Rev Bras Hematol Hemoter 2015 Jan-Feb;37(1):55-7. Epub 2014 Nov 26.
Hospital Privado - Centro Médico de Córdoba, Córdoba, Argentina.
Leukemia 2019 10 27;33(10):2358-2364. Epub 2019 Aug 27.
Institute of Hematology "Lorenzo and Ariosto Seràgnoli", Department of Experimental, Diagnostic and Specialty Medicine, S.Orsola-Malpighi University Hospital, University of Bologna, Bologna, Italy.
Chronic myeloid leukemia is driven by a hybrid gene, BCR-ABL1, that codes for a leukemogenic tyrosine kinase (TK) protein of 210 KDa (p210). Resistance to TK inhibitor (TKI) therapy occurs in relatively few patients, no more than 10%, while persistence of minimal residual disease during TKI therapy occurs in the great majority of patients. Resistance is a cause of death, persistence is compatible with a fairly normal length and quality of life, but may require lifelong treatment. Read More
Acta Haematol 2020 9;143(2):96-111. Epub 2019 Aug 9.
International Research Centre for Medical Sciences, Kumamoto University, Kumamoto, Japan.
The treatment of chronic myeloid leukaemia (CML) requires quantitative polymerase chain reaction (qPCR) to monitor BCR-ABL1 in International Scale (IS). Some normal subjects were found to harbour BCR-ABL1. We performed a systematic review on normal subjects harbouring BCR-ABL1. Read More
Mol Genet Genomic Med 2019 08 17;7(8):e809. Epub 2019 Jun 17.
Medical Research Unit, College of Medicine, Al-Nahrain University, Baghdad, Iraq.
Background: Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the presence of BCR-ABL fusion gene (GenBank accession NC_000022.11). In the vast majority of CML patients, the typical subtype of BCR-ABL transcript are b3a2, b2a2 or both. Read More
Indian J Pathol Microbiol 2019 Apr-Jun;62(2):256-260
Department of Hematology, All India Institute of Medical Sciences, New Delhi, India.
Background: Philadelphia chromosome (Ph): Hallmark of CML is caused by reciprocal translocation between chromosomes 9 and 22 resulting in BCR-ABL fusion protein. Most commonly associated breakpoint with CML is M-bcr in exon 13 or exon 14, producing splice variant b2a2 or b3a2 respectively. The distribution of these transcripts and their influence on clinico-hematological parameters is variable. Read More
Leuk Res 2018 06 4;69:47-53. Epub 2018 Apr 4.
Department of Clinical Laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, PR China. Electronic address:
Fast identification of BCR-ABL fusion genes is critical for precise diagnosis, risk stratification and therapy scheme selection in leukemia. More convenient methods are needed for quickly detection of the BCR-ABL fusion genes. Multiplex fluorescent reverse transcription quantitative real-time PCR (Multiplex RT-qPCR) methods are developed for detection of the at least 14 subtypes of BCR-ABL fusion genes in one tube at a time by using patients' bone marrow samples. Read More