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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper reviews the antiestrogenic and antitumor properties of tamoxifen (NSC-180973; ICI-46474) in the rat. In classic tests for antiestrogenic activity, tamoxifen inhibits the actions of estradiol in the rat uterus and vagina. At the cellular level, tamoxifen inhibits estrogen binding to cytoplasmic estrogen receptors, but although estrogen-receptor units are translocated to the nucleus DNA synthesis does not occur. It is suggested that tamoxifen competes for estrogen receptors in the cytoplasm and the false messenger units block the nuclear acceptors which are normally activated by estradiol-estrogen receptor complexes thereby provoking DNA synthesis. Tamoxifen inhibits the growth of some 7.12-dimethylbenz(a)anthracene-induced rat mammary tumors whereas others continue to grow. Estrogen-stimulated rises in plasma prolactin are only partially inhibited by tamoxifen although at the tumor level, tamoxifen completely blocks estrogen binding. There is a linear correlation (P less than 0.01) between estrogen-receptor levels in tumor biopsies before therapy and tumor responses to 3 weeks of tamoxifen treatment (50 mug/day) i.e., tumors with low levels of estrogen receptors do not respond to therapy whereas tumors with higher levels of estrogen receptors regress. It is suggested that tamoxifen antagonizes the actions of estrogen at the tumor level by blocking the estrogen-receptor mechanism thereby producing tumor regression. Therefore, estrogen-receptor measurements in tumor biopsies before therapy may be a useful predictive test for the tumor response to tamoxifen treatment.
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PMID:Antiestrogenic and antitumor properties of tamoxifen in laboratory animals. 82 17

Estrogen and dihydrotestosterone receptors were detected by agar gel electrophoresis in 224 human mammary tumor biopsies. Approximately half of the tumor specimens revealed measurable amounts of estradiol receptors, whereas only 20% contained dihydrotestosterone receptors. The average concentration of spare estrogetmenopausal than in the premenopausal group, but this was not found to be the case for androgen receptors. The findings presented are discussed with regard to the clinical relevance of multiple assays for various types of receptors in a single tumor.
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PMID:Specific binding of estradiol and dihydrotestosterone in human mammary cancers. 83 Apr 12

Studies suggest that alterations of the endocrine environment may have profound effects on the immunogenicity of tumors and host dependence of a prostatic-specific scretory autoantigen have been shown. The antigen has been identified as the principal source of autoantibodies after parenteral or freezing in situ stimulation. Estrogen suppresses the synthesis of this antigen. Patient survival has been reported to be better after cryoprostatectomy when they did not receive hormone therapy. The palliative effect of estrogenic therapy may be compromised by a reduction in the patient's immunological surveillance. Estrogen may modify the proliferation and differentiation of thymic-dependent lymphocytes into effector lymphocytes. There may be inhibition of specific immune cytolysis of tumor cells. The suppressive effects of estrogens on the synthesis of a prostatic-specific antigen and on immunological responsiveness of the host to the tumor have not been determined. The analogue of an estrogen-sensitive, prostatic-specific antigen has not been definitely identified. However, studies of human carcinomatous prostatic tissues from patients with long-term estrogenic therapy point to a loss or deficiency of normal prostatic tissue-specific antigens.
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PMID:Hormonal epidemiology of prostatic cancer. 86 62

Estrogen (RE) and progestin (RP) cytosol receptors in 379 human breast carcinomas were studied: 281 tumors suitable for surgery, 26 pseudo-inflammatory tumors, 52 metastases, and 20 recurrences. An exchange technique with estradiol for RE and a synthetic compound, R 5020, for RP was used. The results indicate that high rates of RE correlate with postmenopausal women and high rates of RP with premenopausal women. Tumors are considered receptor-positive when the binding site concentration exceeds 100 fmoles/gm tissue. Using this as a base, 32% of the tumors are RE and RP negative. Considering only the positive tumors, 54% contain both receptors, 31% only RE, and 15% only RP. The results support McGuire's hypothesis that both receptors are necessary to obtain a positive response to hormonal therapy. However, a correlation has only been demonstrated with the effects of the hormonal treatments and the presence of the RE receptors.
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PMID:[Estrogen and progestogen cytosol receptors in human breast carcinoma (author's transl)]. 87 43

150 cases of prostate cancer treated with estrogens at the Urology clinic of the Hotel-Dieu from 1963 to 1974 are presented. The men ranged in age from 50 to 91; the majority were 60-69 years. Their clinical stages were 29% Stage 1, no perceptible mass; 43% Stage 2, nodule felt on rectal exam; 13% Stage 3, tumor extended outside the prostate but not metastases, normal prostatic phosphatases; and 15% Stage 4, elevated prostatic phasphatases and metastases. Diagnosis was by urinary symptoms in Stage 2 or above, rectal palpation, and puncture biopsy under local anesthesia. Estrogen treatment consisted of diethylstilbestrol, stilbelstrol diphosphate or TACE (Chlorotraianisene), or estradiol. Estrogen side effects were loss of libido after 1 month, gynecomastia, and nausea. Other treatments included prostatectomy in Stages 1 and 2, cobalt in 5 cases, castration in 3 cases, 1 endo-uretral resection, and 1 hypophysectomy. 50% died in 1 year and 16% were lost to follow up and presumed dead in 1 year; the mean survival of the others was 3 years. Estrogen therapy improved symptoms and reversed tumor growth temporarily in hormone-dependent cancers, but these tumors all escape hormone control eventually.
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PMID:[Course of prostate cancer under estrogen therapy]. 87 31

This letter reports another case of invasive squamous cell carcinoma of the uterine cervix in a patient who had been exposed to diethylstilbestrol (DES) in utero. The patient was a 21-year-old nulliparous white woman. Her mother had taken DES, 25 mg daily, beginning at 6 weeks of gestation and continuing possibly as late as 20 weeks. The mother also took dimenhydrinate, 50 mg once daily. A pelvic examination of the patient at age 19 was normal and the cytologic smear was negative. The patient used an oral contraceptive containing .5 mg of norgestrel and .05 mg of ethinyl estradiol for 3 months. A year later, gynecologic examination and cytologic smear were negative. Subsequently she was treated for trichomonal and monilial vaginitis. Later, leukorrhea and intermenstrual bleeding developed. On examination, an ulcerating exphytic tumor of the cervix was found. Cytologic smear and biopsy showed squamous cell carcinoma. A radical hysterectomy was done with removal of pelvic lymph nodes and the upper 1/3 of the vagina. Endometriosis implants on the colon and on both ovaries were also removed. Follow-up examinations and cytologic smears have been negative to date.
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PMID:Invasive squamous cell carcinoma of the cervix in a diethylstilbestrol-exposed offspring. 93 Sep 82

Altered carbohydrate metabolism associated with fibrosarcomas and chondrosarcomas has been well-documented in past literature. This report describes abnormal carbohydrate metabolism in 2 osteosarcoma patients, and abnormalities in growth hormone and somatomedin serum levels. Experimental evidence is presented showing in vitro suppression of osteosarcoma tumor cell proliferation by 17 beta Estradiol. Estrogen inhibition of linear bone growth, cartilage proliferation, and somatomedin is discussed with reference to possible estrogen therapy in osteosarcoma.
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PMID:Investigation of carbohydrate metabolism and somatomedin in osteosarcoma patients. 105 23

Accurate diagnosis and staging of carcinoma of the prostate is essential to rational management of this disease. Once dissemination outside the periprostatic area is established, treatment is essentially limited to systemic efforts to control or suppress tumor growth and local efforts to minimize secondary effects of tumor deposits. Disseminated tumor limited to pelvic nodes constitute a possible exception to this statement since excisional and radiotherapeutic efforts to eradicate these foci may be successful. At the present time, changes in a number of objective and subjective parameters are utilized to assess the effect of therapeutic endeavors. When these are taken as a group and combined with a clinical judgement, they undoubtedly have merit. On the other hand, when utilized in a relative fashion as isolated indicators of tumor responsiveness or recurrence, their value is limited. Since most patients with disseminated carcinoma of the prostate die from their disease, critical analysis of survival data is at present likely to provide the most accurate assessment of a therapeutic endeavor. Estrogen administration or orchiectomy seem to be the systemic measures which combine relatively limited risk of morbidity with the greatest hope of initially controlling disseminated carcinoma of the prostate. Of these, evidence suggests that low dose estrogen therapy, 1 mg stilbestrol daily, provides the best opportunity for long-term control. Although length of survival does not seem to depend on the time at which the therapy is instituted, our prejudice is usually to start treatment when dissemination is recognized. The hope of providing a longer period of a better life by this practice requires evaluation. Combining local measures such as transurethral resection with systemic measures may add to patient comfort and longevity. Recurrent progression of tumor after initial hormonal measures in often difficult to recognize and accept. In patients with recurrent tumor activity, measures based on the concept of persistence of hormone dependence have produced disappointing results. More sophisticated selection techniques may identify a small group of patients in whom this approach is likely to produce desirable changes. For the most part chemotherapeutic agents hold greater promise of effective therapy in this group of patients.
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PMID:Treatment of stage IV carcinoma of the prostate. 109 57

Drugs that are known to affect breast morphology or breast secretion may be classified into 2 major groups: 1) drugs having a central action on the pituitary or hypothalamus and 2) steroids and several other compounds that act peripherally. Drugs in the 1st group affect lactation through stimulation or suppression of the lactogenic pituitary hormone prolactin. Their action may be directly on the pituitary or indirectly on the hypothalamus where the secretion of hypothalamic prolactin-inhibiting factor is affected. Drugs in the 2nd group act peripherally by exerting their action mainly at the level of breast tubules and acini. The most frequently used are estrogens which stimulate growth of the breast and suppress lactation, and suppress breast cancer in some women. Centrally acting drugs which cause galactorrhea also cause an increase in prolactin secretion, but the presence of estrogen-primed breast tissue is needed. A list of such drugs (including rauwolfia and phenothiazine derivatives, and opiates) is given. The most common mechanism of action by which psychotropic drugs increase prolactin secretion is by interfering with formation or release of dopamine from hypothalamus neurons and its subsequent action via an alpha-adrenergic receptor on hypothalamic cells that secrete prolactin-inhibiting factor. Reserpine and other rauwolfia drugs deplete hypothalamic neurons of catecholamines and prevent their reuptake by nerve endings. Phenothiazines interfere with the action of catecholamines at the alpha-adrenergic receptor sites. Prolonged use of drugs that stimulate pituitary activity may lead to formation of microadenomas of the pituitary. Continuation of galactorrhea for more than 2 weeks after stopping therapy suggest this result. L-dopa suppresses abnormal lactation by reduction in serum prolactin levels. Br-ergocryptine, an ergot derivative, has galactorrhea-blocking and prolactin-suppressing activity but is devoid of alpha-adrenergic activity. Barbiturates and pyridoxine may cause decrease in milk flow of nursing mothers. Peripherally acting drugs consist of estrogen, progesterone, and androgen as well as hypoglycemic-producing agents, thyroid hormone, corticosteroids, and spironolactone. Estrogen is the only steroid effective in suppression of puerperal lactation. There are several steroids effective in causing remission of breast cancer. The presence of an intact pituitary is apparently necessary if estrogens are to be effective in breast cancer. Corticosteroids may be effective in patients insenstive to sex hormones. Cytotoxic agents may be more effective when used in combination with corticosteroids. Galactorrhea occurring in a nulliparous woman taking oral contraceptives is always abnormal and suggests the possibility of a pitutitary tumor. Women with postpill galactorrhea-amenorrhea may also have such tumors. All cases of galactorrhea when sex hormones have been used should be studied for pituitary tumor.
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PMID:Drugs that affect the breast and lactation. 109 75

Transplantable tumor lines were previously established from a variety of estrogen-induced tumors in Nb rats, including tumors of the adrenal cervix, salivary gland, and pancreas, a lymphoma, and a liposarcoma. Spontaneous tumors, however, were found to arise in untreated females and showed the same characteristics. Tumor growth was dependent upon or influenced by estrogen when assessed in estrogenized and unconditioned hosts. Intermitten estrogenization was effective, but tumor growth took place more slowly. The type of response observed led to a new classification of five types of hormone-responsive tumors including tumors inhibited by estrogen. Estrogen-dependent tumor cells might remain dormant indefinitely and not grow in unconditioned animals until stimulated to grow by estrogen. The growth rate of hormone-dependent adrenal carcinomas was related to the amount of estrogen. Tumor growth started more rapidly in the presence of low estrogen dose levels in old rats used as hosts than it did in young rats. Breast carcinomas required the largest amount of estrogen for growth, whereas ovarian thecomas would grow in normal females but not in males. The growth rate in conditioned hosts of most transplanted tumors (some have maintained hormone dependency over 10 years) increased over successive generations. Progression, however, towards a more autonomous state after repeated transplantations was remarkably slow, and a sudden change to autonomy was rarely noted. In contrast, transplants of 9,12-dimethylbenz(a)anthracene-induced mammary carcinomas progressed rapidly to autonomy. Fould's concept of progression (2, 3) has been discussed but the described classification of tumors under hormone influence apparently allows a more detailed analysis of definition of different types of progression.
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PMID:A classification of transplantable tumors in Nb rats controlled by estrogen from dormancy to autonomy. 118 86


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