ArticleGenes & development2011
Regulation of cell growth by Notch signaling and its differential requirement in normal vs. tumor-forming stem cells in Drosophila.
Article in Genes & development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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.
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.
Who cites it
62 citing papers in PubMed, 85 citations in OpenAlex.
- Temporal neuronal differentiation programs safeguard neuronal diversity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dual mitotic bookmarking by GAF and H3K27ac orchestrates differential propagation of cell fate memory in neural development.Nature communications · 2025Article
- Arf1 and ARFGEF2/Sec71 control neuroblast polarity by anchoring nonmuscle myosin II.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Notch Signaling in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025Review
- From the Making of a Neural Lineage to the Making of a Tumor: Lessons from the "Simple" Drosophila Brain.Advances in experimental medicine and biology · 2025Review
- The TRIM-NHL RNA-binding protein Brain Tumor coordinately regulates expression of the glycolytic pathway and vacuolar ATPase complex.Nucleic acids research · 2024Article
- Translation stalling induced mitochondrial entrapment of ribosomal quality control related proteins offers cancer cell vulnerability.Research square · 2024Article
- Ribosome stalling duringPNAS nexus · 2024Article
- The IRE1/Xbp1 axis restores ER and tissue homeostasis perturbed by excess Notch in Drosophila.Developmental biology · 2024Article
- Article
- The transcription elongation factors Spt4 and Spt5 control neural progenitor proliferation and are implicated in neuronal remodeling duringFrontiers in cell and developmental biology · 2024Article
- Ribogenesis boosts controlled by HEATR1-MYC interplay promote transition into brain tumour growth.EMBO reports · 2024Article
- Reverse Electron Transport at Mitochondrial Complex I in Ischemic Stroke, Aging, and Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Characterization of the Notch pathway in nasal polyps of patients with chronic rhinosinusitis: A pilot study.Physiological reports · 2022Article
- Regulation of reverse electron transfer at mitochondrial complex I by unconventional Notch action in cancer stem cells.Developmental cell · 2022Article
- Regulation of Neural Stem Cell Competency and Commitment during Indirect Neurogenesis.International journal of molecular sciences · 2021Review
- Tumor models in various Drosophila tissues.WIREs mechanisms of disease · 2021Review
- Molecular and biological functions of TRIM-NHL RNA-binding proteins.Wiley interdisciplinary reviews. RNA · 2021Review
- Homeodomain protein Six4 prevents the generation of supernumerary Drosophila type II neuroblasts and premature differentiation of intermediate neural progenitors.PLoS genetics · 2021Article
- MYC in Brain Development and Cancer.International journal of molecular sciences · 2020Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cancer stem cells (CSCs) are postulated to be a small subset of tumor cells with tumor-initiating ability that shares features with normal tissue-specific stem cells. The origin of CSCs and the mechanisms underlying their genesis are poorly understood, and it is uncertain whether it is possible to obliterate CSCs without inadvertently damaging normal stem cells. Here we show that a functional reduction of eukaryotic translation initiation factor 4E (eIF4E) in Drosophila specifically eliminates CSC-like cells in the brain and ovary without having discernable effects on normal stem cells. Brain CSC-like cells can arise from dedifferentiation of transit-amplifying progenitors upon Notch hyperactivation. eIF4E is up-regulated in these dedifferentiating progenitors, where it forms a feedback regulatory loop with the growth regulator dMyc to promote cell growth, particularly nucleolar growth, and subsequent ectopic neural stem cell (NSC) formation. Cell growth regulation is also a critical component of the mechanism by which Notch signaling regulates the self-renewal of normal NSCs. Our findings highlight the importance of Notch-regulated cell growth in stem cell maintenance and reveal a stronger dependence on eIF4E function and cell growth by CSCs, which might be exploited therapeutically.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.