receptors in the senile testes. It is speculated that a deficiency of androgen receptor and the presence of estrogen receptor in the testes of patients with TFS lead to insensitivity to androgen as a result of the androgen receptor deficiency and to sensitivity to estrogen as a result of the presence of the estrogen receptor.
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PMID:Preliminary studies on streoid-binding proteins in human testes of testicular feminization syndrome. 68 Jan 94

Biologic properties of breast cancer in men that might reflect alterations in pathogenesis from the disease in women were examined. We studied 22 tumors from males, 18 invasive carcinomas, three of which were papillary, and three in situ tumors of which one was papillary, and one papilloma. Our data support the previously reported high incidence of papillary carcinoma in men. Estrogen receptor status and the expression of cancer-associated antigens recognized by antibodies DF3, B73.2, SP-1, and c-erbB-2 were compared to matched tumors from females. Immunocytochemistry was performed on formalin-fixed, paraffin-embedded sections using standard avidin-biotin techniques; anti-PSA was used to exclude the possibility of metatastic prostate cancer, and 12 cases of gynecomastia were included as nonmalignant controls. The incidence of estrogen receptor positivity was higher in tumors from males (73%) than from females (54%), as has been reported previously. The range of expression of all breast cancer antigens tested in male tumors was similar to that observed in females, but some interesting differences were noted. With the exception of the anti-mucin DF3, all the antibodies reacted only with neoplastic tissues. Expression of the oncoprotein c-erbB-2 was lower (17%) in males than in females (33%), despite the preponderance in men of the large-cell type carcinomas that have been associated with c-erbB-2 expression. Unexpectedly, the pregnancy-associated hormone detected by SP-1 was expressed in 33% of tumors from males and, in contrast to females, was found in less differentiated tumors.
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PMID:Immunocytochemical characterization of male breast cancer. 136 97

The existence of an estrogen receptor and various other sex steroid receptors has been confirmed in prostatic cancer. However, the action mechanism of hormone therapy and relationship between the disappearance of hormone response, which is observed in the recurrence of prostatic cancer, and various sex steroid receptors have yet to be identified. The use of monoclonal antibody ERICA is known as a method of detecting the estrogen receptor in the immuno-histological chemistry method. However, this monoclonal antibody is difficult to use on paraffin sections. Therefore, using monoclonal antibody D5, which allows ER-D5 detection of the estrogen receptor related antigen on paraffin sections, we investigated whether or not estrogen receptors are present in the prostatic cancer preparation and studied the survival rate of prostatic cancer as well as relationship with recurrence. Positive ER-D5 results were obtained in 37 of 93 prostatic cancer cases (39.8%) and in all 20 prostatic hypertrophy cases (100%). ER-D5 tended to be more densely stained in prostatic hypertrophy than in prostatic cancer. The survival rate was obviously higher in the ER-D5 positive prostatic cancer cases than in ER-D5 negative cases for a certain period of time after the start of treatment. Despite differences in the histo-differentiation degree and clinical stage of prostatic cancer, the ER-D5 positive percentage did not change and remained between 35% and 45%. In cases where another prostatic cancer preparation was taken because of recurrence of prostatic cancer, there were no ER-D5 positive cases at the time of recurrence.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Determination of ER-D5 (estrogen receptor related antigen) in prostatic cancer and its significance]. 138 66

The steroid receptor profile in seven prostate cancer metastases was compared with the profile in seven primary prostate cancers. The secondaries were all lymph node metastases, obtained during pelvic lymphadenectomy, preceding radical prostatectomy or irradiation. Cytosol androgen receptor content was higher in metastases, whereas the nuclear androgen receptor content was only one-fourth that in primary cancer. Cytosol progesterone as well as estrogen receptor contents were markedly lower in metastases compared with primary cancer. The steroid receptor profile differed very little between primary cancer and normal tissue. Primary prostatic carcinoma is usually obtained at early stages of the disease, whereas metastases represent a dedifferentiated, more aggressive cell population. This may explain the low amounts of progesterone, estrogen, and nuclear androgen receptor levels. The total androgen receptor content was similar in metastatic and primary disease, however, with a shift towards a cytosolic predominance in metastases. Possibly androgen receptors in metastatic disease are "deactivated."
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PMID:Steroid receptor profile in human prostate cancer metastases as compared with primary prostatic carcinoma. 200 20

Estramustine phosphate, an anti-prostatic cancer agent, was investigated on eleven patients to evaluate the efficacy in a treatment of advanced breast cancers. The daily dose of medication was 840 mg. According to criteria of Japan Society for Cancer Therapy, none was assessed as CR, three as PR, four as NC and PD. The response rate was 27.3%. There was no differences in response rates among estrogen receptor status. A favourable response was observed in postmenopausal patients but no response in premenopausal, as well as a good response in lesions of soft tissue and lung, a poor response in lesions of liver and bone. As to toxicity of estramustine phosphate, gastrointestinal disorders such as nausea, vomiting and diarrhea were noted frequently during the treatment, and a long term administration was not able to perform in premenopausal patients because of vaginal bleeding and discharge, and pain in breast. The estramustine phosphate therapy for advanced breast cancers was regarded as one of modalities for a treatment of postmenopausal patients as a second line therapy. This is the first report in Japan discussing the efficacy of estramustine phosphate for a treatment of breast cancer.
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PMID:[Clinical evaluation of estramustine phosphate in the treatment of patients with advanced breast cancers]. 239 6

Tumor oriented anticancer agents with estrogen as a carrier have been extensively studied since 1950's. Only Estracyt and bestrabucil have been evaluated to be useful in clinical trials. Although the use of estrogen as a carrier for anticancer agents aimed at the development of the anticancer drug for the receptor mediated chemotherapy, these two drugs did not show any affinity to estrogen receptor. The history tells us that the development of anticancer agents for the estrogen receptor mediated chemotherapy is extremely difficult. Estracyt is reported to exert its anticancer effect on prostate cancer through the specific binding to the estramustine binding protein (EMBP) which is present only in the prostate gland and cancer. Bestrabucil shows the selective uptake by the various malignant cells and is indicated that bestrabucil exerts its anti-cancer effects on various malignant tumors including breast cancer and hematopoietic malignancy, through the affinity to malignant cells. The mechanism is unknown and to be elucidated.
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PMID:[Tumor-oriented anti-cancer agent with estrogen as a carrier]. 329 67

Enzyme immuno assay (EIA) of estrogen receptor (ER) has confirmed the results of earlier investigations using steroid binding techniques, namely that ER is present at very low concentrations in samples from metastatic melanoma. Thirty-four of 61 samples (56%) were ER positive with EIA. The corresponding figures using isoelectric focusing (IF) for the steroid binding assay were 16 of these 61 samples (26%). The difference between the methods may be due to difficulties in the interpretation of analytical results for IF at low ER concentration levels or to interference from other 3H-estradiol binding components. Estramustine binding site (EMBS) has been found in samples from 15 of 77 patients (20%) with IF in polyacrylamide gels. Estramustine is, together with estramustine, the cytotoxic metabolite of estramustine phosphate (Estracyt). In analogy to the previously suggested therapeutic significance of estramustine binding protein in the treatment of prostatic cancer, the clinical importance of estramustine phosphate should also be studied in metastatic malignant melanoma in correlation with EMBS status.
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PMID:Estrogen receptor and binding site for estramustine in metastatic malignant melanoma. 331 74

Immunohistochemical investigations of human prostate and human prostate cancer were performed using two different monoclonal antibodies for the demonstration of estrogen receptors (ER). One marked the nuclear estrogen receptor protein (ERICAR, Abbott Laboratories), whereas the other one marked an estrogen receptor-associated cytoplasmic protein (ER-D5 kit, Amersham Buchler). 12 transurethral resection specimens with benign prostatic hyperplasia and 10 prostatic carcinomas were investigated by ERICA. Only in 1 specimen was a focally ERICA-positive basal cell hyperplasia found. The ER-D5 kit yielded a constantly positive reaction of stromal cells, especially smooth muscle cells. Basal cell hyperplasia and squamous metaplasia, alterations which can occur during estrogen application, were always strongly ER-D5-positive. Eleven (13.4%) out of 82 prostate carcinomas were focally positive. The staining results with ER-D5 are in good accordance with biochemical estrogen receptor investigations which demonstrated the estrogen receptors especially in the fibromuscular stroma. Furthermore, the results show that therapeutically applied estrogens do not directly inhibit the growth of prostatic carcinoma, however, the effect is an indirect one by suppressing androgen synthesis of the testis. The different staining results with ER-D5 and ERICA can be explained by the low ER concentration of prostate, the concentration is evidently below the limits of detectability with ERICA.
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PMID:Immunohistochemical estrogen receptor demonstration in the prostate and prostate cancer. 343 7

In vitro cell lines were established from seven biologically distinct in vivo Dunning R3327 rat prostatic tumor sublines. Some of these in vitro cell lines (i.e., G, AT-1, AT-2) retain a low metastatic ability when inoculated back into syngeneic Copenhagen male rats, while others (i.e., AT-3, MAT-LyLu, MAT-Lu) retain a very high metastatic ability. A series of genetic (i.e., DNA content per cell, modal chromosomal number), as well as phenotypic parameters (i.e., morphology, 5 alpha-reductase, androgen receptor, estrogen receptor) were used to validate that the in vitro cell lines retained the major characteristics of the parental in vivo tumor sublines used for their respective establishment. A series of additional characteristics (i.e., morphology, growth rate, saturation density in surface culture, anchorage-dependent and -independent clonogenic potential) were compared between the high vs. the low metastatic in vitro cell lines to determine if a discriminatory parameter could be identified which reproducibly predicted the metastatic abilities of the particular prostatic cancer cell line. While the combination of the in vitro cell lines and their parental in vivo tumor subline will be a valuable tool for developing methods for predicting metastatic ability of prostate cancers, no single parameter yet measured is entirely successful in making this important distinction.
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PMID:Establishment and characterization of seven Dunning rat prostatic cancer cell lines and their use in developing methods for predicting metastatic abilities of prostatic cancers. 377 32


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