Journal
BLOOD
Volume 134, Issue 25, Pages 2242-2248Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood.2019000622
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Funding
- National Institutes of Health, National Heart, Lung, and Blood Institute [R01 HL131835]
- Starr Cancer Consortium [I9-A9-059]
- MPN Research Foundation
- Gabrielle's Angel Foundation for Cancer Research
- K12 award from the National Institutes of Health, National Cancer Insititute [K12CA087723]
- Sanchez and Ferguson Research Faculty Award
- American Society of Hematology-Harold Amos Medical Faculty Development Program award
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Recurrent mutations in calreticulin are present in similar to 20% of patients with myeloproliferative neoplasms (MPNs). Since its discovery in 2013, we now have a more precise understanding of how mutant CALR, an endoplasmic reticulum chaperone protein, activates the JAK/STAT signaling pathway via a pathogenic binding interaction with the thrombopoietin receptor MPL to induce MPNs. In this Spotlight article, we review the current understanding of the biology underpinning mutant CALR-driven MPNs, discuss clinical implications, and highlight future therapeutic approaches.
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