ArticleDevelopmental cell2019
Oncogenic Notch Triggers Neoplastic Tumorigenesis in a Transition-Zone-like Tissue Microenvironment.
Article in Developmental cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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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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.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Macrophage restriction inScience advances · 2026Article
- Leptin Acts as a Peripheral Tropic Signal to Tune Steroidogenesis.bioRxiv : the preprint server for biology · 2026Article
- Unscheduled polyploidy synergizes with oncogenic mutations to enhance genome instability and tumorigenesis.Cancer letters · 2025Article
- Translocation of gut bacteria promotes tumor-associated mortality by inducing immune-activated renal damage.The EMBO journal · 2025Article
- Inflammatory crosstalk: systemic gut-kidney interplay aggravates tumor host mortality.The EMBO journal · 2025Article
- Notch Signaling in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025Review
- Sex-dimorphic tumor growth is regulated by tumor microenvironmental and systemic signals.Science advances · 2024Article
- Hippo effector, Yorkie, is a tumor suppressor in selectProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Topoisomerase I is an evolutionarily conserved key regulator for satellite DNA transcription.Nature communications · 2024Article
- Transient caspase-mediated activation of caspase-activated DNase causes DNA damage required for phagocytic macrophage differentiation.Cell reports · 2024Article
- Topoisomerase I is an Evolutionarily Conserved Key Regulator for Satellite DNA Transcription.bioRxiv : the preprint server for biology · 2024Article
- The antagonistic relationship between apoptosis and polyploidy in development and cancer.Seminars in cell & developmental biology · 2024Review
- Polyploid Cancer Cell Models in Drosophila.Genes · 2024Review
- Larval hematopoietic organs of multiplemicroPublication biology · 2024Article
- The roles of the native cell differentiation program aberrantly recapitulated in Drosophila intestinal tumors.Cell reports · 2023Article
- Ectopic expression of matrix metalloproteinases and filopodia extension via JNK activation are involved in the invasion of blood tumor cells in Drosophila mxc mutant.Genes to cells : devoted to molecular & cellular mechanisms · 2023Article
- Mutual repression between JNK/AP-1 and JAK/STAT stratifies senescent and proliferative cell behaviors during tissue regeneration.PLoS biology · 2023Article
- Modelling Cancer Metastasis inCells · 2023Review
- FBP1 knockdown decreases ovarian cancer formation and cisplatin resistance through EZH2-mediated H3K27me3.Bioscience reports · 2022Article
- Polyploidy in development and tumor models in Drosophila.Seminars in cancer biology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
During the initial stages of tumorigenesis, the tissue microenvironment where the pro-tumor cells reside plays a crucial role in determining the fate of these cells. Transition zones, where two types of epithelial cells meet, are high-risk sites for carcinogenesis, but the underlying mechanism remains largely unclear. Here, we show that persistent upregulation of Notch signaling induces neoplastic tumorigenesis in a transition zone between the salivary gland imaginal ring cells and the giant cells in Drosophila larvae. In this region, local endogenous JAK-STAT and JNK signaling creates a tissue microenvironment that is susceptible to oncogenic-Notch-induced tumorigenesis, whereas the rest of the salivary gland imaginal ring is refractory to Notch-induced tumor transformation. JNK signaling activates a matrix metalloprotease (MMP1) to promote Notch-induced tumorigenesis at the transition zone. These findings illustrate the significance of local endogenous inflammatory signaling in primary tumor formation.
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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 Socratic graph.