Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By employing rat cardiac myocytes in culture and mouse L-1210 leukemia cells, we have compared different anthracycline analogs with respect to their ability to kill cardiac myocytes and tumor cells. Anthracyclines induced a decrease in cellular ATP and glutathione from both cardiac myocytes and L-1210 cells in a time- and concentration-dependent fashion. Moreover, the decrease in ATP in cardiac myocytes was followed by release of the cytoplasmic enzyme lactic acid dehydrogenase and of adenine nucleotides after anthracycline treatment. At very low concentrations of anthracyclines, at which ATP and glutathione were not affected, the drugs induced complete cessation of the growth of L-1210 cells. Some structural alterations in the anthracycline molecule resulted in parallel changes in antitumor activity and in cardiotoxicity. But other structural alterations resulted in dissimilar changes in antitumor activity and cardiotoxicity. Although the results indicate that the structural requirements for inducing cardiotoxicity and antitumor activity may be different, they also indicate that the mechanisms by which anthracycline causes cell death in tumor cells and cardiac myocytes may be the same.
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PMID:Structural requirements for anthracycline-induced cardiotoxicity and antitumor effects. 276 5

A cytotoxic activity, highly selective for neoplastic cells, is expressed by 1-alkyl-2-methoxy-sn-glycero-3-phosphocholine and by other derivatives closely related to the chemical structure of platelet activating factor. The antineoplastic potencies of a new series of analogs tested in HL-60 human leukemia cells and human polymorphonuclear neutrophils are reported. The degree of cytotoxicity was documented according to the ability of each analog to 1) destroy leukemic or normal cells or 2) to release lactic acid dehydrogenase from these cells. An index of selectivity of the analogs for their cytotoxicity toward leukemia cells is presented. Substitution by the twenty carbon branched-chain phytanyl moiety in place of the straight chain alkyl ether-linked group at the sn-1 position of various phospholipid analogs resulted in a 3- to 10-fold reduction in their cytotoxic potency in HL-60 leukemia cells. The enantiomeric isomers (D-forms) of several of the analogs possessed slightly greater phospholipid analogs possessing the sn-2-acetyl (platelet activating factor) or sn-2- propionoyl substituents, both biologically active in their ability to aggregate platelets and to induce hypotension, were relatively innocuous in terms of the measured cytotoxic responses in both HL-60 cells and neutrophils.
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PMID:Cytotoxicity of ether-linked phytanyl phospholipid analogs and related derivatives in human HL-60 leukemia cells and polymorphonuclear neutrophils. 673 56

The case of a 77-year-old male patient who complained of left upper quadrant pain and progressive vomiting. Laboratory examination showed extremely high lactic acid dehydrogenase (LDH) and adult T-cell leukemia antibody (ATLA). The anatomical studies CT, MRI, US and upper GI series substantiated an omental lymphadenopathy which was causing a circumferential compression of portions of the duodenum and jejunum. Gallium-67 citrate (Ga-67) scintigraphy showed high uptake at LUQ. Ultrasound guided biopsy failed to confirm the diagnosis. Irradiation was performed. Ga-67 scintigraphy had a contributory role in clinical subtyping of the disease, planning of treatment, posttreatment assessment and prognostication of adult T-cell lymphoma.
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PMID:Gallium-67 scintigraphy in the treatment and prognosis of acute adult T-cell lymphoma. 963 81