Novel Advances in the Molecular Understanding 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 June 2025 | Viewed by 2460
Special Issue Editors
2. Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China
Interests: MPNs; leukemia; lymphoma; CAR-T; HSCT; GVHD
Interests: Chinese medicine; pharmacology; anti-aging; anti-inflammation
Interests: hematopoiesis; megakaryocytes; myeloproliferative neoplasms; acute myeloid leukemia; myelodysplastic syndrome
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Myeloproliferative neoplasms (MPNs) encompass a diverse group of hematologic malignancies, including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF), as well as post-PV-MF and post-ET-MF. Progression to acute leukemia represents the most dreaded complication of the disease and a significant cause of mortality in MPN patients.
MPNs present a wide spectrum of clinical manifestations and molecular abnormalities, complicating their diagnosis, classification, and treatment. Common driver mutations, such as Janus kinase 2 (JAK2), calreticulin (CALR), and myeloproliferative leukemia virus oncogene (MPL), lead to the constitutive activation of the JAK/STAT signaling pathway, a hallmark of MPN pathogenesis. These driver mutations are essential for the MPN phenotype. Concurrent somatic mutations, including transcription factors (e.g., Runx1), epigenetic regulators (e.g., TET2, ASXL1, and DNMT3A), signaling molecules (e.g., JAKs and NRAS), and splicing factors (e.g., SRSF2 and SF3B), also contribute to MPN development.
Recent advancements in understanding the molecular pathogenesis and genetics of MPNs have prompted the investigation of various therapeutic agents targeting constitutively activated JAK/STAT with JAK inhibitors, such as ruxolitinib, fedratinib, pacritinib, and momelotinib, as well as MEK and ERK kinase inhibitors. While these treatments effectively alleviate clinical symptoms, none have demonstrated the ability to reduce mutant allele burden. The challenge lies in translating scientific discoveries into effective therapies to address this unmet medical need for MPN patients.
This Special Issue aims to present the latest advances in exploring the molecular landscape of MPNs, offering a comprehensive overview of the role of molecular abnormalities in pathogenesis and discussing how these findings might guide treatments targeting vulnerabilities and reduce mutant allele burden in MPNs.
Dr. Wei Chen
Dr. Fei Li
Dr. Qiang Jeremy Wen
Guest Editors
Manuscript Submission Information
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Keywords
- MPNs
- ET
- PV
- PMF
- post-PV-MF
- post-ET-MF
- MDS/MPN
- JAK2
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