By Steffen Koschmieder and Utz Krug
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Additional info for Myeloid Leukemia – Clinical Diagnosis and Treatment
Corbin, A. , Keats, J. , Sawyer, T. , Dalgarno, D. , Deininger, M. , Druker, B. , & Clackson, T. (2009) AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance. Cancer Cell, Vol. 16, No. 5 (November 2009), pp. , Elisseeva, O. , Kim, E. , Udaka, K. & Sugiyama, H. (2000) Human cytotoxic T-lymphocyte responses specific for peptides of the wild-type Wilms' tumor gene (WT1 ) product. Immunogenetics, Vol. 51, No. 2 (February 2000), pp.
D. Anderson Cancer Center (MDACC). MMR and complete molecular response (CMR) rates were 62% and 34%, respectively. 0001). The percentage of patients losing their CCyR was not significantly different between MMR and CMR patients (Cortes, 2005). Press et al. reached similar conclusions. They evaluated 90 CML patients, using a 3-log drop in BCR-ABL values from baseline as a definition of MMR. With a median follow-up of 49 months after the initiation of imatinib, 20 (22%) patients relapsed. Once again, the median BCR-ABL level as detected by RQ-PCR was significantly lower in patients with future stable cytogenetic response compared with those who subsequently relapsed at every time point from 12 to 36 months.
L. (2002) BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid Treatment of Chronic Myeloid Leukaemia: Current Practice and Future Prospects 19 leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90. Blood, Vol. 100, No. 8 (October, 2002), pp. , Vernant, J. , et al. (1993) Bone marrow transplantation for chronic myeloid leukemia: long-term results. Chronic Leukemia Working Party of the European Group for Bone Marrow Transplantation Bone Marrow Transplant, Vol.