By Leo Sachs (auth.), Prof. Dr. W. Hiddemann, Priv.-Doz. Dr. W. Plunkett, Prof. Dr. T. Büchner, Prof. Dr. J. Ritter, B. Wörmann M.D., Ph.D., M. J. Keating M.D., B.S., Prof. Dr. U. Creutzig (eds.)
This quantity, the 5th in a sequence on acute leukemias, focuses really on contemporary easy study effects and novel healing methods to the disorder. features of leukemia cellphone biology, together with differentiation, the mechanisms of drug resistance, the pharmacology of cytostatic brokers and the result of medical trials in relapsed and refractory ailment are coated by way of notable overseas specialists within the respective fields. destiny advancements together with new brokers and new treatment plans reminiscent of unrelated bone marrow transplantation, immunotargeting and gene treatment whole a cutting-edge summery of present wisdom in experimental leukemia therapy.
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Additional info for Acute Leukemias V: Experimental Approaches and Management of Refractory Disease
8. Rabbitts TH. Translocations, master genes, and differences between the origins of acute and chronic leukemias. Cell, 1991,67: 641-644. Cimino G, Lo Coco F, Biondi A, Elia L, Lueiano A, Croce CM, Masera G, Mandelli F, Canaani E. ALL-l gene at chromosome 11q23 is consistently altered in acute leukemia of early infancy. Blood 1993; 82: 544-546. Gu Y, Nakamura T, Alder H, Prasad R, Canaani 0, Cimino G, Croce CM, Canaani E. The t(4;11) chromosome translocation of human acute leukemias fuses the ALL-l gene, related to drosophila trithorax, to the AF-4 gene.
Le6le7JnnwbZ~ "'~... '"... 2 le6l e ? •• ;;J::C~ MV, I ', 120 110,127, 132, 124 :s ::! l. Schematic representation of heterogeneous fusion transeripts in pre-pre- B-ALL. e = exon. Exon assignment as in Table 4 19 Table 5. HRX (A) and FEL (B) exon assignment as in Table 4 e6 e7 e8 n infant adult 0 7 4 6 2 0 6 13 n 7 10 2 19 b c n A B a infant adult n 6 10 0 3 0 0 6 13 16 3 0 19 Table 6. HRX (A) and FEL (B) exon assignment as in Table 4. Data are from Borkhardt et al. Leukemia 1994, Griesinger et al.
Hematopoietic cells from mice defieient in wild-type P53 are more resistant to induction of apoptosis by some agents. Blood 82:1092-1096. 61. , Sachs, L. 1993. Regulation by bcl-2, c-myc and P53 of susceptibility to induction of apoptosis by heat shock and cancer chemotl1erapy compounds in differentiation competent and defective myeloid leukemic cells. , 4: 41-47. 62. R. 1992. Apoptotic cell death induced by c-myc is inhibited by bcl-2. Nature 359: 552-554. 63. I. 1992. Cooperative interaction between c-myc and bcl-2 proto-oncogenes.