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)

Dose response curves were obtained for normal human fibroblasts and for several cell lines derived from human tumors, including melanomas and an osteosarcoma. Most of the tumor lines are similar in radiosensitivity to the normal fibroblasts, except for the melanoma lines, which are significantly more resistant. The two melanoma lines differ, one being much more radioresistant than the other. Potentially lethal damage repair (PLDR) has been studied in these cell lines as well. The extent of PLDR does not appear to correlate with radioresistance; for example, the most resistant melanoma line shows very little repair of PLD. In addition, the normal fibroblasts repair PLD at least as well as any of the tumor derived lines, which casts doubts on the wisdom of introducing into clinical practice inhibitors of PLD until a clear differential between normal tissues and tumors has been demonstrated in vivo. Low dose-rate studies with normal human fibroblasts indicate a smaller dose-rate effect than for most established cell lines of rodent origin. Indeed, in the human cells studied, the effect of sublethal damage repair is quantitatively similar to the repair of potentially lethal damage. Dose response curves for acute and protracted exposures have been obtained for cells derived from patients with cancer-prone syndromes including ataxia telangiectasia (AT) and Bloom's syndrome. Both cell lines are much more radiosensitive than normal human fibroblasts; the AT cells show a dose-rate effect, while Bloom's syndrome cells do not.
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PMID:Response of cells of human origin, normal and malignant, to acute and low dose rate irradiation. 351 54

We studied inherent radiosensitivity/resistance (D0), ability to accumulate sublethal damage (n) and repair of potentially lethal damage (PLDR) in established human tumor cell lines as well as early passage human tumor cell lines derived from patients with known outcome following radiotherapy. Survival 24 hrs after treatment of human tumor cells with X rays in plateau phase cultures is a function of initial damage (D0, n), as well as recovery over 24 hrs (PLDR). A surviving fraction greater than .1 24 hrs following treatment with 7 Gy in plateau phase cultures is associated with tumor cell types (melanoma, osteosarcoma) with a high probability of radiotherapy failure or tumor cells derived from patients who actually failed radiotherapy. Therefore, total cellular recovery following radiation may be an important determinant or radiocurability. Accurate assays of radiotherapy outcome may need to account for all these radiobiological parameters.
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PMID:The maximum recovery potential of human tumor cells may predict clinical outcome in radiotherapy. 357 Aug 93

In a series of 882 retinoblastoma patients, 384 known to have the genetic form of the disease and 498 others, 30 patients developed second primary neoplasms. The spectrum of these second neoplasms is discussed in relation to the forms of treatment used for the retinoblastoma. Cumulative incidence rates of second tumours in the whole series are 2.0% at 12 years after diagnosis and 4.2% after 18 years. For patients with the genetic form of retinoblastoma the cumulative incidence rate after 18 years is 8.4% for all second neoplasms and 6.0% for osteosarcomas alone. The inherent risk among survivors from genetic retinoblastoma of developing an osteosarcoma, excluding all possible effects of treatment, is estimated to be 2.2% after 18 years. Within the field of radiation treatment the cumulative incidence rate for all second neoplasms after 18 years is 6.6% and for osteosarcomas alone 3.7%. There is some evidence that patients with genetic retinoblastoma are particularly sensitive to the carcinogenic effects of radiation. The results also suggest that the use of cyclophosphamide may increase the risk of second primary neoplasms in patients with genetic retinoblastoma. The incidence rates of second primary neoplasms in retinoblastoma survivors reported here are lower than those quoted for previously published series. Evidence from this and other papers strongly suggests an association between retinoblastoma and malignant melanoma.
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PMID:Second primary neoplasms in patients with retinoblastoma. 371 23

The effect of 3-aminobenzamide (3AB), an inhibitor of poly(ADP-ribose) synthetase, on potentially lethal damage repair (PLDR) was investigated in normal human fibroblasts and four human tumor cell lines from tumors with varying degrees of radiocurability. The tumor lines selected were: Ewing's sarcoma, a bone tumor considered radiocurable and, human lung adenocarcinoma, osteosarcoma, and melanoma, three tumors considered nonradiocurable. PLDR was measured by comparing cell survival when cells were irradiated in a density-inhibited state and replated at appropriate cell numbers at specified times following irradiation to cell survival when cells were replated immediately following irradiation. 3AB was added to cultures 2 hr prior to irradiation and removed at the time of replating. Different test radiation doses were used for the various cell lines to obtain equivalent levels of cell survival. In the absence of inhibitor, PLDR was similar in all cell lines tested. In the presence of 8 mM 3AB, differential inhibition of PLDR was observed. PLDR was almost completely inhibited in Ewing's sarcoma cells and partially inhibited in normal fibroblast cells and osteosarcoma cells. No inhibition of PLDR was observed in the lung adenocarcinoma or melanoma cells. Except for the osteosarcoma cells, inhibition of PLDR by 3AB correlated well with radiocurability.
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PMID:Inhibition of potentially lethal radiation damage repair in normal and neoplastic human cells by 3-aminobenzamide: an inhibitor of poly(ADP-ribosylation). 375 79

Radiation cell survival data were obtained in vitro for three cell lines isolated from human tumours traditionally considered to be radioresistant--two melanomas and one osteosarcoma--as well as from a diploid skin fibroblast cell line. One melanoma cell line was much more radioresistant than the other, while the osteosarcoma and fibroblast cell lines were more radiosensitive than either. For cells growing exponentially, little potentially lethal damage repair (PLDR) could be demonstrated by comparing survival data for cells in which subculture was delayed by 6 h with those sub-cultured immediately after treatment. For the malignant cells in plateau phase, which in these cells might be better termed 'slowed growth phase', since an appreciable fraction of the cells are still cycling, a small amount of PLDR was observed, but not as much as reported by other investigators in the literature. The normal fibroblasts, which achieved a truer plateau phase in terms of noncycling cells, showed a significantly larger amount of PLDR than the tumour cells.
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PMID:Potentially lethal damage repair in cell lines of radioresistant human tumours and normal skin fibroblasts. 387 82

Undifferentiated malignant tumors of the oral cavity were diagnosed in six dogs under 2 years of age. The dogs were examined because of pain and swelling of the upper molar or premolar areas. In all six dogs, the tumors were initially misdiagnosed as infections or carnasal abscesses. The differential diagnosis included malignant lymphoma, osteosarcoma, mesenchymal chondrosarcoma, embryonal rhabdomyosarcoma, and malignant melanoma. Electron microscopy of three neoplasms showed that there were no specific features characteristic of carcinoma or sarcoma. Immunoperoxidase studies for cytokeratins, epithelial membrane antigen, actin, myosin, desmin, and vimentin were also negative. We conclude that these tumors be designated undifferentiated malignant tumors of the oral cavity until histogenesis is established.
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PMID:A clinicopathologic and ultrastructural study of undifferentiated malignant tumors of the oral cavity in dogs. 396 83

The chemosensitivity of human tumor xenografts to mitozolomide, 8-carbamoyl-3-(2-chloroethyl)imidazo[5-1-d]-1,2,3,5-tetrazin-4(3H) -one, was studied in 3 different assay systems. In concentrations of 1 to 500 micrograms/ml, mitozolomide completely inhibited the colony-forming ability in soft agar of cell suspensions from sarcomas, melanomas, lung and colon cancers, and a mammary carcinoma. When a panel of tumors of the different histological types was tested for its sensitivity to mitozolomide in vitro, in the 6-day subrenal capsule assay in conventional mice, and, in some cases, as s.c. growing tumors in nude mice, good agreement between the different assay systems was seen. In most cases, a very pronounced antitumor effect was observed. The efficacy of mitozolomide was as good or better than that of the drugs clinically used against the tumor types tested. Tumor size measurements and histological examinations indicated that nude mice carrying a melanoma, a small cell lung cancer, and an osteosarcoma were cured of their tumors. The approach here used for evaluating the effect of a new drug on human cancers may be useful for selecting the tumor types which primarily should be studied in clinical trials. The results indicate that clinical responses to mitozolomide may be anticipated in sarcoma, melanoma, small cell lung cancer, and possibly in colon cancer.
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PMID:Activity of mitozolomide (NSC 353451), a new imidazotetrazine, against xenografts from human melanomas, sarcomas, and lung and colon carcinomas. 397 40

Cultured cell lines of osteosarcoma and normal skin fibroblasts were derived from tissues of five patients with localized osteosarcoma. Testing of pretreatment patient sera in an indirect immunofluorescence assay against both autologous normal fibroblasts and autologous osteosarcoma cells showed cytoplasmic staining. Quantitative absorption of patient sera with human fetal cells removed all reactivity against autologous fibroblasts, but fetal-absorbed sera showed cytoplasmic, membrane, and nuclear fluorescence when tested against autologous osteosarcoma. Testing the five patient sera against all five cell lines showed staining of allogeneic fibroblasts and osteosarcoma by nonabsorbed sera. Following fetal absorption, all reactivity against fibroblasts was removed, with the retention of specific staining of all osteosarcoma cell lines by all five patient sera. Additional testing of sera from normal patients, patients with soft tissue sarcomas, and patients with melanoma showed staining of allogeneic cultured fibroblasts and tumor cells derived from a patient with osteosarcoma. All staining against fibroblasts and tumor cells was eliminated by fetal absorption of the allogeneic sera. Results suggested that fetal neoantigens are expressed in cultured normal and malignant cell lines and that such fetal antigens are recognized by natural antibodies. Absorption of antifetal reactivity allowed demonstration of specific serum reactivity against osteosarcoma cells.
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PMID:Demonstration of specific serologic reactivity in human osteosarcoma. 618 4

The concept of injecting anti-tumor antibodies to localize tumors was first introduced in experimental systems by Pressman (1957). Since then, various trials for tumor detection have been performed using anti-tumor antibodies. In 1970's, the radioimmunodetection of cancer has rapidly developed by the use of radioantibodies to oncofetal proteins such as CEA, AFP and hCG. Recently, there are papers dealing with animal studies of external scanning by the monoclonal antibodies that bind selectively to tumor cells derived from murine teratocarcinoma, human malignant melanoma, human mammary carcinoma and human osteosarcoma. As clinical trials the radiolabeled monoclonal antibodies against CEA or AFP were also used for the radioimmunodetection in patients with CEA or AFP-producing tumors, and the positive rates of the scanning ranged from 40 to 94%. Various related problems are also discussed.
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PMID:[Recent progress in radioimmunodetection for cancer using radio-labeled monoclonal antibodies]. 619 58

Hybridoma cells were derived from a mouse immunized with plasma membranes prepared from the fresh tumor tissues of a patient with malignant fibrous histiocytoma (MFH), a soft tissue sarcoma. Supernatants from the resultant hybridoma clones were screened for positive antibody binding to tumor membranes and negative binding to membrane preparations of normal tissues using a solid-phase radioimmunoassay. Two distinct monoclonal IgG1 (kappa) antibodies, 19-14 and 19-24, were identified that showed identical patterns of reactivity with a large panel of tissues. Both antibodies displayed high levels of binding to membranes prepared from a majority of MFH and osteogenic sarcoma tumors tested. Moderate levels of binding were obtained with melanoma, colorectal carcinoma, and first-trimester fetal membranes. Weak or no significant binding was observed with membranes from a variety of autologous and allogeneic normal adult tissues. Antibody reactivities could be specifically removed by absorption with MFH and osteosarcoma membranes but not with adult muscle membranes. An electrophoretic analysis of immunoprecipitated membrane antigens indicated that antibodies 19-14 and 19-24 reacted with the same protein, a monomer with an approximate molecular weight of 102,000. The antigen was detected in membrane preparations of MFH, osteosarcoma, and first trimester fetus, but was not present in normal adult spleen. However, a small amount of antigen of molecular weight 107,000 was precipitated from a normal adult liver preparation, which suggests that related antigens may be present in low levels in some normal tissues. Antibodies 19-14 and 19-24 also specifically bound to intact, cultured MFH cells, indicating that the relevant antigens were expressed on the outer cell surface.
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PMID:Detection of a human sarcoma-associated antigen with monoclonal antibodies. 629 40


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