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)

Three inhibitors of S-adenosylmethionine-mediated transmethylation, 5'-methylthioadenosine (MTA), 2'-deoxyadenosine and sinefungin, inhibited in vitro invasion by a highly invasive clone (Cl-30) of rat ascites hepatoma cells, AH 130 (AH cells). Difluoromethylthioadenosine (DFMTA), a non-metabolizable derivative of MTA, also caused strong inhibition of invasion at concentrations that did not suppress the growth of the tumor cells. Cl-30 cells precultured in methionine-depleted medium showed decreased invasiveness. DFMTA was also effective on the invasion by fibrosarcoma, B16 melanoma and human lung carcinoma cell lines.
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PMID:Inhibition of in vitro tumor cell invasion by transmethylation inhibitors. 255 19

Administration of rHuIFN-alpha A/D and rMuIFN-gamma as single agents to tumor-bearing mice resulted in a dose-related antitumor effect in each of the six models studied. When the IFNs were given in combination, the effects varied between the tumor systems. No increase in efficacy was seen in mice bearing B16-F10 melanoma or M5076 reticulum cell sarcoma while additive antitumor activity was shown in the KA31 fibrosarcoma and P388 leukemia systems. Mice inoculated with L1210 lymphoma or colon 38 carcinoma, however, revealed enhanced efficacy which was greater than additive. The data also reveal that combination of IFNs alpha and gamma administered to normal and tumor-bearing mice resulted in toxicity which was not predicted by the appropriate doses of the single agents. These studies suggest that combination of IFNs alpha and gamma may provide greater therapeutic utility than the single agents and underscore the need for additional, carefully designed preclinical and clinical efforts.
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PMID:Efficacy and toxicity elicited by recombinant interferons alpha and gamma when administered in combination to tumor-bearing mice. 256 40

The expression of oncogenes in well-characterized B16 melanoma and UV-2237 fibrosarcoma cell variants that exhibit distinct metastatic properties was explored. The search for the expression of 11 different oncogenes revealed that the major oncogene in those two tumor systems is the Kirsten-ras (ki-ras). The results indicate that the amounts of specific ki-ras mRNA and the p21 protein are similar in both low- and high-metastatic counterparts. These results suggest that in these systems there is no apparent direct correlation between the amount and expression of the major cellular oncogene so far identified and the metastatic potential of these tumor cells.
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PMID:Expression of ki-ras oncogene in tumor cell variants exhibiting different metastatic capabilities. 257 34

The expression of tumor-associated transplantation antigens (TATA) by 3 different murine melanomas was examined. A comparison was made between different modes of inducing tumor-rejection activity, including immunization with irradiated cells from tissue culture lines, with irradiated cells from solid tumor lines, and with viable cells growing in footpads (followed by amputation). Melanoma cell lines examined included the spontaneous B16 melanoma, the ultraviolet-light-induced K1735 melanoma, and the dimethylbenzanthracene-induced JB/RH melanoma. The data presented demonstrate that not only do all 3 melanoma lines studied express cell surface antigens sufficient to elicit immune response which result in tumor-rejection activity, but that these antigens show crossreactivity among the 3 melanoma lines studied. The specificity of the TATA appear to be restricted to the melanomas, since crossreactivity was not observed with 2 different fibrosarcoma cell lines, or with 2 sarcoma cell lines. In addition, it was found that both the JB/RH and K1735 melanoma cells release (or shed) cell surface antigens which can elicit tumor rejection activity, and that these antigens can be extracted with aqueous butanol, as has been demonstrated with B16 melanoma.
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PMID:Malignant melanoma: cross-reacting (common) tumor rejection antigens. 257 39

A central feature of tumor metastasis is the migration of malignant cells through interstitial tissues and vascular structures as they spread throughout the body. Various components of the extracellular matrix and of basement membranes, consisting of genetically distinct collagens, proteoglycans, and noncollagenous glycoproteins, are known to modulate certain aspects of cell behavior, including cell movement. Serum spreading factor is a glycoprotein component of human serum that is also found in interstitial tissues. Two native forms are seen in human serum, a Mr 65,000 and a Mr 75,000 component. Spreading factor promotes substratum attachment and spreading of diverse cell types, including epithelial and fibroblastic cells, and will affect the growth rate and differentiation of cells in serum-free culture media. Serum spreading factor was shown to promote the directed migration of the following tumor cell lines in modified Boyden chamber assays: murine melanoma K-1735 (clones M2, M4, and 16); human breast carcinoma MCF-7; and human fibrosarcoma HT-1080. The stimulation of movement occurred over a concentration range of 0.5 to 50 micrograms of serum spreading factor per ml with a maximum response between 5 and 10 micrograms/ml. The maximal response varied with the cell line and ranged from 5- to 50-fold greater migration than control. A monoclonal antibody to spreading factor, previously shown to inhibit the attachment and spreading-promoting activity, abrogated this migration response. Experiments using filters that were precoated with spreading factor indicated that cells could migrate on an insolubilized layer of this protein by haptotaxis. Tumor cell migration to spreading factor in vitro suggests a possible role for this protein in the phenotypic behavior of metastatic cells.
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PMID:Stimulation of haptotaxis and migration of tumor cells by serum spreading factor. 258 Jun 21

Cortisone acetate, locally applied in sustained-release pellets, is effective in inhibiting angiogenesis induced by prostaglandin E1 in the rabbit cornea. The inhibitory effect of cortisone is not increased by addition of heparin. Similar results were obtained with angiogenesis induced by S180 cells. The effects of cortisone with and without heparin were also studied on 5 transplantable murine tumours: 3 variants of B16 melanoma, Lewis lung carcinoma and fibrosarcoma M4. The effect of cortisone in slowing the growth rate of tumours was modestly potentiated by heparin, but no regression of the tumour mass occurred.
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PMID:Effects of cortisone with and without heparin on angiogenesis induced by prostaglandin E1 and by S180 cells, and on growth of murine transplantable tumours. 258 Aug 4

One hundred eighty-five dogs with histologically confirmed, measurable malignant tumors were used in a prospective study to determine the response to 2 doses of the anthracycline antitumor antibiotic, doxorubicin. Eighty-three dogs had been refractory to one or more previous treatment modalities (surgery, n = 54; chemotherapy, n = 22; radiation, n = 10; hyperthermia, n = 1; biological response modifier, n = 1). The extent of neoplastic disease was determined immediately prior to and 3 weeks after 2 doses of doxorubicin were administered (30 mg/m2 of body surface area, iv) 21 days apart. Eighty-four percent (n = 157) of the dogs received 2 doses of doxorubicin and were evaluated. Of the 28 dogs ruled ineligible, 4 had serious side effects to the first dose of doxorubicin, and 24 others acquired complications resulting from their malignant tumors. A partial or complete remission was obtained in 41% (64/157) of all evaluable dogs: 26% (11/43) of the dogs with carcinoma, 67% (42/63) of the dogs with lymphoma, and 22% (11/51) of the dogs with sarcoma. Tumors in which there was at least a 50% volume reduction (partial or complete remission) included malignant lymphoma (42/63), fibrosarcoma (1/14), solid follicular thyroid carcinoma (3/13), mammary adenocarcinoma (2/8), hemangiosarcoma (2/8), osteosarcoma (1/6), circumanal carcinoma (3/5), synovial cell sarcoma (2/3), undifferentiated sarcoma (2/3), nasal adenocarcinoma (1/2), liposarcoma (1/2), infiltrating lipoma (1/1), malignant melanoma (1/1), sclerosing mesothelioma (1/1), and neurofibrosarcoma (1/2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase II evaluation of doxorubicin for treatment of various canine neoplasms. 259 41

Unambiguous 13C-nmr assignments for the widely used pesticide rotenone have been made through the judicious use of APT, CSCM 1D, and selective INEPT spectroscopy. Also, in order to more fully characterize the biologic potential of rotenone, studies were performed with cultured cells. Intense, but nonspecific, activity was observed in the P-388 lymphocytic leukemia, KB carcinoma of the nasopharynx, and a number of human cancer cell types: e.g., HT-1080 human fibrosarcoma, LU-1 lung cancer, COL-2 colon cancer, MEL-2 melanoma, and BC-1 breast cancer cell lines in vitro.
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PMID:13C-nmr spectral assignment and evaluation of the cytotoxic potential of rotenone. 261 25

A new, sensitive automated assay based on the enzyme-linked immunosorbent assay was developed for measuring proteolytic enzyme activity produced by metastatic tumor cells. In this assay, a suitable protein substrate is adsorbed onto the surface of microplates and incubated with dilutions of standard proteinases, viable tumor cells, or tumor-cell-conditioned medium. The loss of immobilized protein due to proteolysis is then detected by means of antibodies directed against the target protein, and is measured by a microplate reader. Both casein and fibronectin were useful as substrates for the assay of various well-defined proteinases. The assay was successfully used to detect degradative activity elaborated by the mouse B16-BL6 melanoma and the human HT1080 fibrosarcoma cell lines. Both cell lines extensively removed immobilized protein substrates when the cells were seeded directly on the protein films. In addition, substrate removal could also be detected in the serum-free culture medium conditioned by the tumor cells. The results indicate that soluble proteinases secreted by tumor cells may be important during tissue invasion.
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PMID:Solubilization of immobilized protein substrates by metastatic tumor cells. 264 47

A phase I study with recombinant human tumor necrosis factor alpha (rhuTNF-alpha; Knoll AG, Ludwigshafen, FRG) in patients with advanced malignant disease was undertaken to evaluate drug toxicity (organ specificity, time course, predictability, reversibility, maximal tolerated dose), effectiveness, antigenicity and pharmacokinetics. TNF was administered as a test dose followed by daily i.v. infusions for 5 days, every 3 weeks (single i.v. infusion lasting 10 min, TNF dissolved in 50 ml 5% human albumin). Dosage was increased in groups of 3 or 4 patients from 0.04 mg/m2 to 0.28 mg/m2. A total of 19 patients with different cancers, including seven large-bowel carcinomas, three chronic myelogenous leukemias, three hypernephromas, two small-cell lung cancers, one malignant melanoma, one malignant lymphoma, one rhabdomyosarcoma and one fibrosarcoma were treated. Major side-effects were chills and fever (maximum 40.4 degrees C, median 38.7 degrees C, 19/19), headache (12/19), nausea and vomiting (12/19) and pronounced (greater than 20%) hypotension (4/19). Acute side-effects could be diminished by paracetamol or indomethacin pretreatment, and with one possible exception no tachyphylaxis to TNF was noted. Mild renal toxicity was seen during TNF treatment. Pharmacokinetic studies showed a serum half-life (t1/2) ranging from 11 min to 17 min for doses from 0.04 mg/m2 to 0.16 mg/m2 and prolonged clearance with t1/2 ranging from 54 min to 70 min in the 0.20-0.28 mg/m2 dose range. No objective antitumor effects were observed in this phase I study.
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PMID:Phase I study of recombinant human tumor necrosis factor alpha in advanced malignant disease. 272 Jul 7


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