Evidence map›Paper›PMID 12509463›Full record

ArticleMolecular and cellular biology2003

Growth suppression of pre-T acute lymphoblastic leukemia cells by inhibition of notch signaling.

Andrew P Weng, Yunsun Nam, Michael S Wolfe, Warren S Pear, James D Griffin, Stephen C Blacklow, Jon C Aster

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
201citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

201 citing papers in PubMed, 1 synthesis or guideline pooled it, 371 citations in OpenAlex.

  1. Pooled it
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  12. Notch-Sox9 Axis Mediates Hepatocyte Dedifferentiation inInternational journal of molecular sciences · 2022
    Article
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  19. Targeting Notch and EGFR signaling in human mucoepidermoid carcinoma.Signal transduction and targeted therapy · 2021
    Article
  20. Genome-Wide Analysis IdentifiesFrontiers in cell and developmental biology · 2021
    Article

141 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Andrew P WengDepartments of Pathology, Brigham and Women's Hospital, Harvard Medical School. Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Yunsun Nam
Michael S Wolfe
Warren S Pear
James D Griffin
Stephen C Blacklow
Jon C Aster
Harvard University · USBrigham and Women's Hospital · USDana-Farber Cancer Institute · USUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Constitutive NOTCH signaling in lymphoid progenitors promotes the development of immature T-cell lymphoblastic neoplasms (T-ALLs). Although it is clear that Notch signaling can initiate leukemogenesis, it has not previously been established whether continued NOTCH signaling is required to maintain T-ALL growth. We demonstrate here that the blockade of Notch signaling at two independent steps suppresses the growth and survival of NOTCH1-transformed T-ALL cells. First, inhibitors of presenilin specifically induce growth suppression and apoptosis of a murine T-ALL cell line that requires presenilin-dependent proteolysis of the Notch receptor in order for its intracellular domain to translocate to the nucleus. Second, a 62-amino-acid peptide derived from a NOTCH coactivator, Mastermind-like-1 (MAML1), forms a transcriptionally inert nuclear complex with NOTCH1 and CSL and specifically inhibits the growth of both murine and human NOTCH1-transformed T-ALLs. These studies show that continued growth and survival of NOTCH1-transformed lymphoid cell lines require nuclear access and transcriptional coactivator recruitment by NOTCH1 and identify at least two steps in the Notch signaling pathway as potential targets for chemotherapeutic intervention.

Indexed as

Receptors, Cell SurfaceSignal TransductionTranscription FactorsAllelesAnimalsApoptosisBlotting, NorthernBlotting, WesternCell CycleCell DivisionCell LineCell Line, TransformedChromosome MappingDNA-Binding ProteinsDose-Response Relationship, DrugDown-RegulationDNA-Binding ProteinsGreen Fluorescent ProteinsLuminescent ProteinsMAML1 protein, humanMembrane ProteinsNOTCH1 protein, humanNotch1 protein, mouseNuclear ProteinsPeptidesPresenilin-1PSEN1 protein, humanReceptor, Notch1Receptors, Cell SurfaceReceptors, NotchRecombinant Fusion ProteinsTrans-ActivatorsTranscription Factors

Identifiers

PMID12509463
PMCPMC151540
OpenAlexW2127125400

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.