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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an evaluation of indium-111-bleomycin as a tumor-imaging agent, 357 whole-body tumor scans were performed in 293 patients. Of 246 studies performed in patients with a variety of active solid tumors, 218 (89%) were true-positive studies and 28 (11%) were false-negative. Of 69 scans in patients thought to be free of tumor after therapy, 32 (46%) were false-positive studies and 37 (54%) were true-negative. The true-positive rates by major tumor type were: adenocarcinoma of gastrointestinal tract origin (95%), lymphoma (88%), melanoma (87%), sarcomas (82%), lung (77%), breast (77%), childhood tumors (71%), gynecologic tumors (70%), and genitourinary tumors (68%). Soft tissue and lymphatic sites of tumor, both above and below the diaphragm, were easily visualized, whereas hepatic and bone marrow sites of involvement were less easily discerned. False-positive uptake with 111In-bleomycin was noted in lungs (6%), gut (3%), mediastinum (2%), normal breast tissue (0.8%), and in occasional inflammatory lesions. In 19 patients with multiple myeloma or leukemia, a pattern of diminished bone marrow uptake associated with abnormal accumulation of 111In-bleomycin in extramedullary sites of involvement was the rule. In another 23 patients in whom scans were performed because an occult tumor was suspected, scanning did not lead to specific diagnosis of tumor in a single instance. We conclude that 111In-bleomycin is a safe, effective, and useful new tumor-imaging agent in the initial staging and followup of patients with a variety of solid tumors. Significant advantages of this agent over other currently available radiopharmaceuticals include: A) a broader spectrum of tumors taking up the radio-pharmaceutical, and B) generally better delineation of abdominal and pelvic disease due to lack of interference from gut uptake.
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PMID:A clinical evaluation of indium-111 bleomycin as a tumor-imaging agent. 4 76

Specimens from various types of Paget disease, other tumors, and certain normal tissues were examined with a battery of histochemical techniques, including the sodium borohydride-potassium hydroxide-PAS method that specifically stains certain sialomucins that are found in terminal parts of the ileum and of the colon. These sialomucins were present in normal anal ducts but were not present in transitional or anal-covering epithelium. A case of perianal Paget disease showed strongly positive staining, both in the underlying mucinous adenocarcinoma and in Paget cells of the affected anal and perianal skin. In contrast, stains of other forms of Paget disease were totally negative with this technique, as well as malignant melanoma and Bowen disease. These results support the theory that Paget disease represents epidermal invasion by malignant cells from underlying tumor.
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PMID:Perianal Paget disease. Histochemical differentiation utilizing the borohydride-KOH-PAS reaction. 5 63

The antineoplastic activity of 5 substances was tested in vivo and in vitro on four different tumours (plasmocytoma and melanoma Fortner III of the Syrian golden hamster, the Walker carcinosarkoma 256 and an adenocarcinoma of the rat). The substances involved were 2,3,5-triethyleniminobenzoquinone-(1,4) (triaziquone), actinomycin D, podophyllinic ethylhydrazide (mitopodozide), bleomycin and adriamycin hydrochloride. The effect of the substances in vivo was measured on the size of the tumour, and in vitro on the incorporation of 3-H-thymidine and 3-H-uridine in short-term incubations of tumour-cell suspensions. No correlation was observed between the 3-H-thymidine incorporation in vitro and the response of the tumours in vivo. On the other hand, the 3-H-uridine incorporation in the tumour-cell suspensions in vitro was in good agreement with the results of therapy in the animal experiments. This is compatible with the results of earlier experiments using other substances to investigate the possible correlation between tumour therapy and in vitro tests.
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PMID:[Correlation of in vitro testing and therapeutical results in animal transplanted tumors after cytostatic treatment]. 5 72

A phase I-II study of cyclocytidine was conducted in 102 patients, 96 of whom had metastatic solid tumors and six of whom had acute leukemia. The drug was administered in 5- or 10-day courses of single daily iv or sc injections of 100-675 mg/m2 day. Two complete and six partial responses were observed in 64 solid tumor patients evaluable for response, 52 of whom had malignant melanoma or adenocarcinoma of gastrointestinal origin. The median duration of the responses was 6 months. An additional seven patients achieved stabilization of their disease for greater than or equal to 2 months. No responses occurred in six patients with acute leukemia. Side effects included nausea and vomiting, postural hypotension, and parotid pain, occurring in approximatley one third of patients receiving greater than 200 mg/m2/day. No myelosuppression was observed in six patients receiving 5-day courses of 100-200 mg/m2/day. Myelosuppressive toxicity became increasingly severe with doses greater than 200 mg/m2/day x 10, related at least in part to prior chemotherapy exposure including the nitrosoureas.
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PMID:Phase I-II evaluation of cyclocytidine. 6 28

To identify soluble cell surface melanoma-associated antigens (MAA), human melanoma cells in culture were radioiodinated by the lactoperoxidase technique and solubilized in non-ionic detergent (NP-40). Labelled MAA were identified by a quantitative double-antibody antigen binding assay and unrelated labelled macromolecules by trichloroacetic acid precipitation. Detergent solubilized 95% of the macromolecule-associated radioactivity. Approximately 8%, presumably MAA, was bound specifically by anti-melanoma serum. In contrast, anti-melanoma serum bound specifically only 0.5 to 1.5% of the acid precipitable radioactivity in control cells iodinated in a similar manner. Specificity was further studied by quantitative serum absorption. Two different melanoma lines were equally effective in inhibiting specific binding of iodinated melanoma lysate, whereas 50-100 times more normal fresh lymphocytes, liver and spleen cells, cultured HeLa or colon adenocarcinoma cells, and 8 times more cultured fetal cells were required to produce similar reductions in specific binding. These studies demonstrate that cell surface human melanoma antigens that differ qualitatively and/or quantitatively from those on normal or malignant allogeneic tissues can be solubilized and identified. These antigens are shared with other melanomas, and some are also present on fetal cells.
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PMID:Identification and solubilization of iodinated cell surface human melanoma associated antigens. 7 Apr 12

This communication describes an automated micro-adherence inhibition assay. Tumor-specific immunity was demonstrated with B16 melanoma and MCA-38 colon adenocarcinoma, both of which are syngeneic to the same strain of mouse (C57B16/J). Abrogation of the leukocyte adherence inhibition (LAI) response of sensitized leukocytes has been demonstrated in the MCA-38 tumor system by the addition of serum from mice bearing MCA-38 progressively growing tumors, a property not present in normal serum. The sensitivity of the system has also been demonstrated by showing that LAI will change prior to a tumor becoming palpable. This microassay has the advantage of being simple, rapid and reproducible, and involves the use of minimal quantities of antigenic preparations and leukocytes, and in addition is amenable to rigorous statistical analysis.
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PMID:Leukocyte adherence inhibition: an automated microassay demonstrating specific antigen recognition and blocking activity in two murine tumor systems. 7 30

The mitogens concanavalin A (Con A) and bacterial lipopolysaccharide (LPS) stimulated normal spleen cells of DBA/2J, CBA/J, and BALB/c mice about equally in the presence of either isologous or homologous serum. This system revealed that sera from mice with five different methylcholanthrene-induced rhabdomyosarcomas inhibited mitogen stimulation of normal spleen cells. Sera from mice with a mammaryadenocarcinoma and spontaneous rhabdomyosarcoma were similarly suppressive. In contrast, sera from mice with melanoma were not inhibitory and often enhanced stimulation. Sera from tumor-bearing animals had the same effects both qualitatively and quantitatively on cells from the strain carrying the tumor and on cells from the other two strains. The mixed lymphocyte response of CBA/J times BALB/c spleen cells was affected exactly as were the responses to mitogen by the various sera. Stimulation by mitogen of mouse lymph-node cells and spleen cells with macrophages removed, as well as that of guinea pig spleen cells, was also inhibited by sera from mice with rhabdomyosarcoma and mammary adenocarcinoma.
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PMID:Effects of sera from tumor-bearing mice on mitogen and allogeneic cell stimulation of normal lymphoid cells. 12 99

To evaluate the relation between histocompatibility antigen phenotypes and solid malignant neoplasms, HL-A type was determined in 633 cancer patients and compared with those of 489 normal controls. HL-A8 was elevated in patients with squamous cancer, melanoma, and adenocarcinoma. The highest incidence occurred in patients with salivary gland adenocarcinoma (67% vs only 17% in normal controls). A threefold increase in HL-A5 was detected in patients with connective tissue sarcomas (28% incidence vs 9% in normal controls). Antigen frequencies did not vary when analyzed by time of diagnosis or interval after treatment. The finding that certain malignant neoplasms have associations with increased frequency of individual HL-A antigens may give clues to cause and genesis for these tumors.
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PMID:Histocompatibility antigens and solid malignant neoplasms. 16 28

The antitumor activity of three preparations of killed Bordetella pertussis (Bp) (Eli Lilly crude and fluid pertussis vaccines and Parke-Davis pertussis vaccine) was studied in the B16 melanoma and CaD2 mammary adenocarcinoma models. In these tumor systems; Bp had weak and variable tumor inhibitory activity and did not augment tumor rejection immunity. The intratumor injection of Bp did not affect the growth of the B16 tumor but significantly inhibited the growth of the CaD2 tumor. However, the established tumor did not regress. Admixture of Bp with B16 cells before inoculation inhibited tumor growth and prolonged survival of inoculated mice. Admixture of Bp with CaD2 cells completely suppressed tumor cell growth in 60% of inoculated mice. Intratumor injection of CaD2 with Bp combined with surgery provided no protection against subsequent development of metastases.
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PMID:Evaluation of antitumor activity of Bordetella pertussis in two murine tumor models. 16 59

Nuclear binding of the AtT-20 cytosol receptor-glucocorticoid complex was studied in a cell-free system using nuclei from steroid-responsive (AtT-20) and nonresponsive (EPO-G1) cell lines, both of which synthesize ACTH. The AtT-20 cell line was derived from a mouse pituitary adenocarcinoma, while the EPO cell line was established from a human malignant melanoma. The nonresponsive EPO cells lacked a cytosol receptor for glucocorticoids, and, when whole cells were incubated with labeled glucocorticoid, they were unable to concentrate the steroid in their nuclei. A cell-free system using AtT-20 cytosol preincubated with labeled glucocorticoid was used to study binding by isolated nuclei. Binding to isolated nuclei from both cell lines was indistinguishable, in terms of temperature sensitivity, binding capacity, and saturability. Sucrose density gradient analyses of KCl extracts of nuclei labeled under these cell-free conditions showed 3.2-3.6 S peaks. In contrast, a 4.0 S peak was observed consistently when unreacted cytosol was analyzed on high-salt gradients, suggesting that interaction with nuclei from both cell lines caused the receptor to alter its sedimentation characteristics. These findings suggest either that all cells contain nuclear acceptor sites and that target cell responsiveness is conferred solely by the presence or absence of the cytosol receptor, or that binding sites detected in isolated nuclei may be different from those observed in intact cells and may, in fact, obscure them.
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PMID:Binding of cytosol receptor-glucocorticoid complexes by isolated nuclei of glucocorticoid-responsive and nonresponsive cultured cells. 17 73


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