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28The BCR-ABL transcript percentparallels the number of leukemic cells
Imatinib Front line therapy in CML Patients:Response MilestonesOptimalSuboptimalFailureWarningBaselineNANANA• High risk;• CCA/Ph+3• CHR and• At least minor CgR(Ph+ < 65%)No CgR> 95%)(Ph+Less than CHRNA6At least PCgR 35%)No CgR> 95%)(Ph+NA12CCgRPCgR1% to 35%)(Ph+Less than PCgR(Ph+ >35%)Less thanMMolR18MMRLess than MMRLess than CCgRNAAny timeduringtreatmentStable or improvingMMR• Loss of MMolR• Mutations 1• Loss of CHR• Loss of CCgR• Mutations 2• CCA/Ph+• Increase intranscriptlevels• CCA/Ph-291. Mutations still sensitive to imatinib 2. Mutations poorly sensitive to imatinibCCA; clonal chromosomal abnormalitiesBaccarani et al, J Clin Oncol., 2009
Page 1 and 2: CML MONITORING INTHE TKI ERAYasser
Page 3 and 4: 2008 WHO CLASSIFICATION OF MPNsPhil
Page 5 and 6: CML Phases5Chronic-phase CML (WHO):
Page 7 and 8: CML: Findings in PBMyelocyteBasophi
Page 9 and 10: Cytogenetic analysisKaryotype:Stand
Page 11 and 12: 11Philadelphia chromosome
Page 13 and 14: 13Iso (17)
Page 15 and 16: Fluorescent In Situ Hybridization(F
Page 17: 17Locations of the breakpoints in t
Page 20 and 21: 20RQ-PCR amplification assays:measu
Page 22 and 23: Use of a conversion factor to conve
Page 24 and 25: ELN 2009: Definitions of ResponseRe
Page 30 and 31: RESISTANCE TO IMATINIB1ry Resistanc
Page 33 and 34: 33Suboptimal response defined by RQ
Page 35 and 36: 13th Congress of the European He
Page 37 and 38: PFS100= 2 log reductions (n=59)
Page 39 and 40: BCR-ABL kinase domain mutations1. D
Page 41 and 42: Mutations critical for 2 nd generat
Page 43 and 44: ABL KINASE DOMAIN MUTATIONS IN IMAT
Page 45 and 46: Faster and deeper molecular respons
Page 47 and 48: Predictive Value of Pretreatment BC
Page 49: 49Thank you!

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