Chronic Myeloproliferative Disorders by Mughal T., Goldman J.M.

By Mughal T., Goldman J.M.

With the recent class of continual myeloproliferative problems, and the increase of curiosity in molecularly specific cures, Informa Healthcare with Dr. Mughal and Dr. Goldman talk about the state of the art developments and new and present implications within the prognosis, remedy, and administration of patients.Filled with cutting edge info in relation to stem-cell transplantations and entire colour images, this well-illustrated textual content may be a necessary source for all practitioners in hematologic oncology.

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Pluk H, Dorey K, Superti-Furga G. Autoinhibition of c-Abl. Cell 2002; 108: 247–59. 51. Smith KM, Yacobi R, van Etten RA. Autoinhibition of Bcr-Abl through its SH3 domain. Mol Cell 2003; 12: 27–37. 52. Nagar B, Hantschel O, Young MA et al. Structural basis for the autoinhibition of c-Abl tyrosine kinase. Cell 2003; 112: 859–71. 53. Hantschel O, Nagar B, Guettler S et al. A myristoyl/ phosphotyrosine switch regulates c-Abl. Cell 2003; 112: 845–57. 54.

Chen SJ, Chen Z, d’Auriol L et al. Ph1+bcr- acute leukemias: implication of Alu sequences in a chromosomal translocation occurring in the new cluster region within the BCR gene. Oncogene 1989; 4: 195–202. 22. Jeffs AR, Wells E, Morris CM. Nonrandom distribution of interspersed repeat elements in the BCR and ABL1 genes and its relation to breakpoint cluster regions. Genes Chromosomes Cancer 2001; 32: 144–54. 23. Bose S, Deininger M, Gora-Tybor J et al. The presence of typical and atypical BCR-ABL fusion genes in leukocytes of normal individuals: biological 34 24.

On the minus side, they carry genetic lesions besides BCR-ABL, their differentiation is blocked and they are remote from the in vivo situation, where the leukemia cells are embedded in their microenvironment. 117 These partially conflicting findings indicate that the transforming capacity of BCR-ABL is dependent on the cellular context, which renders the interpretation of data difficult and has spurred the development of more physiological experimental systems. 118–120 Ba/F3 cells, a murine preB-cell line, and 32D cells, a murine myeloid progenitor cell line, have been used extensively to study BCR-ABL signal transduction and the requirement of BCR-ABL domains for transformation (for review see reference 121).

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