ArticleCell2016
Multi-organ Mapping of Cancer Risk.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.
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
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 165 citations in OpenAlex.
- Large-Scale Genome-Wide Association Study of East Asians Identifies Loci Associated With Risk for Colorectal Cancer.Gastroenterology · 2019Pooled it
- Clonal haematopoiesis is not prevalent in survivors of childhood cancer.British journal of haematology · 2018Trial
- Tumor Anti-Angiogenesis Therapy and Its Influence on Immune Cell Function in the Tumor Microenvironment.Cancer medicine · 2026Review
- Unravelling the genetics and epigenetics of the ageing tumour microenvironment in cancer.Nature reviews. Cancer · 2025Review
- Aging-Related Mechanisms Underlying Carcinogenesis: Therapeutic Opportunities.Aging and disease · 2025Review
- Trans-Scale Insights into Variability in Radiation Cancer Risk Across Tissues, Individuals, and Species.Biology · 2025Review
- Intergenerational Enlargement of Human Organs as a Driver of Increased Cancer Risk?BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Epigenetic ageing clocks: statistical methods and emerging computational challenges.Nature reviews. Genetics · 2025Review
- An evaluation of trends for mesothelioma mortality in American women: Addressing the content of a recent Morbidity and Mortality Weekly Report (MMWR).Toxicology and industrial health · 2025Review
- Tumor Promoters and Opportunities for Molecular Cancer Prevention.Cancer discovery · 2024Review
- Tumor initiation and early tumorigenesis: molecular mechanisms and interventional targets.Signal transduction and targeted therapy · 2024Review
- Quantifying the stochastic component of epigenetic aging.Nature aging · 2024Article
- Smad4 restricts injury-provoked biliary proliferation and carcinogenesis.Disease models & mechanisms · 2024Article
- Article
- An improved epigenetic counter to track mitotic age in normal and precancerous tissues.Nature communications · 2024Article
- Initiation of Cancer: The Journey From Mutations in Somatic Cells to Epigenetic Changes in Tissue-resident VSELs.Stem cell reviews and reports · 2024Review
- On epigenetic stochasticity, entropy and cancer risk.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Increased genomic instability and reshaping of tissue microenvironment underlie oncogenic properties ofScience advances · 2024Article
- Article
- Engineering Heterogeneous Tumor Models for Biomedical Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Cancers are distributed unevenly across the body, but the importance of cell intrinsic factors such as stem cell function in determining organ cancer risk is unknown. Therefore, we used Cre-recombination of conditional lineage tracing, oncogene, and tumor suppressor alleles to define populations of stem and non-stem cells in mouse organs and test their life-long susceptibility to tumorigenesis. We show that tumor incidence is determined by the life-long generative capacity of mutated cells. This relationship held true in the presence of multiple genotypes and regardless of developmental stage, strongly supporting the notion that stem cells dictate organ cancer risk. Using the liver as a model system, we further show that damage-induced activation of stem cell function markedly increases cancer risk. Therefore, we propose that a combination of stem cell mutagenesis and extrinsic factors that enhance the proliferation of these cell populations, creates a "perfect storm" that ultimately determines organ cancer risk. VIDEO ABSTRACT.
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.