By John Swansbury (auth.), John Swansbury (eds.)

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In particular, the leukemic cells respond to all-trans-retinoic acid (ATRA) by proceeding with differentiation and normal apoptosis, so this is used as part of the treatment. The quoted breakpoints on chromosomes 15q and 17q vary widely among different publications; the author favors those proposed by Stock et al. (22). The effect of the presence of secondary abnormalities is uncertain. In one study (23) (in which all secondary abnormalities were combined) they appeared to have no effect, but in others (25,26) the co-occurrence of trisomy 8 reduced the prognosis from good to standard.

38. 10. , et al. (1999) Isochromosome 17q in blast crisis of chronic myeloid leukemia and in other hematologic malignancies is the result of clustered breakpoints in 40 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. Swansbury 17p11 and is not associated with coding TP53 mutations. Blood 94, 225–232. Bennett, J. , Daniel, M. , et al. (1982) The FAB Co-operative Group. Proposals for the classification of the myelodysplastic syndromes. Br. J. Haematol. 51, 189–199. , and Tricot, G. (1985) The 5q- anomaly.

Dyer, M. J. , and Catovsky, D. (1994) Interstitial insertion of retinoic receptor-α gene in acute promyelocytic leukemia with normal chromosomes 15 and 17. Blood 83, 2946–2951. 40. Langabeer, S. , Rogers, J. , et al. (1997a) Incidence of AML1/ETO fusion transcripts in patients entered into the MRC AML trials. Br. J. Haematol. 99, 925–928. 41. Langabeer, S. , Gale, R. , et al. (1997b) Frequency of CBFbeta/MYH11 fusion transcripts in patients entered into the U. K. MRC AML trials. Br. J. Haematol.

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