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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate relapse of hormone-dependent tumour, mice bearing androgen-dependent carcinoma (SC 115) underwent castration or received oestrogen treatment. Since SC 115 consisted of two types of cells, androgen-sensitive round cells and -insensitive spindle-shaped cells, changes in the ratio of the cellular population were examined. After castration, spindle-shaped cells increased temporarily as the tumour regressed, then the round cells increased significantly along with an increase in size of the tumour. Oestrogen treatment did not influence the population. Androgen dependency and the growth rate of round cells were generally preserved in the next generation. Therefore, relapse may occur by an increase in the number of androgen-sensitive round cells.
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PMID:Relapse of androgen-dependent tumour of mouse (Shionogi Carcinoma 115) after castration and oestrogen treatment. 686 20

Androgen responsive and unresponsive Shionogi 115 mouse mammary carcinoma cells have been examined for anchorage-independent growth and tumorigenicity in nude mice. The two cell types exhibit transformed and normal growth characteristics respectively, but both give rise to tumours in nude mice. No correlation between tumorigenicity and transformed characteristics including anchorage-independent growth could be demonstrated.
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PMID:Lack of correlation between transformed characteristics in culture and tumorigenicity of mouse mammary tumour cells. 688 18

A cell line derived from the androgen-responsive Shionogi 115 mouse mammary carcinoma is being used to investigate the changes in cell function accompanying steroid removal from steroid-responsive breast tumor cells. Shiongi 115 mouse mammary carcinoma cells become androgen unresponsive after two weeks of culture in the absence of testosterone although androgen receptors are still present in the cytoplasm and nucleus. Androgen-responsive cells are fibroblastic in appearance, have a low serum requirement, and can proliferate in suspension culture. Unresponsive cells, however, show a flattened morphology, are serum sensitive, and are anchorage dependent. As the androgen receptor mechanism of the unresponsive cells is intact, loss of sensitivity may be caused by a postreceptor defect. To determine the nature of this defect, the temporal relationships of changes in hormone responsiveness, morphology, serum sensitivity, and growth properties have been examined over a period of seven weeks following removal of testosterone from Shionogi 115 mouse mammary carcinoma cell cultures. Responses to testosterone and anchorage independence are both lost over a period of one to two weeks while serum sensitivity increases more slowly during the same period. The most rapid and least reversible change is seen in morphology. It is suggested that hormone responsiveness is related to properties of the cytoskeleton and cell membrane which influence growth rates and multiple sensitivities of tumor cells.
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PMID:Correlation of growth properties and morphology with hormone responsiveness of mammary tumor cells in culture. 744 65

Androgen suppression is the routine approach to the treatment of advanced prostate cancer. Using intermittent androgen suppression by taking the advantage of the reversible action of medical castration results in the maintenance of apoptotic potential. The experiments in the androgen-dependent androgen-dependent Shionogi carcinoma tumor model as well as clinical experience in a group of men with prostate malignancy are presented in this report. These consecutive cycles of androgen withdrawal and replacement afford an improved quality of life when the patient is off therapy. It is possible to reduce toxicity, cost of treatment and to delay tumor progression. Whether survival is affected in a beneficial or adverse way still remains to be studied.
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PMID:[Theoretical considerations and initial clinical results of intermittent hormone treatment of patients with advanced prostatic carcinoma]. 748 55

Bone scans, serum tissue-specific polypeptide antigen (TPS), prostate specific antigen (PSA), and neuron-specific enolase (NSE) were assessed in a total of 80 hormonally treated prostate cancer patients. Thirty-nine patients were free of osseous lesions; in 8 subjects, 3 or fewer scintigraphic hot spots were found; in 29 patients, more than 3 bone lesions were recorded. In 3 patients, a partial contribution of endocrine cell cancer structures was found, while in one patient, a homogeneous small cell carcinoma was detected at autopsy. Measurement of the serum PSA test showed a clear-cut rise from stage D0 subjects to stage D2 patients, with a small number of bone lesions (> or = 3). However, a relative decrease in the mean PSA level was measured with further progression in a number of hot spots in bone (> 3). Androgen threshold that is critical for the induction of the PSA (and PAP) expression seems to differ markedly in various cell subpopulations that arise during adenocarcinoma dedifferentiation. This fact explains not only the rise in serum PSA in the majority of progressive and previously castrated subjects after an initial period of hormonal responsiveness, but also a relative decline of androgen-dependent PSA expression with further tumor progression. Localized disease was accompanied with normal or just slightly elevated TPS concentration. In metastatic tumors, serum TPS values revealed a steady increase with the progression in bone. These data seem to reflect not only an increase in tumor proliferation rate with progressively transformed genome, but also the rise in the number of proliferating cells. The presence of nonepithelial transformed tumor structures, such as small cell cancer within a bulk of adenocarcinoma, reduces or normalizes numerical serotests values of both TPS and PSA even during tumor progression. The extent of such decline depends upon the bulk of the endocrine component. The assessment of the above parameters, especially when associated with elevated plasma NSE concentrations, may help in distinguishing an advanced adenocarcinoma with and without elements of malignant neuroendocrine structures. The proposed approach, modified by applying corresponding organ-specific markers, may be checked for its possible general use in staging protocols of various heterogeneous tumors.
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PMID:A more objective staging of advanced prostate cancer--routine recognition of malignant endocrine structures: the assessment of serum TPS, PSA, and NSE values. 750 85

There is increasing evidence that the course of prostatic carcinoma is determined by a complex interplay between genetic events, paracrine interactions, and hormonal and dietary factors. These latter factors include several ligands of the nuclear receptor family such as androgens, vitamin D3 and retinoids. To test whether thyroid hormones also influence the growth and differentiated function of prostatic carcinoma cells, LNCaP cells were treated with or without triiodothyronine (T3) in the absence or in the presence of other regulatory factors. Exposure of LNCaP cells to T3 for 6 days in the absence of androgens caused a dose-dependent increase in [3H]-thymidine incorporation with a maximal stimulation of 2.5-fold at 10(-9) M T3. Secretion of prostate-specific antigen (PSA) was also stimulated 2-3-fold. The observed effects may well be mediated by a nuclear T3 receptor as evidenced by displaceable T3 binding studies. Combined treatment of LNCaP cells with androgens and T3 revealed intriguing interactions between these two pathways. Below and up to 10(-10) M of the synthetic androgen R1881, the concentration that evokes optimal proliferative responses, T3 stimulated [3H] thymidine incorporation. At higher concentrations of androgens, T3 displayed antiproliferative effects. No androgen-dependent effects on T3 receptor levels were observed. Conversely, T3 increased androgen receptor levels up to twofold. Androgen as well as T3 stimulation of proliferation was abolished by high concentrations of the retinoid 9-cis-retinoic acid. These data add T3 to the list of factors that influence growth and differentiation of prostatic tumor cells and contribute to our understanding of the intricate pathways that ultimately determine the course of prostatic carcinoma.
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PMID:Triiodothyronine modulates growth, secretory function and androgen receptor concentration in the prostatic carcinoma cell line LNCaP. 754 May 69

We have established organ cultures of human prostate for in vitro analysis of the hormone responsiveness of prostatic carcinoma. Tissue samples were obtained from total prostatectomies for localized cancer. Normal prostate tissues with age-related hyperplastic changes were obtained from cystoprostatectomies of bladder cancer patients representing the same age group, and they wer cultivated as controls. The explants of prostates were cultured for 7 days in basal medium containing 5% dextran charcoal-treated fetal calf serum, insulin (0.08 IU/ml), and dexamethasone (10(-7) M) with or without dihydrotestosterone (DHT) (10(-7) M) or estradiol (10(-9) M). Control prostates showed involutive changes of morphology when cultured in basal medium. These changes were prevented by DHT, which also maintained a strong epithelial immunostaining for PSA (prostate specific antigen), which was used as a marker for tissue-specific functions. The concentration of PSA in the medium was high. The rate of [3H]thymidine incorporation into DNA was stimulated by DHT in some cultures of control prostates, but no increase was seen in the others. Androgen stimulation of [3H]thymidine incorporation was consistently inhibited by the antihormone cyproterone acetate. The main morphological response of cultured control prostates to estradiol was induction of squamous metaplasia. This was associated with increased incorporation of [3H]thymidine, which was radioautographically localized to the basal layer of epithelium. Estradiol effects were counteracted by the antihormone toremifene. The expression of androgen receptor mRNA and protein in cultured control prostate was demonstrated by Northern blotting and immunohistochemistry, respectively. Also, the expression of estrogen receptor was demonstrated by the polymerase chain reaction analysis of total mRNA from cultured control and cancer prostate. The cultured explants of prostate cancer maintained the overall morphology of the original carcinoma. However, the presence of DHT improved the morphology of cancerous acini in all better differentiated carcinomas (3 grade I and 5 grade II), and corresponding responses to DHT were observed in the rate of DNA labeling with [3H]thymidine. In 2 of 3 grade I carcinomas, DHT increased DNA synthesis, but in grade II cancers the patterns of hormone responses were more variable. The poorly differentiated grade III prostatic carcinomas did not respond to either hormone as measured by [3H]thymidine uptake, and no hormone effects could be seen in morphology. Immunostaining for PSA differed from that in control prostates: besides cancerous acini, the surrounding stroma was also intensively stained, which suggests unpolarized and impaired secretion of PSA by the cancer cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hormone regulation of human prostate in organ culture. 769 34

The propensity of a cell to undergo apoptosis has been proposed to be a determinant for chemotherapy sensitivity that is not directly dependent on specific drug-target interactions. Androgen-independent prostate cancer is typically refractory to cytotoxic drugs, and we tested whether this is due to a loss of the ability to undergo apoptosis. Exposure of the hormone-insensitive and p53-negative human prostate carcinoma cell line PC-3 to 22 microM cisplatin, 1 microM camptothecin, 10 microM tenoposide, 135 nM vincristine, or 10 microM lovastatin for 72 h caused cell death, internucleosomal DNA fragmentation, and morphological changes typical for apoptosis. One microM cycloheximide prevented anticancer drug-induced apoptosis, whereas high concentration (1 mM) of cycloheximide alone induced apoptosis, indicating that protein synthesis was not needed for these cells to undergo apoptosis. Since cycloheximide affected DNA synthesis and proliferation of PC-3 cells, we tested whether the DNA polymerase inhibitor aphidicolin could also suppress drug-induced apoptosis. In contrast to cycloheximide, aphidicolin inhibited only vincristine-induced apoptosis. Cycloheximide prevented drug-induced changes in cell cycle distribution except for vincristine, while aphidicolin led to an accumulation of cells at the G1-S border independent of the drug used. These data indicate that macromolecular synthesis, active cell cycling, and p53 expression are not required for apoptosis to proceed in this system.
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PMID:Drug-induced apoptosis is not necessarily dependent on macromolecular synthesis or proliferation in the p53-negative human prostate cancer cell line PC-3. 774 12

In order to verify the hypothesized hormone sensibility of the laryngeal carcinoma, we evaluated the level of steroid receptors in this type of neoplasm and correlated this datum with common pathological and clinical prognostic indices. Estrogen and progesterone receptors were evaluated in 105 patients with a squamous cell carcinoma and 2 patients with a mucoepidermoid laryngeal carcinoma. Receptors for androgens and glucocorticoids were evaluated in 35 patients (all with a squamous cell carcinoma). Dosage was performed on fresh neoplastic tissue using the DCC (Dextran Coated Charcoal) method. Estrogen receptors were present in 26 cases (24.3%); progesterone receptors were present in 18 cases (16.8%); both receptors were revealed in 8 patients (7.5%). Androgen receptors were evident in 4 patients (4/35, 11.4%); glucocorticoid receptors were evident in 7 patients (7/35, 20%); both receptors were revealed in 4 (11.4%) cases. No statistical difference with regard to grading, site and extension of the cancer, extralaryngeal tissue involvement or node metastasis was noted in the groups of patients with or without steroid receptors.
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PMID:[The status of receptors in laryngeal carcinoma: a study of receptors for estrogen, progesterone, androgens and glucocorticoids]. 781 44

Androgen (AR) and progesterone (PgR) receptors were measured in 18 samples of normal oral mucosa and of squamous cell carcinoma of the floor of the mouth or the tongue. In a given mean concentration of R1881 (Methyltrienolone) of 8.4 nM in the carcinoma and of 7.9 nM in the normal mucosa, we measured a mean androgen receptor level in the carcinoma smaller than 1.08 fmol/mg protein (< 0.034 fmol/microgram DNA). There was a significant difference (p < 0.05) from the androgen receptor level in the normal mucosa (2.2 fmol/mg protein, 0.082 fmol/microgram DNA). In this experiment, in only 41.2% did we find any PgR receptor in the carcinoma whereas all normal tissue contained PgR, the concentration varied between 0.1 and 3.0 fmol/mg protein (0.01-0.09 fmol/microgram DNA).
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PMID:Androgen and progesterone receptors in oral carcinoma. 802 19


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