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Journal ArticleDOI

Thrombosis in myeloproliferative neoplasms: update in pathophysiology.

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TLDR
In this article, a review summarizes high-impact research in myeloproliferative neoplasms (MPN) from the last 18 months, with a particular focus on basic science findings.
Abstract
Purpose of review This review summarizes high-impact research in myeloproliferative neoplasms (MPN) from the last 18 months, with a particular focus on basic science findings. Recent findings A pseudo-hypoxia state with stabilization of hypoxia-inducible factor (HIFα exists that is central to cell growth, cell renewal, inflammation, and thrombotic potential in MPN hematopoietic cells. Summary HIFα and inflammatory pathways are new therapeutic targets in MPN, with the potential to ameliorate thrombotic risk and perhaps eradicate mutant progenitor cells.

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Citations
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Journal ArticleDOI

Thrombosis in myeloproliferative neoplasms: A clinical and pathophysiological perspective

TL;DR: In this article, the authors outline the incidence, nature, and risk factors for thrombosis in MPNs, give an overview of the mechanisms underlying hypercoagulability and discusses prevention and treatment considerations.
Journal ArticleDOI

Clinical features associated with thrombotic events in children with myeloproliferative neoplasms

TL;DR: Myeloproliferative neoplasms are rare clonal bone marrow disorders characterized by overproduction of mature blood cells, thrombotic complications, and predisposition to progress to acute myeloid leukemia.
References
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Journal ArticleDOI

The evolutionary dynamics and fitness landscape of clonal hematopoiesis

TL;DR: It is shown that positive selection, not drift, is the major force shaping clonal hematopoiesis, and bounds on the number of hematoietic stem cells are provided, and the fitness advantages of key pathogenic variants, at single-nucleotide resolution, as well as the distribution of fitness effects within commonly mutated driver genes.
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Monocyte Conversion During Inflammation and Injury

TL;DR: A brief review of monocytes in mice highlights the plasticity of monocyte subsets and their conversion during inflammation and injury.
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Activation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia.

TL;DR: It is proposed that an early proinflammatory state in the venous milieu, orchestrated by the HIF-induced NLRP3 inflammasome complex, is a key determinant of acute thrombotic events during hypoxic conditions.