Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients entered into phase II trials in metastatic malignant melanoma should be carefully selected in order to ensure that they live long enough to permit a meaningful evaluation of the efficacy of a given drug. In this selection emphasis has been put on performance status. However, also for patients with a good performance status, survival is often short. The purpose of this study has been to identify supplementary prognostic factors as these could be of help in the design of phase II trials. From 1978-1986, 177 consecutive patients were given various chemotherapy regimens for metastatic malignant melanoma in the Norwegian Radium Hospital. About 92% had a performance status of ECOG 0-2. Median survival was 4.0 months (0-30 months). Multivariate survival analysis selected lactate dehydrogenase (LDH) greater than 450 U/l, presence of brain metastases, leukocyte count greater than 10 x 10(9)/l, and erythrocyte sedimentation rate (ESR) greater than 15 mm/h as significant prognostic factors indicating short survival with low probability of surviving 3 months. Patients with normal values of LDH, leukocyte count, and ESR had a median survival of 11.5 months with 94% surviving 3 months. We conclude that this information could have an impact on the design of phase II trials.
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PMID:Regression analyses of prognostic factors in metastatic malignant melanoma. 276 10

Human 253J urinary carcinoma cells and the F1 (low-metastatic) and F10 (high-metastatic) variants of the B16 murine melanoma cell line have been shown to activate heparinized human platelets by an adenosine diphosphate (ADP)-dependent mechanism based on inhibition by creatine phosphate/creatine phosphokinase and the identification of aggregating concentrations (1 to 2 mumol/L) of ADP in cell-free culture supernatants by high-performance liquid chromatography. Aggregation did not occur in citrated samples, and hirudin was without effect. Studies were carried out to determine whether extracellular ADP arose from nonspecific cell damage during cell isolation and manipulation or was a specific process under control of the tumor cells themselves. Tumor cell damage during harvesting was shown not to be a factor because the amounts of ADP produced by the three cell lines (a) were inversely related to the appearance of lactic dehydrogenase in the culture supernatants and (b) were similar when measured in confluent monolayers, either in tumor cells after detachment and resuspension or after crossover studies involving culture in, alternatively, Hanks' balanced salt solution and minimal essential medium. Metabolic control of ADP production was indicated by the fact that (a) it was not dependent on cell number, which suggests feedback inhibition; (b) it was reduced 60% when tumor cells were treated with p-chloromercuribenzene sulfonate; and (c) it was completely abolished in those treated with iodoacetic acid, which might be expected to increase nonspecific leakage. These studies indicate that ADP production by these three lines does not arise due to leakage induced by nonspecific membrane damage during cell harvesting and manipulation but is a discrete process under metabolic control of the tumor cells. Moreover, in B16 murine melanoma cells the ability to produce ADP and to support platelet aggregation appears to be unrelated to metastatic potential insofar as identical results were obtained with the F1 and F10 variants.
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PMID:Platelets in tumor metastasis: generation of adenosine diphosphate by tumor cells is specific but unrelated to metastatic potential. 283 29

Cell lines derived from human melanoma xenografts were characterized for surface markers, karyotype abnormalities, and in vitro drug sensitivity. Xenografts were established using metastatic explants from untreated patients and passaged in nude mice. Cell lines were readily established from melanoma xenografts, and formed colonies when plated in semisolid media. The lines expressed human melanoma-associated and other surface antigens, human lactate dehydrogenase (LDH) isoenzymes, and contained only human chromosomes. They failed to express murine histocompatibility determinants and were negative for murine viruses by mouse antibody production assay. Karyotypes showed abnormalities of chromosomes 3, 6, and 7 similar to other melanomas. In vitro chemosensitivity profiles were compared using cell line and xenograft colony-forming assays. Values were similar for the original xenografts and their cell lines. Xenograft-derived human melanoma lines resemble other melanoma cell lines and primary melanomas with respect to surface antigens and karyotype abnormalities, and are appropriate models for studying in vitro drug sensitivity. When used as a model for transition from solid tumor to cell line, these studies suggest cell lines closely mirror in vitro chemosensitivities of parent tumor cells. However, occasional, unpredictable changes in sensitivity to some drugs occurs during this transition.
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PMID:Use of nude mouse xenografts as preclinical screens. Characterization of xenograft-derived melanoma cell lines. 365 9

Clinical and experimental observations suggest that tumor-induced endothelial cell (EC) injury may be one of several initial events in the establishment of tumor metastases. This work investigates tumor-induced EC injury and the interaction between tumor-damaged EC and platelets. We used cultured bovine EC and extracts of four cultured human malignancies. EC injury was assessed by 51Cr and lactic dehydrogenase (LDH) release. Incubation of EC with melanoma, breast carcinoma or lung carcinoma caused significant LDH and 51Cr release, whereas colon cancer seemed ineffective. Increased adhesion of platelets to tumor-injured EC was noted. These observations indicate that certain varieties of tumor cause EC injury. Adhesion of platelets to tumor-injured EC results in the formation of platelet-tumor thrombi at the endothelial surface, an event that may initiate tumor invasion of the vessel wall.
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PMID:Tumor interaction with vascular endothelium. 366 82

Some enzyme activities and metabolic features of the black Ma melanotic, brown MI melanotic and Ab amelanotic melanomas of hamster were investigated. The activities of hexokinase and phosphofructokinase were similar in all three melanomas, the activity of NAD-dependent glycerol-3-phosphate dehydrogenase was higher in the amelanotic melanoma and that of pyruvate kinase and lactate dehydrogenase were slightly lower in MI than in the other tumors. The activities of citrate synthase, succinate dehydrogenase and malate dehydrogenase were higher in the Ma and MI melanotic melanomas than in the Ab amelanotic melanoma. The rate of labeled CO2 production from 6-14C-glucose, 1,5-14C-citric acid and U-14C-glutamine was about 2 times higher in melanotic melanomas than in amelanotic one, while no significant differences among the three melanomas were found in respect to 1-14C-glucose and U-14C-glycerol-3-phosphate. The production of 14CO2 was much higher from 1-14C-glucose than from 6-14C-glucose in all the melanomas studied. L-DOPA stimulated the production of 14CO2 from 1-14C-glucose much stronger in the Ma and MI melanomas than in the Ab melanoma. In none of the tumors the incorporation from 6-14C-glucose to CO2 was affected by L-DOPA. It is postulated that oxidation of glucose via the pentose phosphate cycle is involved in melanogenesis.
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PMID:Metabolic characterization of three hamster melanoma variants. 406 92

A considerable increase in activity of the following enzymes: succinate dehydrogenase (SDH), lactate dehydrogenase (LDH), beta-hydrogenase (beta-HBDH), cytochrome oxidase (CO), and acid phosphatase (AP) was found in lymph nodes lymphocytes after 1 week of malignant melanoma passage in golden hamster (Mesocricetus auratus Waterhouse). The peripheral blood lymphocytes displayed, too, an increase in activity of all the enzymes mentioned except beta-HBDH and SDH. After 3 weeks of the melanoma growth, the animals affected showed a considerable decrease in activity of all the enzymes studied both in the lymph nodes and in the peripheral blood. The increase in enzymatic activity during the initial phase of tumour growth may be a manifestation of biological activation of the cellular defence of lymphocytes. On the other hand, the decrease in the activity seen at the advanced phase of the disease speaks for an impaired immune response.
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PMID:Activity of some respiratory and lysosomal enzymes of lymphocytes in golden hamster with induced melanoma. 625 28

Gossypol, a yellow pigment from the cotton plant (Gossypium) was found to have anti-tumor cell effects against several tumor cell lines grown in tissue culture. Most sensitive to the drug were melanoma and colon carcinoma cells. After 24 hr of treatment with 10 microM gossypol, over 90% of these cells were killed. A rough correlation existed between very rapidly growing cells and their sensitivity to the drug. For example, slow growing cells, such as normal embryonic lung fibroblasts and mammary adenocarcinoma, were least sensitive, requiring over 30 microM gossypol in order to kill 90% of cells after 48 hr of treatment. These results indicate that gossypol has differential cytotoxic effects against certain tumor cell types, such as melanoma and colon carcinoma, and suggest that it might be of potential therapeutic value. The drug appears to act as a metabolic poison rather than as an agent interfering with DNA synthesis at the concentrations used in the study. Cells sensitive to the drug contain the more cathodic forms of lactate dehydrogenase, lactate dehydrogenases I to III.
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PMID:Differential cytotoxic effect of gossypol on human melanoma, colon carcinoma, and other tissue culture cell lines. 658 64

The clinical findings and response to treatment of leptomeningeal metastases from solid tumors are analyzed in 90 patients treated at Memorial Sloan-Kettering Cancer Center during the period from January 1975 to February 1980. Patients included those who had either typical clinical findings of leptomeningeal tumor or conclusive laboratory evidence supporting the diagnosis. Carcinoma of the breast (46 patients), lung (23 patients) and melanoma (11 patients) were the common primary tumors. Symptoms of leptomeningeal metastasis occurred as the presenting sign in five patients and as late as ten years after the primary tumor was diagnosed in four other patients. Most patients had active systemic disease outside the nervous system. Signs and symptoms could be classified as involving either the brain, cranial nerves, or spinal nerves. Most patients had either symptoms or signs in more than one area at the time the diagnosis was established. The initial spinal fluid examination was abnormal in all but three patients, but only 49 had cytologic evidence of leptomeningeal metastases. Repeated spinal fluid assay yielded a positive cytology in 82 patients. Measurement of biochemical markers, including beta-glucuronidase, carcinoembryonic antigen and lactic dehydrogenase, assisted in the diagnosis. Approximately half of the patients treated by intraventricular methotrexate experienced improvement or stabilization of neurological symptoms for more than a month; median survival was 5.8 months after diagnosis, with a range of 1--29 months. In 18 patients disease was limited to the nervous system, and median survival was eight months, with four patients surviving one year and two patients for two years. Side effects of therapy were, for the most part, minor. We conclude that vigorous treatment of leptomeningeal metastases with intrathecal chemotherapeutic agents improves symptomatology in some patients, and at times prolongs survival.
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PMID:Diagnosis and treatment of leptomeningeal metastases from solid tumors: experience with 90 patients. 689 13

We reviewed the records of 73 patients with primary melanoma of the choroid and ciliary body with metastasis treated at M. D. Anderson Hospital and Tumor Institute between 1973 and 1979. At time of diagnosis of primary melanoma 71 of 73 patients had tumor localized to the eye and were treated with enucleation of the affected eye. The interval from resection of primary tumor to detection of systemic metastases in the 71 patients ranged from one to 201 months (median 43.5 months). Weight loss and abdominal pain due to hepatomegaly were the most common symptoms, and hepatomegaly was the most common physical sign. The liver was the most common site of tumor recurrence, occurring in 44 of 71 patients. Among liver enzymes, serum lactic dehydrogenase was found to be the most sensitive indicator of liver metastasis and was elevated in 96% of patients with tumor in the liver. Liver involvement with tumor was associated with poor response to chemotherapy and significantly poorer survival than involvement of other extracranial sites. The survival duration from time of development of systemic metastasis ranged between one and 31 months (median seven months), with a one-year survival rate of 29%. The median survival of patients from diagnosis of ocular melanoma was 52 months, with a five-year survival rate of 43%.
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PMID:Prognosis in metastatic choroidal melanoma. 724 14

Melanoma is a cutaneous malignancy with an incidence that is rising. Surgery is curative if performed prior to metastasis. Liver metastasis is common and is often associated with an elevation in lactic dehydrogenase. A rise in transaminases is unusual; typically it is low in these patients. We describe a case of metastatic melanoma which presented as severe hepatocellular disease.
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PMID:Severe hepatocellular disease as an unusual presentation of metastatic melanoma. 758 74


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