ReviewCancer journal (Sudbury, Mass.)
Genetics of myeloproliferative neoplasms.
Review in Cancer journal (Sudbury, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- JAK2 rs10974944 is associated with both V617F-positive and negative myeloproliferative neoplasms in a Vietnamese population: A potential genetic marker.Molecular genetics & genomic medicine · 2022Pooled it
- Causal Association Between Thyroid Function and Myeloproliferative Disease: A Two-Sample Mendelian Randomization Study.International journal of endocrinology · 2026Article
- Review
- Molecular Genetics of Thrombotic Myeloproliferative Neoplasms: Implications in Precision Oncology.Diagnostics (Basel, Switzerland) · 2023Review
- The Contribution ofInternational journal of molecular sciences · 2022Review
- Inhibition of proinflammatory signaling impairs fibrosis of bone marrow mesenchymal stromal cells in myeloproliferative neoplasms.Experimental & molecular medicine · 2022Article
- The JAK-STAT pathway: an emerging target for cardiovascular disease in rheumatoid arthritis and myeloproliferative neoplasms.European heart journal · 2021Article
- The Role of Neutrophilic Granulocytes in Philadelphia Chromosome Negative Myeloproliferative Neoplasms.International journal of molecular sciences · 2021Review
- Genomic Analysis of Hematopoietic Stem Cell at the Single-Cell Level: Optimization of Cell Fixation and Whole Genome Amplification (WGA) Protocol.International journal of molecular sciences · 2020Article
- The Rationale for Immunotherapy in Myeloproliferative Neoplasms.Current hematologic malignancy reports · 2019Review
- ASXL1 mutations in Chinese patients with essential thrombocythemia.Experimental and therapeutic medicine · 2018Article
- JAK inhibitors for the treatment of myeloproliferative neoplasms and other disorders.F1000Research · 2018Review
- Review
- Monocyte-Macrophages and T Cells in Atherosclerosis.Immunity · 2017Review
- Mass cytometry analysis reveals hyperactive NF Kappa B signaling in myelofibrosis and secondary acute myeloid leukemia.Leukemia · 2017Article
- LNK/SH2B3 Loss of Function Promotes Atherosclerosis and Thrombosis.Circulation research · 2016Article
- Poly (ADP-Ribose) Polymerase Inhibitor Hypersensitivity in Aggressive Myeloproliferative Neoplasms.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Review
- Role of tyrosine-kinase inhibitors in myeloproliferative neoplasms: comparative lessons learned.OncoTargets and therapy · 2016Review
- Crystal Structure of the FERM-SH2 Module of Human Jak2.PloS one · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In the last decade, genomic studies have identified multiple recurrent somatic mutations in myeloproliferative neoplasms (MPNs). Beginning with the discovery of the JAK2 V617F mutation, multiple additional mutations have been found that constitutively activate cell-signaling pathways, including MPL, CBL, and LNK. Furthermore, several classes of epigenetic modifiers have also been identified, in patients with MPN, revealing a requirement for mutations in other pathways to cooperate with JAK-STAT pathway mutations in MPN pathogenesis. Mutations in the de novo DNA methylation protein, DNMT3A, demethylation machinery, TET2 and related IDH1/2 production of oncometabolite 2-hydroxygluterate, and polycomb complex proteins EZH2 and ASXL1 have opened new pathophysiologic clues into these diseases. The prognostic relevance of these novel disease alleles remains an important area of investigation, and clinical trials are currently underway to determine if these findings represent tractable therapeutic targets, either alone, or in combination with JAK2 inhibition.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.