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Article

FBW7 mutations in leukemic cells mediate NOTCH pathway activation and resistance to gamma-secretase inhibitors.

The Journal of experimental medicine - 6 Aug 2007

O'Neil Jennifer, Grim Jonathan, Strack Peter, Rao Sudhir, Tibbitts Deanne, Winter Christopher, Hardwick James, Welcker Markus, Meijerink Jules P, Pieters Rob, Draetta Giulio, Sears Rosalie, Clurman Bruce E, Look A Thomas

Abstract excerpt

gamma-secretase inhibitors (GSIs) can block NOTCH receptor signaling in vitro and therefore offer an attractive targeted therapy for tumors dependent on deregulated NOTCH activity. To clarify the basis for GSI resistance in T cell acute lymphoblastic leukemia (T-ALL), we studied T-ALL cell lines...

Read the complete abstract on PubMed

Topics

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Share to Amyloid Precursor Protein Secretases
Share to Cell Cycle

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Enzyme Inhibitors

Share to F-Box Proteins

Share to F-Box-WD Repeat-Containing Protein 7

Share to Leukemia

Share to Receptors, Notch

Share to Ubiquitin-Protein Ligases

Source

Open in PubMed Open full text

Identifiers

PMID: 17646409
DOI: 10.1084/jem.20070876
PMCID: PMC2118656

Genes

MYC
NOTCH1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-17646409-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

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FBW7 mutations in leukemic cells mediate NOTCH pathway activation and resistance to gamma-secretase inhibitors.PMID 17646409Read ↗

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Oncogenic NOTCH1 control of MYC and PI3K: challenges and opportunities for anti-NOTCH1 therapy in T-cell acute lymphoblastic leukemias and lymphomas.Semantic proximity Read ↗

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