Myeloproliferative Neoplasms: Diagnosis and Treatment

Inhibition of RhoA-mediated secretory autophagy in megakaryocytes mitigates myelofibrosis in mice

The paper shows that inhibiting RhoA-mediated secretory autophagy in megakaryocytes reduces cytokine secretion and fibrosis in a mouse model of myelofibrosis.

HIF-1 activated by PIM1 assembles a pathological transcription complex and regulon that drives JAK2V617F MPN disease

This study identifies that HIF-1 activation by PIM1 in JAK2V617F-MPNs drives non-canonical transcription complex formation and disease progression.

Wnt-dependent spatiotemporal reprogramming ofbone marrow niches drives fibrosis

The paper shows that Wnt-dependent reprogramming of bone marrow niches drives fibrosis by activating osteolineage cells and altering hematopoietic support.

Logical modelling of myelofibrotic microenvironment predicts dysregulated progenitor stem cell crosstalk

The paper constructs a logical model of the myelofibrotic microenvironment to predict how TPO and TLR signaling disrupt stem cell crosstalk and drive disease progression.

Platelet transcriptome yields progressive markers in chronic myeloproliferative neoplasms and identifies putative targets of therapy

The paper identifies platelet transcriptome markers for predicting disease progression in MPNs and develops a machine learning model to predict advanced MF with high accuracy.

Endothelial JAK2V617F mutation leads to thrombosis, vasculopathy, and cardiomyopathy in a murine model of myeloproliferative neoplasm

This study shows that JAK2V617F mutation in endothelial cells causes thrombosis, vasculopathy, and cardiomyopathy in a murine MPN model, suggesting targeting vasculature as a therapeutic strategy.