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Article

Epigenetic alteration of SOCS family members is a possible pathogenetic mechanism in JAK2 wild type myeloproliferative diseases.

International journal of cancer - 1 Oct 2008

Teofili Luciana, Martini Maurizio, Cenci Tonia, Guidi Francesco, Torti Lorenza, Giona Fiorina, Foà Robin, Leone Giuseppe, Larocca Luigi Maria

Abstract excerpt

In polycythemia vera (PV) and essential thrombocythemia (ET) specific JAK2 mutations constitutively activate the JAK-STAT pathway, explaining biologic findings such as endogenous erythroid colony (EECs) growth or PRV-1 RNA overexpression. Since these markers are detected also in JAK2 wild type patients, we hypothesized that, in these cases, the activation of the JAK-STAT pathway could be produced by a...

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Source

Identifiers

PMID: 18623127
DOI: 10.1002/ijc.23694

Genes

JAK2
MPL

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Epigenetic alteration of SOCS family members is a possible pathogenetic mechanism in JAK2 wild type myeloproliferative diseases.PMID 18623127Read ↗

Methylation of the suppressor of cytokine signaling 3 gene (SOCS3) in myeloproliferative disorders.Semantic proximity Read ↗

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The myeloproliferative disorder-associated JAK2 V617F mutant escapes negative regulation by suppressor of cytokine signaling 3.Semantic proximity Read ↗

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Hypermethylation of the suppressor of cytokine signalling‐1 (<i>SOCS‐1</i>) in myelodysplastic syndromeSemantic proximity Read ↗

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