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)

The effect of angiostatic steroids on pulmonary metastasis was investigated using mice treated with such a steroid before or after intravenous inoculation with Lewis lung carcinoma; cortisone acetate and tetrahydro S, of which the former possesses glucocorticoid activity, and the latter lacks it, were used as the angiostatic steroids. In the presence of heparin, both types of steroids prevented angiogenesis in chick embryo and also pulmonary metastasis in mice when the administration started after cell lodgement. On the other hand, one-shot cortisone treatment before cell inoculation increased the weight of lung colonies to twice that seen in the controls, while tetrahydro S pretreatment did not enhance metastasis. These results revealed that both angiostatic steroids with and without glucocorticoid activity in the presence of heparin inhibited tumor growth in the lungs, and further indicated that cortisone acetate affected the steps of metastasis after the invasion of tumor cells into the blood stream until angiogenesis in the secondary foci, and consequently promoted metastasis, whereas tetrahydro S (which has no glucocorticoid activity) did not affect the steps before angiogenesis. It was thus indicated that the inhibitory effect of angiostatic steroids against tumor growth due to an anti-angiogenic activity was not dependent at all on the metastasis promotion by these steroids having glucocorticoid activity.
Invasion Metastasis 1987
PMID:Effect of angiostatic steroid with or without glucocorticoid activity on metastasis. 244 51

We have evaluated the 7-drug, alternating, high-dose cisplatin regime for germ cell tumours, designated POMB/ACE, in 55 patients with advanced malignant teratomas and 5 patients with bulky metastatic seminomas. All of the latter and 5 of the teratoma patients had relapsed following radiotherapy, chemotherapy or both. The previously untreated teratoma patients included 13 whose tumours were extragonadal. The primary testicular tumour patients comprised 16 with large and 21 with very large volume metastases according to the Medical Research Council criteria. POMB/ACE is effective therapy for poor risk patients with germ cell tumours (including those with the most advanced disease, i.e. hepatic and cerebral metastases) and prolonged treatment after marker normality seems unnecessary. It is a complex regime with significant toxicity and cannot be recommended for the treatment of patients with germ cell tumours who have an excellent prognosis with simpler, shorter and less toxic treatment.
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PMID:Chemotherapy for poor risk germ cell tumours. An independent evaluation of the POMB/ACE regime. 246 34

More than 30% of the colony formation of dispersed tumor cells was inhibited by medroxyprogesterone acetate (MPA) in 2 out of 6 cases of endometrial cancer, in 1 out of 6 cases of cervical cancer, and in 3 out of 12 cases of ovarian cancer. The colony formation inhibited by MPA was not related to clinical stage or histological type. There was no significant difference in the tumor angiogenesis factor (TAF) activity of any case of endometrial, cervical and ovarian cancer between the cortisol-treated group and the controls. TAF activity was inhibited by MPA in 4 out of 6 cases of endometrial cancer, in 5 out of 6 cases of cervical cancer, and in 9 out of 12 cases of ovarian cancer. There was no significant difference in the fibroblast growth factor (FGF) activity of any case of endometrial, cervical and ovarian cancer between the cortisol-treated group and the controls. FGF activity was inhibited by MPA in 3 out of 6 cases of endometrial cancer, in 5 out of 6 cases of cervical cancer, and in 10 out of 12 cases of ovarian cancer. The cases in which the colony formation was inhibited by MPA were not related to the cases in which TAF or FGF activity was inhibited by MPA. Therefore, MPA may reduce neovascularization induced by TAF and FGF, and can depress secondary spreading of some endometrial, cervical and ovarian cancer via the mechanism of terminal process of secondary spreading, regardless of the presence of glucocorticoid actions similar to that of cortisol, and the reduction of cell proliferation.
Invasion Metastasis 1989
PMID:Inhibition of tumor angiogenesis activity by medroxyprogesterone acetate in gynecologic malignant tumors. 247 53

Fourteen patients with incidentally diagnosed carcinoma of the prostate were reviewed. The frequency of the incidental prostatic carcinoma in our clinic was approximately 7.3% of 191 patients operated for benign prostatic hypertrophy. Five patients with focal and well differentiated carcinoma (stage A1) were managed expectantly with no treatment. Two patients with focal and moderately differentiated carcinoma (stage A2) and three patients with stage A1 cancer were treated by means of chlormadinone acetate. Total retropubic prostatectomy and pelvic lymph-node dissection was performed in four patients with diffuse prostatic carcinoma (stage A2). No serious complication occurred without minimal stress incontinence in one patient. Three patients had diffuse residual carcinoma in the total prostatectomy specimens. In one of them capsular penetration of carcinoma cells was discovered. Follow up was performed for 1.5-7 years (mean 43 months) by repeated transrectal needle biopsy, bone scan and serum phosphatase. Metastasis and recurrence have not developed in any patient. Two patients died without evidence of cancer. The remaining patients are alive without evidence of disease. Radical operation is recommended for patients with stage A2 prostatic carcinoma after transurethral resection of prostate.
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PMID:[Treatment of prostatic incidental carcinoma]. 247 36

Evidence is provided to show that two secondary cell-signaling pathways, Ca2+ mobilization and the activation of protein kinase C (PKC), are involved in the induction of spontaneous metastasis in mouse adenocarcinoma cell line SP1. Unlike the parental cells, which were found to be tumorigenic but unable to metastasize from a s.c. site, SP1 cells treated with ionophore A23187 (to mobilize Ca2+) or phorbol 12-myristate 13-acetate (to activate PKC) were able to metastasize spontaneously. Analysis of SP1 cells treated with either agent separately or with both agents simultaneously revealed that both pathways contributed to the final response in a separate and nonsynergistic way. The induced metastatic phenotype in most cases appeared to be heritable. Examination of Ca2+ sources during cell activation by ionophore A23187 suggested that internal Ca2+ was sufficient for the process of induction. Examination of PKC activity and its intracellular distribution during and after treatment of SP1 cells with ionophore A23187 and phorbol 12-myristate 13-acetate were also evaluated. The results suggested that the basal levels of PKC and the activation of the enzyme appear to be involved in the induction of spontaneous metastasis. Taken together, these observations are consistent with the hypothesis that cell-signaling pathways exist which can induce the metastatic phenotype and that this may be related to phosphatidylinositol turnover.
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PMID:Possible involvement of Ca2+ mobilization and protein kinase C activation in the induction of spontaneous metastasis by mouse mammary adenocarcinoma cells. 249 16

High dose medroxyprogesterone treatment was given to 20 patients with metastatic renal cell carcinoma. Distant metastases occurred before the perifascial nephrectomy in 11 patients and following nephrectomy in 9. Tumor deoxyribonucleic acid content was analyzed by flow cytometry in 8 fresh samples from each primary tumor. Four patients had homogeneously diploid primary tumors, 5 had tumors with diploid and aneuploid samples, and all 8 tumor samples were aneuploid in 10 patients. Deoxyribonucleic acid analysis was unsuccessful in 1 patient. One patient with a diploid primary tumor died of an intercurrent disease. Three patients (16 per cent) had objective remissions and 1 had a long-lasting stable disease. Of the 4 patients with any response to medroxyprogesterone acetate treatment 3 had diploid primary tumors, and 1 had 8 diploid and 2 aneuploid samples in the primary tumor. The remaining 14 patients showed no response to treatment and had progressive disease (11 of these patients died within 14 months). All 14 patients had aneuploid primary tumors. The results indicate that tumor ploidy might be related to response to medroxyprogesterone acetate treatment. Deoxyribonucleic acid content seems to be an important parameter to consider in planning treatment of metastatic renal cell carcinoma.
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PMID:Deoxyribonucleic acid content and medroxyprogesterone acetate treatment in metastatic renal cell carcinoma. 214 89

We examined the effect of medroxyprogesterone acetate (MPA) on secondary spreading of endometrial cancer. There was no significant difference in the adhering capacity of dispersed Ishikawa cells (derived from well-differentiated endometrial cancer) to a cell basement membrane matrix, fibronectin or laminin between cells treated with MPA, with cortisol, and without treatment. The adhering capacity of cells treated with cortisol to collagen type IV was higher than that without treatment. However, the adhering capacity was little affected by treatment with MPA. These results indicate that although cortisol may induce the initial process of metastasis by inducing the attachment of tumor cells to the basement membrane of vascular endothelium, MPA has no influence on the attachment, although it has a glucocorticoid action similar to that of cortisol. There was no significant difference in tumor angiogenesis factor (TAF) or fibroblast growth factor (FGF) activity of the tumor extract from Ishikawa cell colonies between cortisol-treated and control group. TAF or FGF activity of the MPA-treated group was lower than that of the control group. MPA may reduce the neovascularization in the terminal process of metastasis via the reduction of TAF and FGF produced by tumor cells, in spite of its glucocorticoid action.
Invasion Metastasis 1989
PMID:Effect of medroxyprogesterone acetate on secondary spreading of endometrial cancer. 252 39

A patient who underwent radical mastectomy was treated by tegafur and tamoxifen. Pulmonary metastases were found four months after operation. Lymphokine activated killer (LAK) and auxiliary interleukin-2 (IL-2) administration was performed, with no change (NC). However, administration of large-dose medroxyprogesterone acetate induced complete disappearance of pulmonary metastases after more than nine months.
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PMID:[Mammary gland carcinoma treated by large-dose medroxyprogesterone acetate of which pulmonary metastases disappeared and a selection of hormone, chemoimmunological treatment]. 252 19

Cloned human cell lines of squamous-cell lung carcinoma and small-cell lung carcinoma were treated with 5-azacytidine (5-azaC), 12-0-tetradecanoyl-phorbol-13 acetate (TPA), retinoic acid (RA), or a combination of these drugs, and the effects on cellular morphology, in vitro growth properties, antigenicity, tumorigenicity and metastatic activity in nude mice were studied. Antigenicity was measured by the expression of major histocompatibility antigens (MHC) and of lung-tumor-associated antigens. 5-AzaC treatment resulted in subclones with shorter population doubling times (from 40-50 hr down to 14-20 hr) and increased cloning efficiencies (from less than 1% to 5-50%). TPA and RA induced loss of proliferative activity in vitro and tumorigenicity in vivo of both lines. This was morphologically associated with the appearance of an abundance of large vaculated cells which by DNA-analysis were all found to be in G0-G1 phase. However, 2 of the 5-azaC-treated subclones were insensitive to both TPA and RA, whereas the remaining subclones (20) all responded like untreated lines to TPA and RA. One of the sublines insensitive to TPA and RA formed metastases in nude mice in contrast to all the other lines used. The density of lung-tumor-associated antigens was significantly reduced by TPA-RA treatment, whereas the expression of MHC antigens was unaffected. In contrast, 5-azaC resulted in some cases in increased density of MHC antigens. The effects of 5-azaC on cellular phenotypes were not directly correlated to the total genomic content of 5-methylcytosine. The data suggest that this experimental system is suitable for studies of phenotypic features of malignant cells as related to cellular differentiation.
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PMID:Modulatory effects of 5-azacytidine, phorbol ester, and retinoic acid on the malignant phenotype of human lung cancer cells. 257 32

The epidemiology, histopathology, diagnosis and staging, and treatment of prostate cancer are reviewed. Prostate cancer, one of the most common malignancies occurring in men over age 50, will strike an estimated 103,000 men in the United States in 1989. More than 95% of prostatic tumors are adenocarcinomas. Tumors are graded on the basis of their degree of differentiation. Most afflicted men initially complain of difficulty in starting the urinary stream and of urinary bleeding, dribbling, and retention. Urinary obstruction may be present in advanced disease, and anemia, anorexia, and bone pain are common in metastatic disease. Prostatectomy and irradiation are used to treat disease localized to the prostate; the prognosis for such patients is good. Survival is diminished in cases of locally advanced and metastatic disease. Symptomatic metastatic disease is treated by hormonal manipulation through orchiectomy and administration of exogenous estrogens (diethylstilbestrol), luteinizing hormone-releasing hormone analogs (leuprolide and goserelin), and antiandrogens (cyproterone acetate, flutamide, and others). Some 70-80% of patients respond to hormonal therapy for periods of up to three years. After relapse occurs, salvage hormonal therapies (aminoglutethimide and ketoconazole) may be attempted to prolong survival. Fluorouracil, doxorubicin, mitomycin, cisplatin, cyclophosphamide, methotrexate, and estramustine have also been administered, with mixed results. Once relapse occurs in prostate cancer patients after initial hormonal therapy, the response to salvage hormonal or cytotoxic therapy is minimal; in the future, total androgen blockade and methods of decreasing drug resistance may be used to prolong survival.
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PMID:Treatment of prostate cancer. 266 30


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