The Philadelphia chromosome in leukemogenesis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-12

AUTHORS

Zhi-Jie Kang, Yu-Fei Liu, Ling-Zhi Xu, Zi-Jie Long, Dan Huang, Ya Yang, Bing Liu, Jiu-Xing Feng, Yu-Jia Pan, Jin-Song Yan, Quentin Liu

ABSTRACT

The truncated chromosome 22 that results from the reciprocal translocation t(9;22)(q34;q11) is known as the Philadelphia chromosome (Ph) and is a hallmark of chronic myeloid leukemia (CML). In leukemia cells, Ph not only impairs the physiological signaling pathways but also disrupts genomic stability. This aberrant fusion gene encodes the breakpoint cluster region-proto-oncogene tyrosine-protein kinase (BCR-ABL1) oncogenic protein with persistently enhanced tyrosine kinase activity. The kinase activity is responsible for maintaining proliferation, inhibiting differentiation, and conferring resistance to cell death. During the progression of CML from the chronic phase to the accelerated phase and then to the blast phase, the expression patterns of different BCR-ABL1 transcripts vary. Each BCR-ABL1 transcript is present in a distinct leukemia phenotype, which predicts both response to therapy and clinical outcome. Besides CML, the Ph is found in acute lymphoblastic leukemia, acute myeloid leukemia, and mixed-phenotype acute leukemia. Here, we provide an overview of the clinical presentation and cellular biology of different phenotypes of Ph-positive leukemia and highlight key findings regarding leukemogenesis. More... »

PAGES

48

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/s40880-016-0108-0

    DOI

    http://dx.doi.org/10.1186/s40880-016-0108-0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1006279816

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27233483


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