Inhibition of acute lymphoblastic leukaemia by a Jak-2 inhibitor View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1996-02

AUTHORS

Naftaly Meydan, Tom Grunberger, Harjit Dadi, Michal Shahar, Enrico Arpaia, Zvi Lapidot, J. Steven Leeder, Melvin Freedman, Amos Cohen, Aviv Gazit, Alexander Levitzki, Chaim M. Roifman

ABSTRACT

ACUTE lymphoblastic leukaemia (ALL) is the most common cancer of childhood. Despite the progress achieved in its treatment, 20% of cases relapse and no longer respond to chemotherapy. The most common phenotype of ALL cells share surface antigens with very early precursors of B cells and are therefore believed to originate from this lineage1,3Characterization of the growth requirement of ALL cells indicated that they were dependent on various cytokines, suggesting paracrine and/or autocrine growth regulation4–6. Because many cytokines induce tyrosine phosphorylation in lymphoid progenitor cells, and constitutive tyrosine phosphorylation is commonly observed in B-lineage leukaemias7,8, attempts have been made to develop protein tyrosine kinase (PTK) blockers of leukaemia cell growth9,10. Here we show that leukaemic cells from patients in relapse have con-stitutively activated Jak-2 PTK. Inhibition of Jak-2 activity by a specific tyrosine kinase blocker, AG-490, selectively blocks leukaemic cell growthin vitro and in vivo by inducing programmed cell death, with no deleterious effect on normal haematopoiesis. More... »

PAGES

645-648

Journal

TITLE

Nature

ISSUE

6566

VOLUME

379

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/379645a0

    DOI

    http://dx.doi.org/10.1038/379645a0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1027170927

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/8628398


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