Interleukin 7 and thymic stromal lymphopoietin: From immunity to leukemia

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

doi:10.1007/s00018-013-1337-x

Interleukin 7 and thymic stromal lymphopoietin: From immunity to leukemia

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

Sheba Medical Center at Tel Hashomer
Tel Aviv University
Migal Galilee Technology Center Israel
Tel Hai Academic College
University of California at San Diego

Research output: Contribution to journal › Review article › peer-review

42 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 language	English
Pages (from-to)	365-378
Number of pages	14
Journal	Cellular and Molecular Life Sciences
Volume	71
Issue number	3
DOIs	https://doi.org/10.1007/s00018-013-1337-x
State	Published - Feb 2014
Externally published	Yes

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).

Funders
Waxman Cancer Foundation
Israel Cancer Research Fund
Swiss Re Foundation
Israel Science Foundation

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

CRLF2
IL7 receptor alpha
JAK1
JAK2
Leukemia
Thymic stromal lymphopoietin

Access to Document

10.1007/s00018-013-1337-x

Cite this

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title = "Interleukin 7 and thymic stromal lymphopoietin: From immunity to leukemia",

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.",

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author = "Noa Tal and Chen Shochat and Ifat Geron and Dani Bercovich and Shai Izraeli",

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). ",

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AU - Izraeli, Shai

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AB - 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.

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Interleukin 7 and thymic stromal lymphopoietin: From immunity to leukemia

Abstract

Bibliographical note

Funding

UN SDGs

Keywords

Access to Document

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