Disease relevance of Leukemia P388

• Adriamycin and menogarol are anthracyclines which cause more than 100% increase in life span of mice bearing P388 leukemia and B16 melanoma [1].
• In vivo, the spectrum of activity of 4'-iodo-4'-deoxydoxorubicin is comparable to that of DXR, but the new compound has higher activity against murine P388 leukemia resistant to DXR and against pulmonary metastases from Lewis lung carcinoma [2].
• Chemoimmunotherapy of B 16 melanoma and P388 leukemia with cyclophosphamide and pyrimidinones [3].
• In in vivo experiments, MGBCP depleted spermidine and spermine in the P388 leukemic ascites cells, and prolonged the survival time of mice bearing P388 leukemia [4].
• Calcium influx blockers, diltiazem, nicardipine, nifedipine, niludipine, and nimodipine, which possess coronary vasodilator activity, greatly enhanced the cytotoxicity of vincristine (VCR) in tumor cells and especially in VCR-resistant sublines of P388 leukemia (P388/VCR) and human K562 myelogenous leukemia [5].

High impact information on Leukemia P388

• The active compounds isolated from the tunicate, didemnins A, B, and C, are depsipeptides, and didemnin B (a derivative of didemnin A) is the component active at the lowest concentration in inhibiting viral replication in vitro and P388 leukemia in vivo [6].
• The same strategy produced no better results than giving either MTX or TMTX alone to (C57BL/6 x DBA/2)F1 mice bearing murine leukemia P388 cells [7].
• Four main patterns were evident: a transport-related multidrug-resistance pattern (three sublines), a pattern similar to that for a murine P388 leukemia subline resistant to amsacrine, and two patterns not observed previously [8].
• Because the development of resistance to cancer chemotherapeutic agents represents a major limitation of cancer chemotherapy, we investigated the mechanism of resistance by murine P388 leukemia to camptothecin (topoisomerase I inhibitor) or amsacrine (topoisomerase II inhibitor) [9].
• Cisplatin and melphalan given ip exert a synergistic therapeutic effect against ascitic P388 leukemia in mice and have different dose-limiting toxic effects as well as favorable pharmacokinetic characteristics in ip phase I studies [10].

Chemical compound and disease context of Leukemia P388

• Biochemical parameters of resistance of an adriamycin-resistant subline of P388 leukemia to emetine, an inhibitor of protein synthesis [11].
• Resistance and cross-resistance of cultured leukemia P388 cells to vincristine, adriamycin, adriamycin analogs, and actinomycin D [12].
• Treatment with n-acetylcysteine also increased the nonprotein sulfhydryl content of P388 leukemia cells nearly threefold; however, it did not after the chemotherapeutic activity of doxorubicin against this murine tumor [13].
• The biochemical basis for the resistance of murine leukemia P388 to 5-fluorouracil (FUra) was systematically investigated by examining the transport and metabolism of FUra, or its anabolites, as well as the inhibition of enzymes and processes known to be affected by the drug [14].
• Schedule-dependent variations in the response of murine P388 leukemia to cyclophosphamide in combination with interferons-alpha/beta [15].

Biological context of Leukemia P388

• Formation and persistence of DNA single- and double-strand breaks stimulated by doxorubicin, 9-deoxydoxorubicin, or 4-demethyl-6-deoxydoxorubicin in murine leukemia P388 cells were compared in relation to drug DNA affinity, cellular pharmacokinetics, and cytotoxicity [16].
• Multifactorial resistance to adriamycin: relationship of DNA repair, glutathione transferase activity, drug efflux, and P-glycoprotein in cloned cell lines of adriamycin-sensitive and -resistant P388 leukemia [17].
• The dibenzo[1,4]dioxin-1-carboxamides are active against wild-type P388 leukemia in vitro and in vivo, with structure-activity relationships resembling those for both the acridine-4-carboxamide and phenazine-1-carboxamide series of DNA-intercalating antitumor agents [18].
• Rapid kinetics of the interaction between daunomycin and drug-sensitive or drug-resistant P388 leukemia cells [19].
• In this study we observed that alpha-hederin caused a dose- and time-dependent increase in apoptosis of murine leukemia P388 cells [20].

Anatomical context of Leukemia P388

• Cloned lines of Adriamycin (ADR)-sensitive and -resistant P388 leukemia have been established, including P388/ADR/3 and P388/ADR/7 that are 5- and 10-fold more resistant than the cloned sensitive cell line P388/4 (Cancer Res., 46: 2978, 1986) [17].
• P-glycoprotein expression and modulation of cell-membrane morphology in adriamycin-resistant P388 leukemia cells [21].
• MS-209 at 1-10 microM completely reversed resistance against vincristine (VCR) in vitro in multidrug-resistant variants of mouse leukemia P388 cells (VCR-resistant P388/VCR and Adriamycin (ADM)-resistant P388/ADM) and human leukemia K562 cells (VCR-resistant K562/VCR and ADM-resistant K562/ADM) [22].
• Proton NMR longitudinal relaxation times (T1; 10.7 MHz; 37 degrees C) were measured in the kidneys and blood serum of mice inoculated with P388 leukemia, and/or treated with the chemotherapeutic drug cis-diamminedichloroplatinum(II) (cis-Pt) [23].
• The anti-cancer drug aclarubicin (2.0 mg/kg body weight) was injected into the left popliteal lymph node (the primary draining node of the foot-pad region) or into the tail vein, 8 days after a subcutaneous inoculation of 5 x 10(5) P388 leukemia cells/mouse in the left hind paw foot-pad of mouse (donor) [24].

Gene context of Leukemia P388

• Reversal of P-glycoprotein-dependent resistance to vinblastine by newly synthesized bisbenzylisoquinoline alkaloids in mouse leukemia P388 cells [25].
• Reversal of drug sensitivity in MDR subline of P388 leukemia by gene-targeted antisense oligonucleotide [26].
• The sensitivity of camptothecin-resistant mouse leukemia P388/ CPT45 cells, which fail to express detectable top1, was similar to the sensitivity of wild-type P388 cells, suggesting that top1 is not a critical target for the antiproliferative activity of Et743 [27].
• Following the parenteral administration of tiazofurin, 2-beta D-ribofuranosylthiazole-4-carboxamide (thiazole nucleoside, TR), a potent but reversible inhibitor of IMP dehydrogenase is generated in subcutaneous nodules of the P388 leukemia [28].
• In ascitic P388 leukemia the antineoplastic activity of CDDP given ip was not reduced significantly [29].

Analytical, diagnostic and therapeutic context of Leukemia P388

• Adriamycin (ADR) (NSC-123127) uptake and retention in ADR-sensitive P388 leukemia (P388/S) and ADR-resistant P388 leukemia (p388/R) cells were compared by fluorometry and laser flow cytometry (FCM) and were correlated with cytotoxic effects [30].
• Finally, in vivo combination studies demonstrated that nontoxic doses of the ardeemins with DX significantly improved the chemotherapeutic effects in B6D2F1 mice bearing DX-resistant P388 leukemia, and nude mice bearing human MX-1 mammary carcinoma xenografts [31].
• Mouse leukemia (P388) cells were incubated in cell culture medium containing nitrogen mustard [2-chloro-N-(2-chloroethyl)-N-methylethanamine] for 4 h [32].
• Enhanced levels of cyclic AMP, adenosine(5')tetraphospho(5')adenosine and nucleoside 5'-triphosphates in mouse leukemia P388/D1 after treatment with cis-diamminedichloroplatinum(II) [33].
• Electron microscopy of cultured P388 leukemia cells revealed morphological differences between the Adriamycin-resistant (P388/ADR) and -sensitive (P388/0) cell lines [21].

References