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 chain on acute leukemias, focuses quite on contemporary simple examine effects and novel healing methods to the illness. elements of leukemia phone biology, together with differentiation, the mechanisms of drug resistance, the pharmacology of cytostatic brokers and the result of medical trials in relapsed and refractory disorder are coated by way of remarkable overseas specialists within the respective fields. destiny advancements together with new brokers and new treatments comparable to unrelated bone marrow transplantation, immunotargeting and gene remedy entire a state of the art summery of present wisdom in experimental leukemia therapy.
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Extra resources for Acute Leukemias V: Experimental Approaches and Management of Refractory Disease
Coupling of growth and differentiation in normal myeloid precursors and the breakdown of this coupling in leukemia. Int. J. Cancer 32: 127-134. 58. A. 1991. The P53 tumor suppressor gene. Nature 351: 453-456. 59. , Oren M. 1991. Wild type P53 induces apoptosis of myeloid leukaemic cells that is inhibited by interleukin 6. Nature 352: 345-347. 60. , Sachs, L. 1993. Hematopoietic cells from mice defieient in wild-type P53 are more resistant to induction of apoptosis by some agents. Blood 82:1092-1096.
Corral J, Forster A, Thompson S, Lampert F, Kaneko Y, Slater R, Kroes WG, van der Schoot CE, Ludwig W-D, Karpas A, Pocock C, Cotter F, Rabbitts TH. Acute leukemias of different lineages have similar MLL gene fusions encoding related chimerie pro teins resulting from chromosomal translocations. PNAS 1993; 90: 8538-8542. 16. Borkhardt A, Repp R, Haupt E, Brettreich S, Buchen U, Gossen R, Lampert F. Molecular analysis of MLL-I/AF4 recombination in infant acute lyrnphoblastic leukemia. Leukemia 1994; 8: 549-553.
Ii) to characterize HRX-FEL fusion genes by sequence determination in different age groups. Twenty-three pre-pre-B-ALL (7 infants, 14 adults and two celllines) were selected either based on cytogenetic demonstration of t(4;1l) (n=I2, group A) or on a CD15/CDw65+ pre-pre-B-ALL phenotype, highly suggestive of a t(4;1l) (n = 10, group B). HRX-FEL-fusion gene transcripts were detected in 13 of 13 pre-pre-B- ALL in group A and in 9 of 10 adult pre-pre-BALL in group B. More than one HRX-FEL-fusion gene amplification product was detected in 4 of 22 pre-pre-B-ALL, suggesting differential splicing of fusion genes.
Acute Leukemias V: Experimental Approaches and Management of Refractory Disease 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.)