ArticleFrontiers in oncology2026
FDX1 is associated with CALR abundance and JAK-STAT-related inflammatory signaling in myeloproliferative neoplasms.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Myeloproliferative neoplasms (MPNs) are driven by constitutive cytokine-receptor signaling, yet the metabolic programs associated with driver genotype and inflammatory remodeling remain incompletely defined. Methods: Here we integrated a 60-case clinical MPN cohort, the GSE174060 Affymetrix Human Transcriptome Array 2.0 microarray dataset, immune deconvolution, exploratory feature prioritization, the GSE228995 mouse single-cell RNA sequencing (scRNA-seq) dataset, human-sample validation, and functional perturbation assays to investigate whether cuproptosis-related metabolism is associated with total calreticulin (CALR) abundance and Janus kinase-signal transducer and activator of transcription (JAK-STAT)-related inflammatory signaling. GSE174060 included 36 samples: 6 essential thrombocythemia (ET), 11 polycythemia vera (PV), 9 primary myelofibrosis (PMF), 4 secondary myelofibrosis (SMF), and 6 healthy control (HC) samples. Results: Clinically, CALR-mutated cases were enriched for thrombocytosis and distinctive megakaryocytic abnormalities, while inflammatory and fibrotic features tracked with higher interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and lactate dehydrogenase (LDH). Microarray-based transcriptomic analyses identified an MPN-associated cuproptosis-related and immune-response program, and consensus clustering separated samples into exploratory transcriptomic clusters. Within this expression-derived partition, Discussion: These findings support an association between FDX1 perturbation, total CALR abundance, STAT5-associated signaling, and inflammatory output in MPN, but do not establish direct regulation of mutant CALR or mutant CALR-MPL signaling.
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