By A. F. List, C. M. Spier, W. S. Dalton (auth.), Prof. Dr. W. Hiddemann, Prof. Dr. T. Büchner, Priv. Doz. Dr. B. Wörmann, Prof. Dr. W. Plunkett, Prof. Dr. M. Keating, Prof. Dr. M. Andreeff (eds.)
This can be the 3rd quantity during this sequence on tools of treating acute leukemia. a number of drug resistance is mentioned, besides using human granulocyte-macrophage CSF, the position of stem cellphone issue, and simple points of mobile biology and pharmakokinetics. there's additionally a entire part facing relapse treatment and postremission remedy. The publication hence offers the clinician with instructions to be used in daily perform.
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Extra resources for Acute Leukemias: Pharmacokinetics and Management of Relapsed and Refractory Disease
Ludwig! Introduction Tumor-cell resistance to cytotoxic drugs is thought to be a major cause of failure in the chemotherapy of malignant tumors. One type identified as multi drug resistance (MDR) in experimental systems including human tumor cell lines was first described in 1970 in Chinese hamster lung and P388 leukemia cells . Resistant tumor cells exhibit decreased sensitivity, not only to the initial drug used to promote resistance but also to a variety of structurally diverse molecules to which they have not been previously exposed (reviewed in ).
Curt GA, Carney DN, Cowan KH, Jolivet J, Bailey BD, Drake JC, Kao-Shan CS, Minna 21 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 22 JD, Chabner BA (1983) Unstable methotrexate resistance in human small cell cancer associated with double minute chromosomes. N Engl J Med 308: 199-202 Trent JM, Buick RN, Olson S, Horns RC Jr, Schimke RT (1984) Cytologic evidence for gene amplification in methotrexate-resistant cells obtained from a patient with ovarian adenocarcinoma. J Clin Oncol 2: 8-15 Sirotnak FM, Moccio DM, Kelleher LE, Goutas LJ (1981) Relative frequencey and kinetic properties of transport defective phenotypes among methotrexate-resistant L1210 clonal cells derived in vivo.
Lmollh per mg protein found both in our previous studies and a recent report by Dedhar and colleagues . Eighteen patients' samples were evaluated for formation of MTX polyglutamates. No significant differences were seen in the total amount of MTX plus polyglutamates between the two neoplasms, suggesting that transport resistance is not a common mechanism of intrinsic MTX resistance in ANLL. However, although the total MTX plus polyglutamates was the same in ANLL and ALL, we found lower levels of long chain polyglutamates formed in ANLL ceIls than in ALL ceIls, although the amounts of long chain polyglutamates formed by ANLL blast cells were quite variable, and some ANLL patient samples formed as much MTX polyglutamates as the pediatric ALL blast cells.
Acute Leukemias: Pharmacokinetics and Management of Relapsed and Refractory Disease by A. F. List, C. M. Spier, W. S. Dalton (auth.), Prof. Dr. W. Hiddemann, Prof. Dr. T. Büchner, Priv. Doz. Dr. B. Wörmann, Prof. Dr. W. Plunkett, Prof. Dr. M. Keating, Prof. Dr. M. Andreeff (eds.)