ReviewNature reviews. Cancer2024
Beyond genetics: driving cancer with the tumour microenvironment behind the wheel.
Review in Nature reviews. Cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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
98 citing papers in PubMed.
- Current landscape and emerging trends of PD-1/PD-L1 research in prostate cancer: A data-driven atlas from multidatabase integration.Human vaccines & immunotherapeutics · 2026Article
- Compartment-Specific Immunohistochemical Alterations Along the Colorectal Adenoma-Carcinoma Continuum.Digestive diseases and sciences · 2026Article
- GLG1 in cancer-associated fibroblasts promotes bladder cancer growth while limiting tumor apoptosis.Apoptosis : an international journal on programmed cell death · 2026Article
- Intratumoral microbiota in the growth of CRC and lung cancer: Comprehensive insights from etiology to therapy.iScience · 2026Review
- Integrated Transcriptomic Analysis and Machine Learning Identify THY1 as a Key Regulator of Cancer-Associated Fibroblast Infiltration, Promoting Malignant Progression and Immune Escape in Gastric Cancer.Journal of gastroenterology and hepatology · 2026Article
- Article
- Molecular Mechanisms of Tumor Pathogenesis.Cells · 2026Article
- DNA Methylation as a Programmable Information Layer: From Molecular Marks to Disease State Engineering.International journal of molecular sciences · 2026Review
- Review
- Automatic Coregistration of High-Resolution MALDI-MSI and Raman Imaging Applied to Cardiac Tissue of Fabry Disease Mouse Models.Analytical chemistry · 2026Article
- Tumor heterogeneity: development, mechanisms, and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Tendon stem/progenitor cells in heterotopic ossification: functional regulation, molecular mechanisms and targeted therapeutic strategies.Journal of orthopaedic translation · 2026Review
- Review
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- Extracellular Vesicles in the Biology and Liquid Biopsy Diagnostics of Pediatric High-Grade Glioma - Emerging Findings and Opportunities.Journal of extracellular biology · 2026Review
- Remembering inflammation increases cancer risk.Nature reviews. Cancer · 2026Article
- Beyond the chaos: How architecture structures tumour biology.The FEBS journal · 2026Review
- Multifaceted roles of miR‑124 in cancer: Molecular mechanisms and clinical prospects (Review).International journal of oncology · 2026Review
- Poor prognosis outcome tumors, bacteria-infected tumors and nanodrugs: current evidence and hypotheses towards a paradigm change for treatment.Cancer biology & medicine · 2026Review
- Layers of Hope: How Graphene and Nanostructures Hold Promise for Cancer Therapy.International journal of molecular sciences · 2026Review
38 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
3 authors.
Funding
Abstract
Cancer has long been viewed as a genetic disease of cumulative mutations. This notion is fuelled by studies showing that ageing tissues are often riddled with clones of complex oncogenic backgrounds coexisting in seeming harmony with their normal tissue counterparts. Equally puzzling, however, is how cancer cells harbouring high mutational burden contribute to normal, tumour-free mice when allowed to develop within the confines of healthy embryos. Conversely, recent evidence suggests that adult tissue cells expressing only one or a few oncogenes can, in some contexts, generate tumours exhibiting many of the features of a malignant, invasive cancer. These disparate observations are difficult to reconcile without invoking environmental cues triggering epigenetic changes that can either dampen or drive malignant transformation. In this Review, we focus on how certain oncogenes can launch a two-way dialogue of miscommunication between a stem cell and its environment that can rewire downstream events non-genetically and skew the morphogenetic course of the tissue. We review the cells and molecules of and the physical forces acting in the resulting tumour microenvironments that can profoundly affect the behaviours of transformed cells. Finally, we discuss possible explanations for the remarkable diversity in the relative importance of mutational burden versus tumour microenvironment and its clinical relevance.
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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.