ArticleThe Journal of clinical investigation2014
Long-lived intestinal tuft cells serve as colon cancer-initiating cells.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 265 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.
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.
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Who cites it
265 citing papers in PubMed, 391 citations in OpenAlex.
- Building and regenerating intestines by manipulating intestinal stem cells.Nature reviews. Gastroenterology & hepatology · 2026Review
- Pan-cancer analysis and mechanistic insights of tuft cell-like tumors.Genes & diseases · 2026Review
- Translational insights and clinical challenges of targeting cancer stem cells.Signal transduction and targeted therapy · 2026Review
- Tuft cells protect against intestinal inflammation through histone deacetylase 3.Mucosal immunology · 2026Article
- Testican-1 activates Wnt/β-Catenin signaling to drive colorectal cancer progression.Oncogenesis · 2026Article
- Gastrointestinal tuft cells: Recent insights and next questions.Science immunology · 2026Review
- MDA5-MAVS and interferon-lambda signaling in the intestinal epithelium limit murine astrovirus infection.Mucosal immunology · 2026Article
- A Rare T-Cell Factor 4 Lineage-negative Epithelial Stem Cell Supports Wound Repair and APC-deletion-induced Colon Tumorigenesis.bioRxiv : the preprint server for biology · 2026Article
- Article
- KIT supports small intestinal tuft cell hyperplasia.Science advances · 2026Article
- Viral mimicry acts as a tumor suppressor in colitis.Nature communications · 2026Article
- Plasticity and stringency: rethinking stem cell division modes.Biochemical Society transactions · 2026Review
- Perspectives on gastric cancer: the central role of gastrin in carcinogenesis byFrontiers in oncology · 2026Review
- Tuft cell-mediated pathogen sensing and inflammation resolution.Biochemical Society transactions · 2025Review
- Organ-Specific Dedifferentiation and Epigenetic Remodeling in In Vivo Reprogramming.Aging cell · 2025Review
- Tumor necrosis factor promotes doublecortin-like kinase 1 expression and cellular reprogramming in intestinal epithelial cells leading to neoplastic transformation.Cell communication and signaling : CCS · 2025Article
- Clinical applications of circulating tumor cells in metastasis and therapy.Journal of hematology & oncology · 2025Review
- Intestinal tuft cell subtypes represent successive stages of maturation driven by crypt-villus signaling gradients.Nature communications · 2025Article
- c-KitCell death and differentiation · 2025Article
- Balancing Regeneration and Resistance: Targeting DCLK1 to Mitigate Gastrointestinal Radiation Injury and Oncogenesis.Cancers · 2025Review
205 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
17 authors at 5 institutions in 3 countries.
Funding
Abstract
Doublecortin-like kinase 1 protein (DCLK1) is a gastrointestinal tuft cell marker that has been proposed to identify quiescent and tumor growth-sustaining stem cells. DCLK1⁺ tuft cells are increased in inflammation-induced carcinogenesis; however, the role of these cells within the gastrointestinal epithelium and their potential as cancer-initiating cells are poorly understood. Here, using a BAC-CreERT-dependent genetic lineage-tracing strategy, we determined that a subpopulation of DCLK1⁺ cells is extremely long lived and possesses rare stem cell abilities. Moreover, genetic ablation of Dclk1 revealed that DCLK1⁺ tuft cells contribute to recovery following intestinal and colonic injury. Surprisingly, conditional knockdown of the Wnt regulator APC in DCLK1⁺ cells was not sufficient to drive colonic carcinogenesis under normal conditions; however, dextran sodium sulfate-induced (DSS-induced) colitis promoted the development of poorly differentiated colonic adenocarcinoma in mice lacking APC in DCLK1⁺ cells. Importantly, colonic tumor formation occurred even when colitis onset was delayed for up to 3 months after induced APC loss in DCLK1⁺ cells. Thus, our data define an intestinal DCLK1⁺ tuft cell population that is long lived, quiescent, and important for intestinal homeostasis and regeneration. Long-lived DCLK1⁺ cells maintain quiescence even following oncogenic mutation, but are activated by tissue injury and can serve to initiate colon cancer.
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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.