Contemporary and future strategies in polycythemia vera.
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Summary
None of the existing therapies have proven the ability to deplete the underlying malignant clone, or definitively reduce the risk of disease, leaving a large area of unmet need.
- Type
- review
- Published
- 2022-06-01
- Cited by
- 2
- References
- 83
- OpenAlex
- https://openalex.org/W4289830475
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:251377744
Keywords
Polycythemia vera, Medicine, Myelofibrosis, Intensive care medicine, Constitutional symptoms
References
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- Busulfan in patients with polycythemia vera or essential thrombocythemia refractory or intolerant to hydroxyurea
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- Past, present, and future hepatitis C treatments.
- Somatic mutations of JAK2 exon 12 in patients with JAK2 (V617F)-negative myeloproliferative disorders.
- Cardiovascular events and intensity of treatment in polycythemia vera.
- JAK2V617F negatively regulates p53 stabilization by enhancing MDM2 via La expression in myeloproliferative neoplasms
- A phase II study of Givinostat in combination with hydroxycarbamide in patients with polycythaemia vera unresponsive to hydroxycarbamide monotherapy
- Histone Deacetylase Inhibitors: Potential in Cancer Therapy
- Combination treatment in vitro with Nutlin, a small-molecule antagonist of MDM2, and pegylated interferon-α 2a specifically targets JAK2V617F-positive polycythemia vera cells.
- Mechanisms of Thrombogenesis in Polycythemia Vera
- The histone deacetylase inhibitor ITF2357 selectively targets cells bearing mutated JAK2V617F
- Platelet activation and inhibition in polycythemia vera and essential thrombocythemia.
- Aspirin-insensitive thromboxane biosynthesis in essential thrombocythemia is explained by accelerated renewal of the drug target.
- Long-term survival and blast transformation in molecularly annotated essential thrombocythemia, polycythemia vera, and myelofibrosis.
- Hepcidin and iron regulation, 10 years later.
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