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)

Although current hormonal therapy of prostate cancer may not appear to have altered survival appreciably, there have been considerable changes that may significantly affect the future management of this disease. A number of new hormonal agents have been introduced that still require definition of their therapeutic efficacy. Megestrol acetate, a hormonal agent with multiple sites of action in androgen metabolism, has recently been investigated in the treatment of patients with metastatic and locally advanced disease, and in those patients whose disease progresses with other hormonal therapies. Megestrol acetate plus mini-dose diethylstilbestrol (DES) is associated with fewer side effects than standard-dose DES and has equivalent therapeutic efficacy in the treatment of patients with metastatic disease. In patients with locally advanced disease that may benefit from hormonal cytoreduction, megestrol acetate is effective and well tolerated. Megestrol acetate has a role in the palliation of patients with progressive disease despite initial hormonal therapy. Considerable controversy surrounds the therapy of carcinoma of the prostate; further studies are required to define optimal hormonal therapy.
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PMID:Megestrol acetate in the treatment of metastatic carcinoma of the prostate. 146 22

A pilot study was undertaken to compare mitomycin C plus oral high-dose medroxyprogesterone acetate (MMPA) to cyclophosphamide+doxorubicin+ fluorouracil (CAF). Thirty-four women were randomized at first relapse to receive MMPA or CAF. Patients were balanced with respect to age, performance status, hormone receptor status, prior adjuvant treatment, site of metastases, and number of metastatic sites. On MMPA 9/18 objective responses occurred and on CAF 12/18. Median time to treatment failure was 5.7 months on MMPA and 7.6 months on CAF; median survival on MMPA was 22.5 months and on CAF 16.7 months. Although there were more objective responses on CAF, this was not statistically significantly different, and CAF was associated with significantly more hemopoietic toxicity. It is concluded that mitomycin C should be further studied in front-line regimens for patients with metastatic breast cancer.
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PMID:Mitomycin C + high-dose medroxyprogesterone versus cyclophosphamide+doxorubicin plus fluorouracil as first-line treatment for metastatic breast cancer. 146 78

In a phase II study, 24 patients with metastatic prostatic cancer were treated with mitomycin C 15 mg/m2 i.v. every 6 weeks, combined with aminoglutethimide 250 mg twice a day. A low dose of 37.5 mg cortisone acetate was supplied daily to compensate for adrenal cortical suppression. A partial response was demonstrated in 4 of 24 evaluable patients with bi-dimensionally measurable metastases. Stable disease occurred in 8 patients over a period of more than 6 months. Within the maximum cumulative dose limit of 2 mg/kg body weight mitomycin C, toxicity was observed in 21 cases, including 2 deaths due to treatment toxicity. The poor response rate and high toxicity suggest that the addition of aminoglutethimide does not enhance the effect of mitomycin C in these patients.
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PMID:Mitomycin C and aminoglutethimide in the treatment of metastatic prostatic cancer: a phase II study. 146 62

Thirty nine patients with metastatic breast cancer, all previously treated with chemotherapy including anthracycline, were given Elliptinium acetate (80 mg/m2/day) and a continuous infusion of Vinblastine (2 mg/m2/day) for 3 consecutive days every 4 weeks. Twenty nine patients had measurable metastatic disease. Nine (31%) achieved a partial response. No complete response was observed. Median duration of response was 6 months. The response rate was dependent on the number of metastatic sites and independent of the number of previous chemotherapy regimes. Side effects were dry mouth (27 patients), vomiting (9), neutropenia (3 patients with grade IV, 2 with grade III), muscle cramps (5) and thrombosis (3). Xerostomia and vomiting contributed to weight loss and fatigue (8 patients). We conclude that Elliptinium-Vinblastine combination has moderate activity as second line treatment in metastatic breast cancer. This combination causes xerostomia and fatigue with moderate myelosuppression.
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PMID:Phase II study of a combination of elliptinium and vinblastine in metastatic breast cancer. 148 4

Sixty patients with advanced breast cancer unresponsive to tamoxifen have been randomised to receive four course of mitozantrone, 14 mg m-2 (n = 30) intravenously every 3 weeks (9 weeks total) or megesterol acetate, 160 mg bd (n = 30). One in three patients (11 from each group) had substantial disease control for a minimum period of 6 months i.e., lack of progression; seven patients (23%) showed objective response to mitozantrone compared to four (13%) receiving megesterol. Non-progressive disease occurred in all sites, including visceral metastases and receptor negative patients. There were no significant differences between treatment groups in the median time (5 months each) to disease progression response duration or survival (13 months megesterol, 11 months mitozantrone) from commencing second-line therapy. Toxicity was considerably higher in the mitozantrone group. Second-line hormonal therapies can produce similar therapeutic results as those achieved from a short course of a 'short option' single agent cytotoxic in patients who were previously thought hormone insensitive. Provided that the patient does not have life threatening disease a trial of megesterol acetate is worth consideration in that it does not prejudice subsequent response to combination cytotoxic chemotherapy.
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PMID:A randomised trial of second-line hormone vs single agent chemotherapy in tamoxifen resistant advanced breast cancer. 150 15

Monoclonal antibodies (mAb) raised against human peritoneal macrophages were selected for their non-reactivity with freshly sampled blood cells. One of these mAb, AMH152, initially non-reactive, bound to monocytes after 18 h of culture, a property which was not shared by an unrelated antibody of the same isotype (IgG1). The induction of the expression of the antigen detected by AMH152 on monocytes in culture was not influenced by the addition of serum or by the substrate used, plastic that favoured adhesion or teflon bags. Overnight incubation at 4 degrees C in adhesion conditions did not enable antigen expression. A 1-h treatment with phorbol myristate acetate or formyl-methionyl-leucyl-phenylalanine did not increase AMH152 binding. Culturing monocytes with cycloheximide tended to inhibit antigen expression. These observations suggested that antigen expression represents an active phenomenon, requiring protein synthesis. The antigen recognized by mAb AMH152 could be visualized on sections of formalin-fixed and paraffin-embedded tissues. Macrophages of healthy lymphoid organs and tissues that expressed CD68 antigen failed to bind AMH152. In contrast, chronic inflammatory lesions, like those of sarcoidosis, tuberculosis and cat scratch disease, contained epithelioid and multinucleated giant cells that reacted with AMH152. In serous exudates of cancer metastases, 10-40% of macrophages were also stained. The antigenic material was essentially present at the cell periphery. Thus, mAb AMH152 recognized a surface antigen, detectable on paraffin-embedded tissue sections, and which accompanied differentiation of monocytes into inflammatory cells. The expression of this antigen on monocytes in culture suggests that these cells underwent an activation process, even when maintained for some hours in teflon bags and in a serum-free medium.
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PMID:Monoclonal antibody AMH152 reacts with human monocytes in culture and with inflammatory macrophages. 156 45

Nine patients with multiple metastases including liver from breast cancer were treated with transarterial chemoembolization through hepatic artery using 40-50 mg of 4'-epi-adriamycin and Lipiodol, followed by 800-1,200 mg/day of medroxyprogesterone acetate. Of 9 patients thus treated, there were 4 partial response (44%), 2 no change and 3 progressive disease. Duration of disease control ranged from 4 to 46 months (mean 24.5 months). Seven out of 9 patients died within 6 to 37 months (mean 15.3 months) after diagnosis of liver metastases. The 3- and 5-year survival rates were 45% and 11%, respectively. We conclude that this therapy is a useful treatment modality for controlling liver metastases of breast cancer.
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PMID:[Combination of transarterial chemoembolization and endocrine therapy for liver metastases of breast cancer]. 165 31

Gelatinolytic and collagenolytic proteinases were separately isolated by different extraction methods from the mouse ascites hepatoma MH134, and from rat ascites hepatoma AH109A. The activities of two proteinases in each extract showed no significant differences, but after trypsin activation the activities of proteinases from the highly metastatic MH134 were significantly increased compared to the enzyme activities in AH109A, which has low metastatic potential. The total activities of collagenase and gelatinase were increased 7.2- and 5.1-fold; their specific activities were increased 5.2- and 4.8-fold, respectively. Gelatinase and collagenase from MH134 were characterized on gelatin zymography. The gelatinase had a molecular weight of 99 and activation by 4-aminophenylmercuric acetate (APMA) or trypsin resulted in its conversion to 79 or 79-95 kD, respectively. The collagenase revealed a major gelatinolytic band at 89 kD, which was converted to 85 and 70 kD by APMA-activation, and a minor gelatinolytic band at 60 kD. These proteinases could degrade native type I collagen to small fragments in a cooperative manner. Trypsin inhibitor, which affects the trypsin activation of latent gelatinase, was extracted together with gelatinase. The inhibitory activity of the enzyme from AH109A showed a 4.1-fold higher specific activity and 3.7-fold greater total activity than that from MH134. The proteinase(s) capable of activating the gelatinase was also extracted from MH134.
Clin Exp Metastasis
PMID:Sequential degradation of interstitial collagen by metalloproteinases extracted from tumors of murine ascites hepatomas. 165 24

I have reported a rare case of hypercalcemia associated with small cell carcinoma of the lung. Our patient initially had small cell carcinoma of the right bronchial orifice, with metastases to the mediastinum and the lumbar vertebrae. Complete remission was achieved with chemotherapy over the next 3 years, but then three metastatic foci were found in the brain. Subsequently, recurrent small cell carcinoma was identified in the lung, and chemotherapy was resumed. The patient's condition deteriorated over the following 2 months. When intravenous saline failed to control hypercalcemia, octreotide acetate was given. The serum calcium level returned to normal and remained stable, without any other intervention, until the day after octreotide therapy was discontinued. I have discussed hypercalcemia due to bronchogenic carcinoma in terms of incidence in relation to histologic type, mechanisms of pathogenesis, and current treatment methods.
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PMID:Octreotide acetate therapy for hypercalcemia complicating small cell carcinoma of the lung. 131 35

Squamous cell carcinomas (SCC) of the mouse skin were produced by three different protocols of chemical carcinogenesis, i.e., complete carcinogenesis with 7,12-dimethylbenz(a)anthracene (DMBA) two-stage carcinogenesis with DMBA as initiator, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) as promoter and three stage carcinogenesis with DMBA, TPA and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) as third-stage agent or progressor. Tumors were sequentially studied at weeks 38-52 of treatment. Although no significant differences in the rate of appearance of gamma-glutamyl transpeptidase (GGT) could be seen, a larger number of SCC produced by complete carcinogenesis protocols were GGT-negative. This coincided with the higher grade of malignancy of these tumors as evaluated by histopathology. In general terms high-grade tumors were seen more frequently in the complete carcinogenesis experiment than in the other two protocols. SCC produced by complete carcinogenesis also exhibited a markedly higher DNA index than the SCC from the other experimental groups. All three protocols were very effective in producing late metastasizing tumors, and no significant differences could be established in the incidence of spontaneous lung metastasis. This shows that, contrary to general knowledge, if adequately observed for more than 40 weeks, SCC of the murine skin is able to metastasize in the lung in approximately 30% of cases. Nevertheless, complete carcinogenesis-induced SCC were usually of higher histological grade, a proportion of these were GGT-negative and produced more multiple or diffuse metastases than the tumors induced by the multistage protocols.
Invasion Metastasis 1991
PMID:Metastatic potential of mouse skin carcinomas produced by different protocols of chemical carcinogenesis. 168 75


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