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Article

Epigenetic regulation of the Ink4a-Arf (Cdkn2a) tumor suppressor locus in the initiation and progression of Notch1-driven T cell acute lymphoblastic leukemia.

Experimental hematology - 1 Apr 2013

Volanakis Emmanuel J, Boothby Mark R, Sherr Charles J

Abstract excerpt

Activating mutations of NOTCH1 and deletion of the INK4A-ARF (CDKN2A) tumor suppressor locus are two of the most frequent genetic alterations in T cell acute lymphoblastic leukemia (T-ALL). In a murine model of T-ALL induced by the intracellular domain of Notch1 (ICN1), the genetic interaction between ICN1 signaling and Arf inactivation is developmentally stage-specific, with a more pronounced requirement for Arf...

Topics

Animals
Binding Sites
Bone Marrow Cells
Cell Line
Cell Transformation, Neoplastic
Cells, Cultured
Coculture Techniques
Cyclin-Dependent Kinase Inhibitor p16
Disease Progression
Dogs

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Epigenesis, Genetic

Flow Cytometry

Gene Expression

Mice

Mice, Inbred C57BL

Mice, Knockout

Mice, Transgenic

Mutation

Source

Open in PubMed Open full text

Identifiers

PMID: 23178376
DOI: 10.1016/j.exphem.2012.11.006
PMCID: PMC3860824

Genes

NOTCH1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-23178376-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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Epigenetic regulation of the Ink4a-Arf (Cdkn2a) tumor suppressor locus in the initiation and progression of Notch1-driven T cell acute lymphoblastic leukemia.PMID 23178376Read ↗

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