Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A simple procedure for the assay of specific estrogen receptors in breast cancer tissue is described. Estrogen receptors were detected in 74% of primary tumors, 71% of skin metastases and 63% of lymph node metastases. Postmenopausal patients and younger oophorectomized women had estrogen receptor-containing tumors more frequently, and at higher levels, than uncastrated, premenopausal, patients. The stability of estrogen receptors was not affected by the transportation of samples from distant hospitals, providing that they were kept frozen in Tris buffer, pH 8.0, at all times.
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PMID:Experience with a simple method for estrogen receptor assay in breast cancer. 0 1

Estrogen-dependent renal adenocarcinoma and normal proximal tubules of the hamster kidney exhibit junctional differences. Although both cell types possess gap junctions, the neoplastic cells have in addition a cytoplasmic configuration of gap-junctional membrane (annular nexuses) not found in the kidneys of untreated or estrogenized hamsters or in the nontumorous kidney adjacent to the adenocarcinoma. The presence of these unique structures in the renal tumor and its abdominal metastases was demonstrated by electron microscopy with the use of lanthanum impregnation. A possible correlation between these structures and the estrogen sensitivity of the kidney neoplasm is made.
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PMID:Junctional specialization in estrogen-induced renal adenocarcinomas of the golden hamster. 16 65

Forty-one patients with metastatic carcinoma of the prostate (stage IV) were treated with diethylstilbestrol or bilateral orchidectomy or both and followed for a period of two years. The effect of treatment was determined every six months and was based on the size and consistency of the primary lesions on rectal palpation, the effects on pain, obstructive symptoms, osseous metastases, level of serum prostatic acid phosphatase and on the overall clinical evaluation of the patient. Bilateral orchidectomy was as effective as a combination of bilateral orchidectomy and diethylstilbestrol therapy. Diethylstilbestrol given alone was less effective. The poorer results obtained were attributed to the failure of many patients to adhere strictly to their estrogen regimen. Rectal digital palpation of the prostate as well as an estimation of the level of serum prostatic acid phosphatase is recommended in developing countries for all male patients over 50 years of age seen at the hospital.
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PMID:Effect of estrogen therapy on metastatic carcinoma of the prostate. 59 Dec 15

Horones as a therapeutic agent are practically not used in gynecologic oncology, because gynecological malignomas are hormonally independent. Therapeutically succesful in only the use of Progesterone in metastases and relapses of endometrial cancer and of Estrogen in the palliative treatment of cervical cancer relapses. However, significant results are obtained by cytostatic therapy, particularly in carcinomas of the ovary and in choriocarcinomas; the therapy is somewhat less successful in the cancer of the oviduct and vulva, while in the cancer of the cervix and vagina it is not successful at all. Polychemotherapy is recommended because it results in better remissions and is less aggressive.
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PMID:[Cytostatic and hormonal therapy on oncologic gynecology (author's transl)]. 75 24

Because a few ovarian adenocarcinomas respond favorably to endocrine therapy, we tested the hypothesis that some ovarian adenocarcinomas have functional similarity with sex-hormone-sensitive endometrial and breast tumors. Cytosols from 23 ovarian adenocarcinomas and 27 control tissues were examined for receptorlike estrogen and/or progestin binding. Eight of 16 primary ovarian adenocarcinomas had estrogen and/or progestin receptorlike components; among the metastases tested, one third retained estrogen binding. No correlations were found between binding characteristics and histopathologic grade. The presence of estrogen binding in a lung lesion helped confirm recurrent ovarian disease. Estrogen binding occurred in specimens from women with no histories of exposure to exogenous estrogen. Because tamoxifen and nafoxidine could inhibit estradiol binding, it is likely that antiestrogens will prove beneficial against some ovarian cancers.
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PMID:Estrogen and progestin binding in cytosols of ovarian adenocarcinomas. 76 18

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

Gonadal dysgenesis was diagnosed in a 24-year-old patient presenting with primary amenorrhea. Because of her concern over poor breast development, .25 mg/day stilbestrol was prescribed. She was not seen again until 4 years later when she was admitted to hospital for heavy vaginal bleeding of uterine origin. Stilbestrol therapy was stopped. The uterus was enlarged, and curettings showed striking changes in the epithelium and the presence of cartilagelike material. Hysterectomy was performed a month later, and histological examination showed changes similar to those seen earlier but no penetration of the myometrium. The histological features were extremely variable, but the lesion was put in the adenosquamous category. The presence of cartilage in this type of lesion has not been previously reported. The 4-year stilbestrol treatment is shorter than the 5-year-plus average treatment duration reported in other cases of estrogen-induced malignant change. Although it may be suspected that the longer the duration of estrogen treatment, the more likely the chance of myometrial invasion and spread beyond the uterus, no fatal case has been found of such metastases. However, it is now agreed that cyclic estrogen-progestogen therapy for gonadal dysgenesis is safer.
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PMID:Oestrogen-induced endometrial carcinoma in a patient with gonadal dysgenesis. 113 6

Previously we have shown that a murine mammary carcinoma cell line, designated SPI, grows and metastasizes more efficiently in the mammary gland than in the subcutis. In this report, we examine the tissue specificity of this phenomenon. Our results show that SPI cells grow best in the mesenteric and ovarian fat pads and well in the mammary gland, but very poorly in the subcutis or peritoneal cavity. Massive dissemination of tumors from the ovarian and mesenteric sites occurs to the liver, spleen and diaphragm. In contrast, metastases from the mammary site occur primarily in the lung. Co-transplantation of a threshold number of SPI cells with mammary or ovarian fat fragments into the subcutis results in increased tumor growth, whereas very few tumors form in sham controls receiving no fat fragments. Removal of the ovaries of donor and recipient mice abrogates tumor growth in adipose tissue transplants. Estrogen can stimulate growth of SPI in adipose tissue sites, whereas progesterone inhibits growth. In contrast, in vivo growth of a stable metastatic variant selected from SPI cells was not inhibited by progesterone. SPI cells growing in ovarian and mesenteric fat pads showed increased expression of estrogen receptors and progesterone receptors, as well as detectable levels of epidermal-growth-factor receptors, whereas receptor levels decreased to baseline on tumors in the subcutis. The levels of estrogen-receptor mRNA reflect the corresponding functional expression of receptors; this finding suggests that the regulation of estrogen-receptor expression in this system is, at least in part, at the mRNA level. Our results are consistent with the model that adipose tissue exerts an estrogen-dependent positive regulatory effect on primary SPI tumor growth, and promotes the formation of metastases.
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PMID:Capacity of adipose tissue to promote growth and metastasis of a murine mammary carcinoma: effect of estrogen and progesterone. 131 63

Cisplatin/etoposide/bleomycin (DEB) was given as an outpatient regimen in a novel weekly schedule to 27 patients with recurrent and/or widely metastatic cancer of the head and neck region. Six of these patients also received mitomycin (DEB/M) when their disease failed to respond after at least three weekly DEB doses. All but three patients had been treated previously with radiotherapy directed to the primary site and regional nodal disease; four had also received chemotherapy with cisplatin or carboplatin. Before treatment with DEB, 19 patients had distant metastases. Of an intended 12 doses per patient, a mean of 8.2 was achieved. Myelosuppression was the major toxicity, with neutropenia in 45% of patients and significant anemia in 26%. The overall response rate to DEB in 27 patients was 59%, increasing to 70% after the addition of mitomycin. There were two complete and 17 partial responses. The median duration of response was 12 weeks and median survival was 6 months, with 20% of patients surviving 1 year. We conclude that the relatively short survival time together with the significant toxicity of the DEB/M regimen does not warrant its routine use in clinical practice. However, this regimen, or one patterned on it, should be evaluated in combination with radiotherapy as the initial treatment for selected patients with previously untreated head and neck cancer.
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PMID:Treatment of recurrent and metastatic head and neck cancer with cisplatin/etoposide/bleomycin. 138 40


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