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Targeted therapy of polycytemia vera patients

D I Shikhbabaeva, V A Shuvaev, I S Martynkevich

    Voprosy Onkologii
    |November 27, 2018
    PubMed

    Insights

    The JAK2V617F mutation discovery revolutionized myeloproliferative neoplasms (MPN) research. Targeted JAK inhibitors offer new hope for polycythemia vera (PV) patients resistant to standard treatments.

    Area of Science:

    • Hematology
    • Oncology
    • Molecular Biology

    Background:

    • The JAK2V617F mutation is central to the pathophysiology of Philadelphia chromosome-negative myeloproliferative neoplasms (MPN).
    • This mutation has emerged as a critical therapeutic target, particularly in polycythemia vera (PV).

    Purpose of the Study:

    • To review the molecular-genetic basis of polycythemia vera (PV) pathogenesis.
    • To explore novel therapeutic strategies, specifically JAK inhibitors, for PV treatment.
    • To assess the efficacy and safety of JAK inhibitors in patients resistant or intolerant to standard therapies.

    Main Methods:

    • Literature review of molecular-genetic features in PV pathogenesis.
    • Review of studies on JAK inhibitors as targeted therapy for PV.
    • Analysis of clinical trial data, including the RESPONSE trial for ruxolitinib.

    Main Results:

    • JAK2 mutation identification opened new avenues for understanding and treating Ph-negative MPN.
    • JAK inhibitors represent a significant advancement in targeted therapy for PV.
    • Ruxolitinib demonstrated efficacy and safety in clinical trials for PV patients.

    Conclusions:

    • Targeted therapy with JAK inhibitors offers improved outcomes and quality of life for PV patients.
    • Understanding JAK2 mutation is key to developing effective treatments for MPN.
    • JAK inhibitors are a promising alternative for patients with hydroxycarbamide or interferon-refractory PV.

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