ArticleeLife2016
Neural stem cell-encoded temporal patterning delineates an early window of malignant susceptibility in Drosophila.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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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.
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Who cites it
53 citing papers in PubMed, 80 citations in OpenAlex.
- Psc and Su(z)2 safeguard intestinal stem cell identity and prevent chinmo-dependent tumorigenesis.EMBO reports · 2026Article
- A tumor-suppressive role of the PRC1 Polycomb epigenetic complex in the maintenance of adult Drosophila intestinal stem cell identity.PLoS genetics · 2026Article
- Age-related decline in niche self-renewal factors drives testis aging via Hairless, Imp, and Chinmo.Science advances · 2026Article
- Temporal neuronal differentiation programs safeguard neuronal diversity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Decoding neuronal diversity: Mechanisms governing neural cell fate in Drosophila.Current opinion in neurobiology · 2025Review
- In vivo AGO-APP identifies a module of microRNAs cooperatively preserving neural progenitors.PLoS genetics · 2025Article
- Epigenetic Regulation in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025Review
- DNA repair in tumor radioresistance: insights from fruit flies genetics.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Seven-up acts in neuroblasts to specify adult central complex neuron identity and initiate neuroblast decommissioning.Development (Cambridge, England) · 2024Article
- Spt5 interacts genetically with Myc and is limiting for brain tumor growth inLife science alliance · 2024Article
- Seven-up acts in neuroblasts to specify adult central complex neuron identity and initiate neuroblast decommissioning.bioRxiv : the preprint server for biology · 2023Article
- 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 · 2023Article
- Dedifferentiation-derived neural stem cells exhibit perturbed temporal progression.EMBO reports · 2023Article
- CRISPR/Cas9 and FLP-FRT mediated regulatory dissection of the BX-C of Drosophila melanogaster.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Article
- Review
- Imp and Syp mediated temporal patterning of neural stem cells in the developing Drosophila CNS.Genetics · 2022Review
- Single cell RNA-seq analysis reveals temporally-regulated and quiescence-regulated gene expression in Drosophila larval neuroblasts.Neural development · 2022Article
- Regulation of developmental hierarchy inScience advances · 2022Article
- chinmo-mutant spermatogonial stem cells cause mitotic drive by evicting non-mutant neighbors from the niche.Developmental cell · 2022Article
- Non-autonomous regulation of neurogenesis by extrinsic cues: aOxford open neuroscience · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Pediatric neural tumors are often initiated during early development and can undergo very rapid transformation. However, the molecular basis of this early malignant susceptibility remains unknown. During Drosophila development, neural stem cells (NSCs) divide asymmetrically and generate intermediate progenitors that rapidly differentiate in neurons. Upon gene inactivation, these progeny can dedifferentiate and generate malignant tumors. Here, we find that intermediate progenitors are prone to malignancy only when born during an early window of development while expressing the transcription factor Chinmo, and the mRNA-binding proteins Imp/IGF2BP and Lin-28. These genes compose an oncogenic module that is coopted upon dedifferentiation of early-born intermediate progenitors to drive unlimited tumor growth. In late larvae, temporal transcription factor progression in NSCs silences the module, thereby limiting mitotic potential and terminating the window of malignant susceptibility. Thus, this study identifies the gene regulatory network that confers malignant potential to neural tumors with early developmental origins.
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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.