Mutation-Driven S100A8 Overexpression Confers Aberrant Phenotypes in Type 1 -Mutated MPN.

Numerous pathogenic exon 9 mutations have been identified in myeloproliferative neoplasms (MPN), with type 1 (52bp deletion; ) and type 2 (5bp insertion; ) being the most prevalent. Despite the universal pathobiology of MPN driven by various mutants, it is unclear why different mutations result in diverse clinical phenotypes. Through RNA sequencing followed by validation at the protein and mRNA levels, we found that S100A8 was specifically enriched in but not in MPN-model cells.

The Genomic Landscape in Philadelphia-Negative Myeloproliferative Neoplasm Patients with Second Cancers.

Patients with myeloproliferative neoplasms (MPNs) are characterized by systemic inflammation. With the indolent nature of the diseases, second cancers (SCs) have emerged as a challenging issue in afflicted patients. Epidemiological studies have confirmed the excessive risk of SCs in MPNs, but little is known about their molecular basis.

Clinicopathological characteristics and treatment outcome in obese patients with diffuse large B-cell lymphoma.

Background: Aberrant MYC and BCL2 expression, cell of origin (COO), and National Comprehensive Cancer Network international prognostic index (NCCN-IPI) are commonly used for risk assessment and treatment decision in patients with diffuse large B-cell lymphoma (DLBCL). Although obesity has been shown to be of predictive value in DLBCL patients, it remains unclear whether it retains its prognostic relevance after those aforementioned novel factors being taken into consideration.

Methods: Patients with DLBCL were identified retrospectively in a single institute and data were collected through electronic databases and pharmacy records.

Real-world experience with Ropeginterferon-alpha 2b (Besremi) in Philadelphia-negative myeloproliferative neoplasms.

Background/purpose: Ropeginterferon alpha-2b (Ropeg) is a novel pegylated interferon-alpha recently approved for the treatment of polycythemia vera (PV) in Europe. However, other than data from clinical trials, little is known about this agent in real world practice.

Methods: A compassionate use program employing Ropeg for treating patients with unmet medical need was initiated in Taiwan in 2017.

Molecular heterogeneity unravelled by single-cell transcriptomics in patients with essential thrombocythaemia.

Significant phenotypic heterogeneity exists in patients with all subtypes of myeloproliferative neoplasms (MPN), including essential thrombocythaemia (ET). Single-cell RNA sequencing (scRNA-Seq) holds the promise of unravelling the biology of MPN at an unprecedented level of resolution. Herein we employed this approach to dissect the transcriptomes in the CD34 cells from the peripheral blood of seven previously untreated ET patients and one healthy adult.

Enhanced Risk for Specific Somatic Myeloproliferative Neoplastic Mutations in Patients with Stroke.

Background: Somatic mutations of Janus kinase 2 (JAK2V617F), calreticulin (CALR), and myeloproliferative leukemia virus oncogene (MPL) are the major clonal molecules that drive the pathogenesis of myeloproliferative neoplasms (MPN). It is well recognized that MPN patients carry an excessive risk of thrombohemorrhagic complications. However, little is known about the prevalence of these clonal markers in patients with cerebral vascular disease.

Aberrant let7a/HMGA2 signaling activity with unique clinical phenotype in -mutated myeloproliferative neoplasms.

High mobility group AT-hook 2 (HMGA2) is an architectural transcription factor that is negatively regulated by microRNA through binding to it's 3'-untranslated region. Transgenic mice expressing with a truncation of its 3'-untranslated region has been shown to exhibit a myeloproliferative phenotype. To decipher the axis in myeloproliferative neoplasms, we employed an model supplemented with clinical correlation.