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Technical aspects and clinical applications of measuring BCR‐ABL1 transcripts number in chronic myeloid leukemia
American journal of hematology, 2009-08, Vol.84 (8), p.517-522
Foroni, Letizia
Gerrard, Gareth
Nna, Emmanuel
Khorashad, Jamshid Sorouri
Stevens, David
Swale, Bryony
Milojkovic, Dragana
Reid, Alistair
Goldman, John
Marin, David
2009
Details
Autor(en) / Beteiligte
Foroni, Letizia
Gerrard, Gareth
Nna, Emmanuel
Khorashad, Jamshid Sorouri
Stevens, David
Swale, Bryony
Milojkovic, Dragana
Reid, Alistair
Goldman, John
Marin, David
Titel
Technical aspects and clinical applications of measuring BCR‐ABL1 transcripts number in chronic myeloid leukemia
Ist Teil von
American journal of hematology, 2009-08, Vol.84 (8), p.517-522
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2009
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by a triphasic clinical course, the morphologic expansion of a terminally differentiated myeloid cell and the presence of the BCR‐ABL1 fusion gene, the hallmark of CML. The fusion gene is usually, but not always, associated with a Philadelphia chromosome, the result of a reciprocal exchange of genetic material between chromosome 22 and chromosome 9, which leads to the production of the activated BCR‐ABL1 gene and oncoprotein. The breakpoint in the BCR gene occurs commonly downstream of exons e13 or e14 (M‐BCR) and less frequently downstream of exons e1 and e2 (m‐BCR). Less than 1% of cases carry a breakpoint downstream of exon 6 or 8 (“variant fusion genes”) or exon 19 (μ‐BCR). Breakpoints in the ABL1 gene cluster upstream of exon a2 (or of exon a3 in less than 5% of patients with CML). Conventional cytogenetic, fluorescence in situ hybridization, and molecular testing for the BCR‐ABL1 fusion gene are key investigations for the diagnosis and monitoring of CML. Treatment using tyrosine kinase inhibitors has revolutionized the management of CML with hematologic and cytogenetic response within 12–18 months observed in >85% of patients. Nevertheless, between 15 and 20% of patients may evolve to blastic phase. Measurement of low level or “minimal” residual disease using molecular tests is becoming the gold‐standard approach to measure response to therapy due to its higher sensitivity compared to other routine techniques. The technical aspects and clinical applications of molecular monitoring will be the main focus of this article. Am. J. Hematol., 2009. © 2009 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0361-8609
eISSN: 1096-8652
DOI: 10.1002/ajh.21457
Titel-ID: cdi_proquest_miscellaneous_746053521
Format
–
Schlagworte
Biological and medical sciences
,
Chromosomes, Human, Pair 22 - genetics
,
Chromosomes, Human, Pair 22 - metabolism
,
Chromosomes, Human, Pair 9 - genetics
,
Chromosomes, Human, Pair 9 - metabolism
,
Exons - genetics
,
Fusion Proteins, bcr-abl - antagonists & inhibitors
,
Fusion Proteins, bcr-abl - biosynthesis
,
Fusion Proteins, bcr-abl - genetics
,
Hematologic and hematopoietic diseases
,
Humans
,
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy
,
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology
,
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
,
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
,
Medical sciences
,
Monitoring, Physiologic - methods
,
Neoplasm, Residual
,
Philadelphia Chromosome
,
Protein Kinase Inhibitors - therapeutic use
,
Remission Induction
,
RNA, Messenger - biosynthesis
,
RNA, Messenger - genetics
,
RNA, Neoplasm - biosynthesis
,
RNA, Neoplasm - genetics
,
Time Factors
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