ReviewNature immunology2002
Natural selection of tumor variants in the generation of "tumor escape" phenotypes.
Review in Nature immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 452 papers, 3 of them syntheses 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
452 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,033 citations in OpenAlex.
- Liquid-liquid phase separation drives immune signaling transduction in cancer: a bibliometric and visualized study from 1992 to 2024.Frontiers in oncology · 2025Pooled it
- Design of new drugs for medullary thyroid carcinoma.Frontiers in oncology · 2022Pooled it
- Neutrophil-to-lymphocyte ratio as prognostic indicator in gastrointestinal cancers: a systematic review and meta-analysis.Oncotarget · 2017Pooled it
- Trial
- Pleiotropic effects of BET inhibition broadly boost tumor immunogenicity to CD8Oncoimmunology · 2026Article
- Modular Vaccine Robots for Spatiotemporal Programming of the CD4Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Targeting cytokine/chemokine signaling to convert immunologically cold tumors into hot: Emerging strategies in cancer immunotherapy.Acta pharmaceutica Sinica. B · 2026Review
- Microplastics inhibit macrophage bioenergetics impairing homeostatic function and immune responsiveness.bioRxiv : the preprint server for biology · 2026Article
- Pyroptosis: Turning Up the Heat on Cancer.Annual review of immunology · 2026Review
- Lymphodepleting preconditioning impairs host antitumor immunity induced by adoptive T cell therapy in mouse models.Nature communications · 2026Article
- Identification of a biologically coherent three gene immune signature predictive of immunotherapy benefit in gastric adenocarcinoma.Discover oncology · 2026Article
- Metabolomic profiling and anti-tumor function of canine NK cells in tumor interaction.BMC veterinary research · 2026Article
- Advancing adoptive T cell therapy in ovarian cancer: barriers, innovations, and emerging platforms.Journal for immunotherapy of cancer · 2026Review
- Innate immunity in tumour immunoediting and immunosurveillance.The EMBO journal · 2026Review
- Biomarkers for predicting and monitoring the efficacy of cancer vaccines.Frontiers in oncology · 2026Review
- Investigating the Consequences of Aneuploidy in Cancer and Normal Tissue.Advances in experimental medicine and biology · 2026Review
- Modeling immunotherapies in live 3D human cancer tissue bioreactors.Theranostics · 2026Article
- Article
- Recent advances in targeting protein degradation for tumor immunotherapy.Journal of hematology & oncology · 2025Review
- Immunological surveillance against cancer across mammals.Nature communications · 2025Article
392 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
2 authors at 1 institution in 1 country.
Funding
Abstract
The idea that tumors must "escape" from immune recognition contains the implicit assumption that tumors can be destroyed by immune responses either spontaneously or as the result of immunotherapeutic intervention. Simply put, there is no need for tumor escape without immunological pressure. Here, we review evidence supporting the immune escape hypothesis and critically explore the mechanisms that may allow such escape to occur. We discuss the idea that the central engine for generating immunoresistant tumor cell variants is the genomic instability and dysregulation that is characteristic of the transformed genome. "Natural selection" of heterogeneous tumor cells results in the survival and proliferation of variants that happen to possess genetic and epigenetic traits that facilitate their growth and immune evasion. Tumor escape variants are likely to emerge after treatment with increasingly effective immunotherapies.
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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.