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)

Zinc, testosterone and dihydrotestosterone concentrations have been measured in normal prostatic tissue and in specimens obtained from untreated patients with benign prostatic hyperplasia (BPH) and carcinoma of the prostate (CaP). The metal--androgen relationship was examined and related to the pathological condition of the patients. The evidence suggests that discriminant analysis combining the hormonal data into a single variable is a reliable test for distinguishing between BPH and CaP patients. We have observed that the high Zn values found in BPH specimens were always associated with a DTH:T ratio greater than 1. Androgen tissue ratios less than 1 were characteristic of all CaP specimens, and these were usually preceded by a reduction in prostatic Zn concentration. Since these patterns, particularly those associated with neoplasia, precede the clinical manifestations, they may be used as an index for predicting the onset of carcinoma in the prostate gland. They may also be of value in monitoring the progress of the disease.
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PMID:Cancer of the prostate: early diagnosis by zinc and hormone analysis? 8 14

The metabolism of radioactive testosterone, 5alpha-dihydrotestosterone, 4-androstene-3beta,17beta-diol or 4-androstene-3alpha,17beta-diol by the human cell line NHIK 3025, derived from a carcinoma of the uterine cervix, was studied. The cells were grown in Eagle's minimal essential medium (MEM) with a steriod concentration of 10-(7) M for 4 days. Androgen metabolism by this cell line is essentially the same as for other androgen-responsive cells. The most interesting testosterone metabolite in this system is 4-androstene-3beta,17beta-diol, and the separation of this compound from 4-androstene-3alpha,17beta-diol and the two corresponding 5alpha-reduced diols is described. Since 4-androsterone-3beta,17beta-diol is a more potent growth factor for these cells than testosterone, the small conversion of testosterone to 4-androstene-3beta, 17beta-diol observed could be responsible for the growth stimulation by testosterone.
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PMID:Androgen metabolism in relation to growth stimulation by a uterine cell line. 56

Androgen-dependent and androgen-independent (autonomous), cloned, cultured cell lines of the androgen-dependent mouse mammary adenocarcinoma, Shionogi carcinoma 115, have been established. Growth of the dependent cells requires the presence of androgen, provided they are growth in suspension culture in medium containing dextran-charcoal-treated fetal calf serum. The growth rate of autonomous cells in the presence or absence of DHT is similar to that of dependent cells grown in its presence. An agar culture method has been developed that enables the proportion of dependent and autonomous cells in mixed populations to be determined. Autonomous cells appear in dependent clones, and their frequency increases with increasing time of subculture. Dependent cells form tumors preferentially in male animals and dependent cell cytosols contain significant amounts (approximately 300 femtomoles per mg protein) of a specific androgen-binding macromolecule. Autonomous cells formed tumors equally well in both male and female mice, and autonomous cell cytols contain very low levels (less than or equal to 7 femtomoles per mg protein) of the specific androgen-binding macromolecule(s). These studies delineate a system which can be used to investigate the mechanism of steroid hormone-dependent and autonomous tumor growth, and the transitions between the hormone-dependent and autonomous states.
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PMID:Development of methods for the quantitative in vitro analysis of androgen-dependent and autonomous Shionogi carcinoma 115 cells. 83 42

Human prostatic acid phosphatase (PAcP) is a tissue-specific differentiation antigen and is the major phosphotyrosyl (p-tyr) protein phosphatase in normal differentiated prostate epithelial cells. In prostate carcinomas, cellular PAcP has a low expression. We examined the expression of cellular PAcP activity and its correlation with cell growth that may lead us to understand the role of tyrosine phosphorylation in human prostate cells. LNCaP cells, which expressed the highest cellular PAcP activity, had the slowest growth rate and the lowest p-tyr level among three human prostate carcinoma cell lines: LNCaP, DU145, and PC-3. This inverse correlation was further examined in LNCaP cells, since these cells remain hormone-sensitive. Androgen, a classical stimulator of prostate cells, stimulated the growth of LNCaP cells while cellular PAcP activity decreased and p-tyr levels increased. This phenomenon was also observed when cells were treated with epidermal growth factor and fetal bovine serum. Both epidermal growth factor and fetal bovine serum stimulated the growth of LNCaP cells whereas cellular PAcP activity decreased. Furthermore, when cell growth was arrested at low temperatures (23 degrees C), cellular PAcP activity was elevated. To establish the relationship of cellular PAcP activity with cell growth rate, we transfected a complementary DNA encoding the full length PAcP protein into another human prostate carcinoma line, PC-3, that lacks endogenous PAcP. Two stable transfectants, designated PC-18 and PC-416 cells, were obtained and shown to express PAcP mRNA transcribed from the transfected complementary DNA. The expression of PAcP activity in PC-416 cells, but not PC-18 cells, was associated with a lower p-tyr level and a slower growth rate than control cells transfected with the expression vector alone. In conclusion, in LNCaP cells, the stimulated cell growth is associated with an increased p-tyr level and a decreased cellular PAcP activity. In PAcP complementary DNA-transfected PC-416 cells, the low level of p-tyr corresponds to a slow growth rate.
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PMID:Expression of human prostatic acid phosphatase activity and the growth of prostate carcinoma cells. 138 Aug 86

In vivo effects of androgen withdrawal and substitution on human androgen receptor (hAR) expression were evaluated in the androgen-dependent human prostatic carcinoma tumor line PC-82. By application of several antibodies reactive with different epitopes of the hAR molecule, hAR protein expression was studied in tumor transplants by immunohistochemistry and immunoblotting. hAR messenger RNA (mRNA) levels were quantitated in PC-82 tumor tissue with a S1-nuclease protection assay. Most PC-82 tumor cells (> 97%) from testosterone-supplemented mice displayed nuclear hAR protein expression immunohistochemically. The almost complete reduction of nuclear hAR immunoreactivity within 5 days after androgen withdrawal (< 10%) was restored after androgen substitution within 1 day. The immunochemical data were confirmed by Western blot analysis. In contrast, no significant changes were observed in hAR mRNA content of PC-82 cells after 5 days of androgen withdrawal. Correlating hAR expression with proliferative activity of PC-82 tumor tissue during endocrine manipulation, a rapid, castration-induced decline of the percentage of bromodeoxyuridine-labeled cells accompanied the loss of hAR. Androgen substitution in castrated male mice restored the proliferative activity. However, this increase of proliferative activity lagged at least 24 h behind the normalization of the hAR protein level. In contrast to the steroid receptor down-regulation by homologous ligands observed in other experimental models, our data support the concept of hAR up-regulation by androgen. Since the hAR mRNA content of PC-82 tumor tissue was hardly affected by castration, expression of the hAR in PC-82 is thought to be modulated by translational and/or posttranslational mechanisms.
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PMID:Regulation of androgen receptor expression in the human heterotransplantable prostate carcinoma PC-82. 144 39

The leading cause of cancer in males in the United States, prostate cancer accounts for 22% of all new cancers, with 132,000 new cases projected to be diagnosed in 1992. While localized prostate cancer can be cured, up to two thirds of patients present with advanced disease. Androgen deprivation remains the mainstay of treatment for advanced prostate carcinoma. Recurrent disease, however, is invariably refractory to further hormone manipulations. The development of hormone-resistant tumor cells may be explained either by a multi-clones theory, by mutation of previously sensitive tumor cell clones, or, most likely, by both mechanisms. Thus, vigorous efforts are needed to develop nonendocrine treatment approaches. Such efforts have been complicated by the difficulty of assessing therapeutic response in patients with prostate cancer, because the typical metastatic bone lesions seen in these patients are difficult to measure accurately and patients seldom have disease in the lung, lymph nodes, or soft tissue. A variety of single chemotherapeutic agents have been tested against recurrent disease, with widely divergent response rates achieved. Trials of chemohormonal therapy have likewise proved disappointing to date. Preliminary results from an ongoing trial of oral etoposide in patients with recurrent prostate cancer are discussed.
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PMID:Etoposide in the treatment of hormone-refractory advanced carcinoma of the prostate. 148 54

We have demonstrated that differential housing alters the growth rate of the androgen-responsive Shionogi mouse mammary carcinoma (SC115). In the present study we wished to determine if changes in plasma levels of hormones or a shift in the responsiveness of the tumor cells to hormones was responsible for the differential tumor growth rates observed. Plasma testosterone and corticosterone levels were assayed 24 h, 3 days and 1 week post tumor cell/vehicle injection. Also 3 weeks post injection androgen and glucocorticoid receptor binding capacity (Bmax) and binding affinity (Kd) and the in vitro responsiveness of tumor cells to dihydrotestosterone and hydrocortisone were measured. At 24 h post injection, plasma testosterone levels were significantly increased in mice with large tumors, but remained low in mice with small tumors. Plasma corticosterone levels were significantly elevated in mice with small tumors compared to those of mice with large tumors at all time points measured. Androgen and glucocorticoid receptor binding capacity and binding affinity of tumor cells did not differ among groups. Further, all groups tested had the ability to respond to dihydrotestosterone and hydrocortisone in vitro. These data indicate that an effect of housing condition on plasma levels of steroid hormones may, in part, mediate the differential tumor growth rates observed in this model.
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PMID:Endocrine mediation of psychosocial stressor effects on mouse mammary tumor growth. 151 12

Androgen receptors have been found in human larynx and androgens have been supposed to play an important role in promoting the growth of laryngeal carcinomas. The molecular mechanism underlaying this phenomenon is not at all understood. Aim of this work was to investigate the effects of two androgens (testosterone and dihydrotestosterone) on insulin receptor mRNA levels and insulin binding activity as well as on either metabolic or growth-promoting actions of insulin in a human larynx carcinoma cell line (HEp-2). We found that HEp-2 cells express a high affinity insulin receptor. Both androgens significantly increase insulin receptor mRNA levels and insulin receptor number in HEp-2 cells. Insulin action, evaluated either as total glucose utilization or as [3H]thymidine incorporation into DNA, significantly increased in HEp-2 treated with androgens in comparison to control cultures. Altogether, our data allow us to speculate that the increased insulin effectiveness we observed in the larynx carcinoma cell line HEp-2 after androgen treatment might be involved in the regulation of larynx cancer cells growth.
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PMID:Androgens increase insulin receptor mRNA levels, insulin binding, and insulin responsiveness in HEp-2 larynx carcinoma cells. 151 77

We investigated for the first time the relationships among all the different steroid receptor classes and between steroid receptor status and lymph node involvement in laryngeal carcinoma. Androgen (AR), oestrogen (ER), progesterone (PR) and glucocorticoid (GR) receptors were assayed in the high-speed soluble fraction and in the nuclear extract from 73 carcinomas of the larynx. Forty-one, 26, 15, and 13 tumours expressed cytosolic GR, ER, AR, and PR, respectively, while 33, 26, 13 and 13 biopsies were nuclear-positive for GR, ER, AR, and PR, respectively. Data obtained in histologically-proven non-cancerous larynx (N = 20) compared to those obtained in the malignant specimens showed a significant loss of ER and PR in cancerous larynx over that in the non-cancerous tissue. Lymph node metastases were evaluated in only 53 of the 73 patients and they were noted in 22 cases (41.5%). No significant relationships were found either among the different classes of steroid receptors or between steroid receptors and lymph node involvement. Despite the apparent absence of any interrelationships among the different receptors or tendency towards metastasis, the presence of steroid receptors would justify the use of hormonal manipulations which could be effective in the management of this disease.
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PMID:Steroid receptor status in malignant and non-malignant larynx. 161 93

Shionogi Carcinoma 115 (SC 115) is an androgen-dependent mouse tumor. Chiba Subline 2 (CS 2) is an androgen-independent subline derived from SC 115. CS 2 contains androgen receptors (AR), but is refractory to androgen and does not exhibit androgen-related responses which are observed in SC 115. In the present study the structure and function of AR in SC 115 and CS 2 are examined using cloned cells. There were no gross rearrangements or deletions in the AR genes of these cell lines when compared by Southern blot analysis with the AR gene in the mouse seminal vesicle. SC 115 and CS 2 expressed AR mRNA of normal size. When the cDNA containing DNA- and androgen-binding domains of the AR genes of both cell lines were amplified by polymerase chain reaction, no mutations were found in these regions. SC 115 and CS 2 were transfected with a plasmid containing a long terminal repeat of mouse mammary tumor virus linked to the chloramphenicol acetyltransferase (CAT) gene. Androgen stimulation of these transfectants resulted in equal elevation of CAT activity. These results indicated that the androgen-independent CS 2 contained functionally normal AR which were identical to those in the androgen-dependent parent tumor.
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PMID:Loss of androgen dependency with preservation of functional androgen receptors in androgen-dependent mouse tumor (Shionogi Carcinoma 115). 163 20


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