Evidence map›Paper›PMID 26657768›Full record

ArticleDevelopment (Cambridge, England)2016

Genes implicated in stem cell identity and temporal programme are directly targeted by Notch in neuroblast tumours.

Evanthia Zacharioudaki, Benjamin E Housden, George Garinis, Robert Stojnic, Christos Delidakis, Sarah J Bray

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Notch Signaling in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025
    Review
  2. Article
  3. Indirect neurogenesis in space and time.Nature reviews. Neuroscience · 2024
    Review
  4. Article
  5. Growth deregulation and interaction with host hemocytes contribute to tumor progression in a Drosophila brain tumor model.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  7. Review
  8. Article
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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

6 authors at 3 institutions in 2 countries.

Evanthia ZacharioudakiDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3DY, UK Institute of Molecular Biology and Biotechnology, FORTH-Hellas, Heraklion, Crete 70013, Greece Department of Biology, University of Crete, Heraklion, Greece GR71409.
Benjamin E HousdenDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3DY, UK.
George GarinisInstitute of Molecular Biology and Biotechnology, FORTH-Hellas, Heraklion, Crete 70013, Greece Department of Biology, University of Crete, Heraklion, Greece GR71409.
Robert StojnicDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3DY, UK Cambridge Systems Biology Centre, University of Cambridge, Cambridge CB2 1QR, UK.
Christos DelidakisInstitute of Molecular Biology and Biotechnology, FORTH-Hellas, Heraklion, Crete 70013, Greece Department of Biology, University of Crete, Heraklion, Greece GR71409 delidaki@imbb.forth.gr sjb32@cam.ac.uk.
Sarah J BrayDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3DY, UK delidaki@imbb.forth.gr sjb32@cam.ac.uk.
University of Cambridge · GBFoundation for Research and Technology Hellas · GRUniversity of Crete · GR

Funding

Medical Research Council G0800034Medical Research Council MR/L007177/1
6 · The paper itself

Abstract

Notch signalling is involved in a multitude of developmental decisions and its aberrant activation is linked to many diseases, including cancers. One example is the neural stem cell tumours that arise from constitutive Notch activity in Drosophila neuroblasts. To investigate how hyperactivation of Notch in larval neuroblasts leads to tumours, we combined results from profiling the upregulated mRNAs and mapping the regions bound by the core Notch pathway transcription factor Su(H). This identified 246 putative direct Notch targets. These genes were highly enriched for transcription factors and overlapped significantly with a previously identified regulatory programme dependent on the proneural transcription factor Asense. Included were genes associated with the neuroblast maintenance and self-renewal programme that we validated as Notch regulated in vivo. Another group were the so-called temporal transcription factors, which have been implicated in neuroblast maturation. Normally expressed in specific time windows, several temporal transcription factors were ectopically expressed in the stem cell tumours, suggesting that Notch had reprogrammed their normal temporal regulation. Indeed, the Notch-induced hyperplasia was reduced by mutations affecting two of the temporal factors, which, conversely, were sufficient to induce mild hyperplasia on their own. Altogether, the results suggest that Notch induces neuroblast tumours by directly promoting the expression of genes that contribute to stem cell identity and by reprogramming the expression of factors that could regulate maturity.

Indexed as

AnimalsDrosophilaDrosophila melanogasterDrosophila ProteinsNeural Stem CellsReceptors, NotchTranscription FactorsDrosophila ProteinsReceptors, NotchTranscription FactorsDrosophilaGene regulationNeuroblastNotchStem cell

Identifiers

PMID26657768
PMCPMC4725341
OpenAlexW2288694327

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.