PMID- 26637731
OWN - NLM
STAT- MEDLINE
DCOM- 20161005
LR  - 20161230
IS  - 1520-4383 (Electronic)
IS  - 1520-4383 (Linking)
VI  - 2015
DP  - 2015
TI  - Molecular monitoring in CML and the prospects for treatment-free remissions.
PG  - 257-63
LID - 10.1182/asheducation-2015.1.257 [doi]
AB  - Monitoring treatment responses in chronic myeloid leukemia (CML) is based on 
      complete blood counts (CBCs) to determine hematologic response, karyotyping of 
      bone marrow metaphase cells to delineate cytogenetic response and quantitative 
      reverse transcription polymerase chain reaction (qPCR) to quantify expression of 
      BCR-ABL1 mRNA (molecular response; MR) in peripheral blood. Fluorescence in situ 
      hybridization (FISH) to identify BCR-ABL1 in interphase nuclei and mutational 
      analysis of the BCR-ABL1 kinase domain (KD) are used in certain clinical 
      circumstances. As most patients treated with tyrosine kinase inhibitors (TKIs) 
      achieve complete cytogenetic responses (CCyRs), qPCR with its increased 
      sensitivity and dynamic range has become the main tool used to monitor CML 
      patients. Landmark analyses of large TKI trials have established MR milestones 
      that identify patients with high risk of failure, are the basis of consensus 
      management guidelines, and have led to a strong push toward qPCR test 
      standardization. Today many laboratories report BCR-ABL1 qPCR results on the 
      international scale (IS), a system based on the conversion of laboratory-specific 
      numerical values to conform to a universal scale. The fact that qPCR is 
      technically demanding and liable to assay variations poses considerable 
      challenges for its routine clinical use. This is important as the prevalence of 
      patients on chronic TKI therapy increases and critical clinical decisions are 
      made based on qPCR results, for example if discontinuation of TKI therapy should 
      be considered. Here we will review the current state of molecular monitoring in 
      CML, focusing on qPCR, the definition of TKI failure and the results of TKI 
      discontinuation studies.
CI  - (c) 2015 by The American Society of Hematology. All rights reserved.
FAU - Deininger, Michael W
AU  - Deininger MW
AD  - Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah; and 
      Division of Hematology and Hematologic Malignancies, The University of Utah, Salt 
      Lake City, Utah.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Hematology Am Soc Hematol Educ Program
JT  - Hematology. American Society of Hematology. Education Program
JID - 100890099
RN  - 0 (Protein Kinase Inhibitors)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.2 (Fusion Proteins, bcr-abl)
SB  - IM
MH  - Blood Cell Count
MH  - DNA Mutational Analysis
MH  - Fusion Proteins, bcr-abl/metabolism
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*diagnosis/drug therapy/genetics
MH  - Medical Oncology/methods
MH  - Mutation
MH  - Polymerase Chain Reaction
MH  - Prognosis
MH  - Protein Kinase Inhibitors/therapeutic use
MH  - Protein Structure, Tertiary
MH  - Protein-Tyrosine Kinases/antagonists & inhibitors
MH  - Remission Induction
MH  - Risk
EDAT- 2015/12/08 06:00
MHDA- 2016/10/07 06:00
CRDT- 2015/12/06 06:00
PHST- 2015/12/06 06:00 [entrez]
PHST- 2015/12/08 06:00 [pubmed]
PHST- 2016/10/07 06:00 [medline]
AID - 2015/1/257 [pii]
AID - 10.1182/asheducation-2015.1.257 [doi]
PST - ppublish
SO  - Hematology Am Soc Hematol Educ Program. 2015;2015:257-63. doi: 
      10.1182/asheducation-2015.1.257.