Interleukin 7 and thymic stromal lymphopoietin: From immunity to leukemia

Noa Tal, Chen Shochat, Ifat Geron, Dani Bercovich, Shai Izraeli

Research output: Contribution to journalReview articlepeer-review

39 Scopus citations

Abstract

Cancer is often caused by deregulation of normal developmental processes. Here, we review recent research on the aberrant activation of two hematopoietic cytokine receptors in acute lymphoid leukemias. Somatic events in the genes for thymic stromal lymphopoietin and Interleukin 7 receptors as well as in their downstream JAK kinases result in constitutive ligand-independent activation of survival and proliferation in B and T lymphoid precursors. Drugs targeting these receptors or the signaling pathways might provide effective therapies of these leukemias.

Original languageEnglish
Pages (from-to)365-378
Number of pages14
JournalCellular and Molecular Life Sciences
Volume71
Issue number3
DOIs
StatePublished - Feb 2014
Externally publishedYes

Bibliographical note

Funding Information:
The “hijacking” of the TSLP receptor by the aberrant expression of CRLF2 probably provides some survival advantage for B cell precursors, but is insufficient for leukemic transformation. This hypothesis is supported by the detection of additional mutations in the TSLP pathway in the majority of leukemias overexpressing CRLF2. These mutations are either in CRLF2 and IL7RA subunits of the TSLP receptor or in the signaling components downstream (Fig. a).

Funding

The “hijacking” of the TSLP receptor by the aberrant expression of CRLF2 probably provides some survival advantage for B cell precursors, but is insufficient for leukemic transformation. This hypothesis is supported by the detection of additional mutations in the TSLP pathway in the majority of leukemias overexpressing CRLF2. These mutations are either in CRLF2 and IL7RA subunits of the TSLP receptor or in the signaling components downstream (Fig. a).

FundersFunder number
Waxman Cancer Foundation
Israel Cancer Research Fund
Swiss Re Foundation
Israel Science Foundation

    Keywords

    • CRLF2
    • IL7 receptor alpha
    • JAK1
    • JAK2
    • Leukemia
    • Thymic stromal lymphopoietin

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