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 |
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Pages (from-to) | 365-378 |
Number of pages | 14 |
Journal | Cellular and Molecular Life Sciences |
Volume | 71 |
Issue number | 3 |
DOIs | |
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 | Funder number |
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Waxman Cancer Foundation | |
Israel Cancer Research Fund | |
Swiss Re Foundation | |
Israel Science Foundation |
Keywords
- CRLF2
- IL7 receptor alpha
- JAK1
- JAK2
- Leukemia
- Thymic stromal lymphopoietin