ArticleLeukemia2007
Epigenetic alterations complement mutation of JAK2 tyrosine kinase in patients with BCR/ABL-negative myeloproliferative disorders.
Article in Leukemia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- DNA Methylation in Ph-Negative Myeloproliferative Neoplasms: Prognostic Role and Therapeutic Implications.Current issues in molecular biology · 2025Review
- Molecular Genetics of Thrombotic Myeloproliferative Neoplasms: Implications in Precision Oncology.Diagnostics (Basel, Switzerland) · 2023Review
- Molecular determinants of pathogenesis and clinical phenotype in myeloproliferative neoplasms.Haematologica · 2017Review
- Myelofibrosis: an update on drug therapy in 2016.Expert opinion on pharmacotherapy · 2016Review
- miR-203 and miR-221 regulate SOCS1 and SOCS3 in essential thrombocythemia.Blood cancer journal · 2016Article
- The role of small adaptor proteins in the control of oncogenic signalingr driven by tyrosine kinases in human cancer.Oncotarget · 2016Review
- Article
- Rapid and robust reversion to essential thrombocythemia on treatment with Decitabine in a case of hydroxyurea-induced t-MDS/AML.Clinical case reports · 2016Article
- JAK kinase targeting in hematologic malignancies: a sinuous pathway from identification of genetic alterations towards clinical indications.Haematologica · 2015Review
- SOCS proteins in regulation of receptor tyrosine kinase signaling.Cellular and molecular life sciences : CMLS · 2014Review
- Mechanistic insights into activation and SOCS3-mediated inhibition of myeloproliferative neoplasm-associated JAK2 mutants from biochemical and structural analyses.The Biochemical journal · 2014Article
- The role of suppressors of cytokine signalling in human neoplasms.Molecular biology international · 2014Review
- Genetic basis of MPN: Beyond JAK2-V617F.Current hematologic malignancy reports · 2013Review
- Methylation profiling of SOCS1, SOCS2, SOCS3, CISH and SHP1 in Philadelphia-negative myeloproliferative neoplasm.Journal of cellular and molecular medicine · 2013Article
- JAK2 mutants (e.g., JAK2V617F) and their importance as drug targets in myeloproliferative neoplasms.JAK-STAT · 2013Review
- SOCS, inflammation, and cancer.JAK-STAT · 2013Review
- JAK/STAT signaling in hematological malignancies.Oncogene · 2013Review
- SOCS proteins in development and disease.American journal of clinical and experimental immunology · 2013Article
- Epigenetic dysregulation of secreted frizzled-related proteins in myeloproliferative neoplasms complements the JAK2V617F-mutation.Clinical epigenetics · 2012Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An acquired autoactivating mutation with a V617F amino-acid substitution in the JAK2 tyrosine kinase is frequently found in BCR/ABL-negative myeloproliferative disorders (MPD). Hypermethylation of CpG islands within gene promoter regions is associated with transcriptional inactivation and represents an important mechanism of gene silencing in the pathogenesis of hematopoietic malignancies. In this study, we determined the DNA methylation status of 13 cancer-related genes in the context of JAK2 mutations in 39 patients with MPD. Genes analyzed for hypermethylation were SOCS-1, SHP-1, E-cadherin, MGMT, TIMP-2, TIMP-3, p15, p16, p73, DAPK1, RASSF1A, RARbeta2 and hMLH1. We found at least one hypermethylated gene in 15/39 MPD patient specimens, and in 6/39 samples aberrant methylation of the negative cytokine regulator SOCS-1 was present. The JAK2V617F mutation was found in 21/39 patients as determined by allele-specific polymerase chain reaction. Hypermethylation of SOCS-1 was observed in 3/21 patients with an autoactivating JAK2 mutation and in 3/18 patients with wild-type JAK2. Our results suggest that epigenetic inactivation of SOCS-1 may be a complementary mechanism to the JAK2V617F mutation in the pathogenesis of MPD that leads to dysregulation of JAK-STAT signal transduction and thus contributes to growth factor hypersensitivity.
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