Abstract |
A line of P388 leukemia resistant to mitomycin C (MMC) was successfully developed in vivo by treating mice bearing parental P388 (P388/0) with MMC followed by serial passage of the surviving leukemic cells. From this P388/MMC line, a subline was derived by not treating the passage mice with MMC (P388/MMC-NP); resistance to MMC was stable for as many as 56 weeks of transplantation. The chemosensitivities of each P388 line to assorted anticancer drugs were compared in vivo. Both P388/MMC and P388/MMC-NP had similar patterns of drug cross-resistance and collateral sensitivity. With respect to alkylating agents (e.g. cyclophosphamide, Platinol and chlorambucil), there was generally a partial degree of cross-resistance, sometimes only detectable at suboptimal dose levels. With respect to DNA binders or intercalators (e.g. actinomycin D, luzopeptin A, amsacrine, doxorubicin), the extent of cross-resistance varied from none (dihydoxyanthraquinone) to marked ( doxorubicin). Antimitotic inhibitors ( vinblastine and vincristine) were completely cross-resistant, as were some miscellaneous natural agents ( rebeccamycin, VP-16, sesbanimide, and elsamicin, a chartreusin analog). Antimetabolites (e.g. methotrexate and 6-thioguanine) showed no cross-resistance and even demonstrated some occasional evidence of collateral effectiveness.
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Authors | W C Rose, J B Huftalen, W T Bradner, J E Schurig |
Journal | In vivo (Athens, Greece)
(In Vivo)
1987 Jan-Feb
Vol. 1
Issue 1
Pg. 47-52
ISSN: 0258-851X [Print] Greece |
PMID | 2979764
(Publication Type: Journal Article)
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Chemical References |
- Antineoplastic Agents
- Mitomycin
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Topics |
- Animals
- Antineoplastic Agents
(therapeutic use)
- Drug Resistance
- Leukemia P388
(drug therapy, physiopathology)
- Mice
- Mice, Inbred DBA
- Mice, Inbred Strains
- Mitomycin
(therapeutic use)
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