# Molecular and Functional Platelet Abnormalities in Myeloproliferative Neoplasms

**Authors:** Ann X. Wang, Belinda B. Guo, Matthew D. Linden

PMC · DOI: 10.3390/cells15060555 · Cells · 2026-03-19

## TL;DR

This review explores how platelet abnormalities in myeloproliferative neoplasms (MPNs) offer insights into disease mechanisms and potential biomarkers for diagnosis and risk assessment.

## Contribution

The paper highlights novel platelet-based biomarkers and molecular signatures for understanding and managing MPNs.

## Key findings

- Platelets in MPNs show functional and molecular changes that reflect disease pathophysiology.
- Platelet transcriptomics and proteomics can identify disease-specific signatures in MPNs.
- Platelet-based approaches may improve diagnosis, prognosis, and risk stratification in MPNs.

## Abstract

Blood platelets are derived from megakaryocytes with functions extending beyond hemostasis to inflammation, immunity, and cancer. Myeloproliferative neoplasms (MPNs) are clonal stem cell disorders driven by somatic mutations affecting JAK-STAT signaling, leading to excessive myeloid proliferation. Thrombosis affects approximately one-fifth of patients at diagnosis and remains elevated throughout the disease course, while the paradoxical coexistence of bleeding further complicates clinical management. In addition, MPNs may progress to advanced disease stages, including bone marrow fibrosis and transformation to acute myeloid leukemia, leading to ineffective hematopoiesis, worsening symptom burden, and poor clinical outcomes. This review outlines how peripherally circulating platelets provide a unique window into MPN pathophysiology, with emphasis on their functional and molecular abnormalities. We summarize current understanding of platelet-mediated hemostatic imbalance across MPN subtypes. We discuss the potential of platelet transcriptomics and proteomics to reveal disease-specific signatures. We further highlight emerging platelet-associated candidates with potential utility as dynamic biomarkers for both the pathological marrow niche and thrombotic and bleeding risk. Together, these insights underscore the potential of platelet-based approaches to complement existing diagnostic and prognostic strategies in MPNs.

## Linked entities

- **Diseases:** myeloproliferative neoplasms (MONDO:0020076), acute myeloid leukemia (MONDO:0015667)

## Full-text entities

- **Genes:** VWF (von Willebrand factor) [NCBI Gene 7450] {aka F8VWF, VWD}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, JAK1 (Janus kinase 1) [NCBI Gene 3716] {aka AIIDE, JAK1A, JAK1B, JTK3}, LGALS1 (galectin 1) [NCBI Gene 3956] {aka GAL1, GBP}, CEP55 (centrosomal protein 55) [NCBI Gene 55165] {aka C10orf3, CT111, MARCH, URCC6}, H2AX (H2A.X variant histone) [NCBI Gene 3014] {aka H2A.X, H2A/X, H2AFX}, THPO (thrombopoietin) [NCBI Gene 7066] {aka CAMT2, MGDF, MKCSF, ML, MPLLG, THC9}, STAT5A (signal transducer and activator of transcription 5A) [NCBI Gene 6776] {aka MGF, STAT5}, SELP (selectin P) [NCBI Gene 6403] {aka CD62, CD62P, GMP140, GRMP, LECAM3, PADGEM}, GP6 (glycoprotein VI platelet) [NCBI Gene 51206] {aka BDPLT11, GPIV, GPVI}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, CALR (calreticulin) [NCBI Gene 811] {aka CALR1, CRT, HEL-S-99n, RO, SSA, cC1qR}, MPL (MPL proto-oncogene, thrombopoietin receptor) [NCBI Gene 4352] {aka C-MPL, CD110, MPLV, THCYT2, THPOR, TPOR}, SERPINH1 (serpin family H member 1) [NCBI Gene 871] {aka AsTP3, CBP1, CBP2, HSP47, OI10, PIG14}, HSP90B2P (heat shock protein 90 beta family member 2, pseudogene) [NCBI Gene 7190] {aka GRP94P1, GRP94b, HSP, HSPCP2, TRA1P1, TRAP1}, AURKA (aurora kinase A) [NCBI Gene 6790] {aka AIK, ARK1, AURA, BTAK, PPP1R47, STK15}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, CD34 (CD34 molecule) [NCBI Gene 947], CD40LG (CD40 ligand) [NCBI Gene 959] {aka CD154, CD40L, HIGM1, IGM, IMD3, T-BAM}, JAK2 (Janus kinase 2) [NCBI Gene 3717] {aka JTK10}, RAP1B (RAP1B, member of RAS oncogene family) [NCBI Gene 5908] {aka K-REV, RAL1B, THC11}, CCND1 (cyclin D1) [NCBI Gene 595] {aka BCL1, D11S287E, PRAD1, U21B31}, TPO (thyroid peroxidase) [NCBI Gene 7173] {aka MSA, TDH2A, TPX}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, HSPB2 (heat shock protein family B (small) member 2) [NCBI Gene 3316] {aka HSP27, Hs.78846, LOH11CR1K, MKBP}
- **Diseases:** Platelet Hypofunction (MESH:D000309), cardiovascular disease (MESH:D002318), thrombocytosis (MESH:D013922), hemostatic defects (MESH:D020141), MF (MESH:D055728), injury to (MESH:D014947), ET (MESH:D013920), PV (MESH:D011087), Bleeding (MESH:D006470), stroke (MESH:D020521), tumorigenesis (MESH:D063646), platelet abnormalities (MESH:D001791), vascular injury (MESH:D057772), gastrointestinal or intracranial hemorrhage (MESH:D006471), metastasis (MESH:D009362), AML (MESH:D015470), lymphoid malignancies (MESH:D008223), hypercoagulability (MESH:D019851), thromboembolic (MESH:D013923), thrombocytopenia (MESH:D013921), Thrombosis (MESH:D013927), inflammation (MESH:D007249), AvWS (MESH:D014842), hematologic malignancies (MESH:D019337), fibrotic disorders (MESH:D009358), platelet count abnormalities (MESH:D011225), myocardial infarction (MESH:D009203), fibrosis (MESH:D005355), MPNs (MESH:D009369)
- **Chemicals:** baricitinib (MESH:C000596027), Ca2+ (-), ruxolitinib (MESH:C540383), MLN8237 (MESH:C550258), aspirin (MESH:D001241), thromboxane (MESH:D013931)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]
- **Mutations:** serine/threonine, MPLW515L, JAK2 (V617F

## Full text

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## Figures

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## References

87 references — full list in the complete paper: https://tomesphere.com/paper/PMC13024808/full.md

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Source: https://tomesphere.com/paper/PMC13024808