The Biology and Pathogenesis of Chronic Myeloid Leukemia View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2016

AUTHORS

Bradley Chereda , Junia V. Melo

ABSTRACT

Chronic myeloid leukaemia (CML) is a myeloproliferative disorder of the haemopoietic stem cell. Understanding the molecular biology of CML began with the discovery of the Philadelphia chromosome. This genomic abnormality is the result of a t(9;22) translocation, which gives origin to a BCR-ABL1 fusion gene. The research focus thereafter shifted to characterising the functional consequence of BCR-ABL1. It was demonstrated that this fusion protein is capable of hijacking a vast repertoire of cellular functions to drive myeloid hyperplasia, which is characteristic of the initial, chronic phase of the disease. Without successful intervention, it will progress into blast crisis, resembling an acute leukaemia, which is aggressive and invariably fatal. Although it is hypothesised that additional genomic/genetic alterations are needed for this evolution, the exact causes have yet to be defined. The answer behind advanced disease may be intertwined with the other unsolved issue in CML, that being characterisation of primitive CML cells. This chapter introduces the clinical and cell biology of CML and describes examples of genes with important roles for CML stem cell abnormalities and blast crisis. More... »

PAGES

17-39

References to SciGraph publications

Book

TITLE

Chronic Myeloid Leukemia

ISBN

978-3-319-33197-3
978-3-319-33198-0

Author Affiliations

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-319-33198-0_2

DOI

http://dx.doi.org/10.1007/978-3-319-33198-0_2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1020245126


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203 schema:description Chronic myeloid leukaemia (CML) is a myeloproliferative disorder of the haemopoietic stem cell. Understanding the molecular biology of CML began with the discovery of the Philadelphia chromosome. This genomic abnormality is the result of a t(9;22) translocation, which gives origin to a BCR-ABL1 fusion gene. The research focus thereafter shifted to characterising the functional consequence of BCR-ABL1. It was demonstrated that this fusion protein is capable of hijacking a vast repertoire of cellular functions to drive myeloid hyperplasia, which is characteristic of the initial, chronic phase of the disease. Without successful intervention, it will progress into blast crisis, resembling an acute leukaemia, which is aggressive and invariably fatal. Although it is hypothesised that additional genomic/genetic alterations are needed for this evolution, the exact causes have yet to be defined. The answer behind advanced disease may be intertwined with the other unsolved issue in CML, that being characterisation of primitive CML cells. This chapter introduces the clinical and cell biology of CML and describes examples of genes with important roles for CML stem cell abnormalities and blast crisis.
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