ArticleCurrent biology : CB2012
Live imaging of tumor initiation in zebrafish larvae reveals a trophic role for leukocyte-derived PGE₂.
Article in Current biology : CB, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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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Who cites it
56 citing papers in PubMed, 104 citations in OpenAlex.
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- Zebrafish Models to Study the Crosstalk between Inflammation and NADPH Oxidase-Derived Oxidative Stress in Melanoma.Antioxidants (Basel, Switzerland) · 2022Review
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- Cell Type-Specific Transcriptome Profiling Reveals a Role for Thioredoxin During Tumor Initiation.Frontiers in immunology · 2022Article
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- Tumor-Associated Inflammation: The Tumor-Promoting Immunity in the Early Stages of Tumorigenesis.Journal of immunology research · 2022Review
- TLR7 ligation augments hematopoiesis in Rps14 (uS11) deficiency via paradoxical suppression of inflammatory signaling.Blood advances · 2021Article
- Melanoma models for the next generation of therapies.Cancer cell · 2021Review
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- Damage-Induced Calcium Signaling and Reactive Oxygen Species Mediate Macrophage Activation in Zebrafish.Frontiers in immunology · 2021Article
- Telomere shortening produces an inflammatory environment that increases tumor incidence in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
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3 authors at 2 institutions in 1 country.
Funding
Abstract
Epidemiology studies and clinical trials have suggested that the use of non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, can significantly reduce the incidence of and mortality associated with many cancers, and upregulation of the COX2-PGE(2) pathway in tumor microenvironments might drive several aspects of cancer progression. For these reasons, the mechanisms linking COX blockade and cancer prevention have long been an area of active investigation. During carcinogenesis, COX-2 is expressed both by malignant epithelial cells and by tumor-associated stromal cells, including macrophages, but the observation that NSAIDs are most effective in cancer prevention in APC(min/+) mice if the mice are treated from conception suggests that the COX-2/PGE(2) pathway might also be critical at the earliest stages of tumor development. In this study we take advantage of the translucency and genetic tractability of zebrafish larvae to investigate the involvement of inflammatory cells at cancer initiation, when transformed cells first arise in tissues. We previously showed that innate immune cells supply early transformed cells with proliferative cues and, by using complementary pharmacological and genetic experiments, we now show that prostaglandin E(2) (PGE(2)) is the trophic signal required for this expansion of transformed cells. Our in vivo observations at these early stages of cancer initiation provide a potential mechanistic explanation for why long-term use of low doses of NSAIDs, including aspirin, might reduce cancer onset.
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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.