Beyond JAK Inhibition: Molecular Pathogenesis and Novel Therapeutic Strategies for the Treatment of Myeloproliferative Neoplasms (MPNs)
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".
Deadline for manuscript submissions: 30 April 2024 | Viewed by 3187
Special Issue Editor
Special Issue Information
Dear Colleagues,
The BCR/ABL-negative myeloproliferative neoplasms (MPNs), driven by mutations in JAK2, calreticulin (CALR), or the thrombopoietin receptor (MPL), are unified by the presence of constitutive JAK/STAT signaling. As such, JAK inhibitors have become an important therapeutic approach for treating MPN patients, particularly those with myelofibrosis for whom hematopoietic stem cell transplantation (HSCT) is not an option. However, although these agents impart profound clinical benefit, they are not curative and fail to alter disease progression.
Because of the shared presence of aberrant JAK/STAT signaling, MPN driver mutations have long been thought of as overlapping in their mechanisms of hematopoietic transformation. However, in recent years, evidence of their distinct molecular and cellular effects has begun to emerge. Understanding the mechanisms underlying the differential molecular pathogenesis of each MPN driver, and exploiting this knowledge to identify unique, targetable dependencies for each mutation, will help to move the needle towards the development of novel, highly specific and potentially curative treatment strategies for MPNs.
This Special Issue will highlight work that sheds light on the molecular mechanisms underlying the pathogenesis of mutant JAK2, CALR, and MPL-driven MPNs, and the targetable dependencies unique to each that may represent new therapeutic avenues. This work will provide invaluable insight into the future of MPN treatment, in which the elucidation of basic molecular mechanisms will give way to rationally designed therapies and precision medicine to cure patients without HSCT.
Dr. Shannon Elisabeth Elf
Guest Editor
Manuscript Submission Information
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Keywords
- philadelphia-negative myeloproliferative neoplasms (MPNs)
- mechanisms of disease pathogenesis
- novel molecular dependencies
- molecular targeted therapies
- immunotherapies
