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Open research questions in Myeloproliferative Neoplasms: Diagnosis and Treatment

109 gap statements mined from Myeloproliferative Neoplasms: Diagnosis and Treatment papers in our 4.5M-paper local library, which holds 642 papers on the topic — drawn mostly from each paper's own stated research gap, future-work, challenge and limitation notes, and its abstract. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one.

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What the literature leaves open

  • Although standardized proce- dures and clinical integration are still lacking, studies indicate that quantitative JAK2 allele burden may aid in guiding thera- peutic decisions and tracking treatment response [9, 17, 24].

    Polycythaemia Vera and JAK2 Variant: A Molecular Perspective on Diagnosis and Management · 2026 · DOI

  • Post-transplant strategies, such as maintenance therapies and measurable residual dis- ease (MRD)-guided approaches, are critical considerations that warrant further exploration.

    Treosulfan-Based Conditioning in Allogeneic Stem Cell Transplantation for Myelofibrosis: A Systematic Review · 2026 · DOI

  • Few studies have evaluated the role of alloHSCT, focusing specifically in patients with BP-MF[15–17]. However, the optimal bridging therapy before transplantation remains controversial, and in daily clinical practice, it should be selected primarily based on the patient's performance status.

    Outcomes of allogeneic hematopoietic stem cell transplantation in patients with blast phase myelofibrosis: molecular signature and intensive chemotherapy matter · 2026 · DOI

  • The next phase of progress in MF will depend on better predictive biomarkers, more standardized use of genomic data, earlier identification of biologically aggressive disease, and more deliberate integration of clinical-trial strategies into routine care. Combination therapy and biologically matched approaches may further shift practice away from symptom control alone, but their value will still depend on whether they improve meaningful clinical outcomes in clearly defined patient subsets (6, 13, 19). Equally important is the refinement of selection frameworks that help clinicians decide when a JAK inhibitor is sufficient, when it

    Precision medicine in myelofibrosis: from molecular profiling to personalized therapy · 2026 · DOI

  • The ability of RBCs to promote thrombosis is multifactorial, with several underlying mechanisms that are probably needed in concert. Although RBCs are not known to be the drivers of thrombotic events, the studies cited in this review are important elements supporting the active role of RBCs in this pathological manifestation in PV and ET. While the direct relationship between a high red cell count and thrombosis is well-known, the intrinsic defects of RBCs from PV and ET patients are new contributors that need to be investigated in depth in order to elucidate their role and pave the way for new biomarkers (Table 1) and therapeutical strategies. Table 1. RBC-related biomarkers for prediction of thrombotic events in PV and ET patients.

    Red Blood Cell Contribution to Thrombosis in Polycythemia Vera and Essential Thrombocythemia · 2024 · DOI

  • Prospective studies with longer follow-up are warranted to validate these survival outcomes and evaluate the long-term safety of early cytore- ductive intervention in low-risk patients.

    Clinical Profile and Treatment Outcomes of Polycythemia Vera: A Single-Center Retrospective Study from North India · 2026 · DOI

  • As a con- ceptual framework, however, the thrombotic niche remains to be prospectively validated, and future work must deter- mine whether it improves prediction or treatment selection beyond existing risk models before it can be considered a clinically actionable construct.

    Beyond the JAK2 mutation: The inflammasome, clonal stability, and the thrombotic niche in myeloproliferative neoplasms · 2026 · DOI

  • 2 Strengths and limitations This study has several noteworthy strengths. Further investigation of predictive biomarkers, including baseline allele burden and mutational profile, may help identify patients most likely to benefit from therapy.

    Efficacy and safety of ropeginterferon in myeloproliferative neoplasms: a systematic review and meta-analysis · 2026 · DOI

  • While the association between cancer and heart failure (HF) is well recognised, most cardio-oncology studies concentrate on systolic dysfunction and HFrEF, leaving HFpEF underexplored.

    More than blood: echocardiographic evidence of HFpEF in polycythemia vera · 2026 · DOI

  • Whilst malignant context directs the role of HIFs within oncogenesis, these mechanisms are not well characterised.

    JAK2V617F reprograms Hypoxia Inducible Factor-1 to induce a non-canonical hypoxia regulon in myeloproliferative neoplasms · 2026 · DOI

  • Whether elevated counts increase thrombosis risk, define a distinct clinical subtype, or influence disease progression has not been systematically explored.

    Clinical and molecular characterization of thrombocytosis in transient abnormal myelopoiesis · 2026 · DOI

  • INTRODUCTION: Aquagenic pruritus (AP) is an underrecognized condition in which patients perceive itch following contact with water on clinically non-lesional skin.

    Aquagenic Pruritus Questionnaire: Predicting Myeloproliferative Neoplasms in Patients with Aquagenic Pruritus · 2025 · DOI

  • The significance of ruxolitinib-induced JAK2 hyperphosphorylation is not well understood.

    Ruxolitinib mediated paradoxical JAK2 hyperphosphorylation is due to the protection of activation loop tyrosines from phosphatases · 2025 · DOI

  • However, studies directly comparing patient- and physician-reported ratings are lacking.

    Comparison of recognition of symptom burden in MPN between patient- and physician-reported assessment – an intraindividual analysis by the German Study Group for MPN (GSG-MPN) · 2025 · DOI

  • Despite the activation of JAK/STAT signaling and its influence on the proliferation of malignant cells is well studied in patient samples and JAK2- and CALR-mutated cell systems, there exists limited information about the link between interferon (IFN)-γ signaling and bone marrow (BM) environment alterations.

    Association of the composition of the bone marrow tumor microenvironment in BCR::ABL1-negative myeloproliferative neoplasms with IFN-γ signaling and driver mutations · 2025 · DOI

  • Weakly activating JAK2 germline variants have been associated with MPN risk, but the underlying mechanisms remain unclear.

    Germline Jak2-R1063H mutation interferes with normal hematopoietic development and increases risk of thrombosis and leukemic transformation · 2025 · DOI

  • However, the association between CHIP and the risk of pulmonary embolism remains unknown.

    Clonal hematopoiesis of indeterminate potential and the risk of pulmonary embolism: an observational study · 2024 · DOI

  • Crizotinib carries an FDA hepatotoxicity warning, yet analysis of the FAERS database suggests that the severity of its hepatotoxicity risks, including progression to hepatitis and liver failure, might be underreported.

    The involvement of the Stat1/Nrf2 pathway in exacerbating Crizotinib-induced liver injury: implications for ferroptosis · 2024 · DOI

  • However, the underlying mechanism remains poorly understood, and effective intervention strategies are lacking.

    The involvement of the Stat1/Nrf2 pathway in exacerbating Crizotinib-induced liver injury: implications for ferroptosis · 2024 · DOI

  • Further study of the role of EMH may offer valuable insights into emergency hematopoiesis and therapeutic approaches against cancer.

    Extramedullary hematopoiesis in cancer · 2024 · DOI

  • Myeloproliferative neoplasms (MPN) are associated with inferior pregnancy outcome, however, little is known about fertility and childbearing potential in women with MPN.

    Childbirth rates in women with myeloproliferative neoplasms · 2024 · DOI

  • Although multiple genetic events are thought to play a role in promoting progression of the myeloproliferative neoplasms (MPN), the individual events that are associated with the development of more aggressive disease phenotypes remain poorly defined.

    HMGA2 overexpression with specific chromosomal abnormalities predominate in CALR and ASXL1 mutated myelofibrosis · 2024 · DOI

  • Due to the relatively small population of this subgroup persons, multi-center collaboration is warranted to verify this hypothesis.

    Concerns regarding myelofibrosis-type megakaryocyte dysplasia · 2024 · DOI

  • The lack of a well-validated model that includes molecular predictors of thrombosis. The need for more research to validate associations for markers other than JAK2.

    Genomic profiling for thrombosis risk prediction in myeloproliferative neoplasms · 2026 · DOI

  • The study identifies a gap in the understanding of mitochondrial dysfunction in JAK2 V617F-positive MPN patients. The study highlights the need for further research into the underlying mechanisms of mitochondrial dysfunction in MPN patients.

    Analysis of mitochondrial function and antioxidant capacity in JAK2 V617F-positive chronic myeloproliferative neoplasms · 2026 · DOI

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109 gap statements have been mined from Myeloproliferative Neoplasms: Diagnosis and Treatment papers in our 4.5M-paper local library, which holds 642 papers on the topic; the gaps come from whichever of those papers state one. They are mostly the research gaps the authors state and the papers' abstracts, plus future-work, limitations and challenges passages. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one, so you can read the original claim in context.

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