ArticleNature2024
Titration of RAS alters senescent state and influences tumour initiation.
Erratum issuedAbstract read
In one paragraph
Article in Nature, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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
23 citing papers in PubMed.
- Cellular senescence: six decades of discovery and reinvention.The EMBO journal · 2026Review
- UHRF1 overexpression generates distinct senescent states with different Tp53 dependencies.EMBO reports · 2026Article
- Engineering editopes through programmable RNA editing toward tumor neoantigen generation.The EMBO journal · 2026Article
- Immune surveillance and immune evasion of senescent cells.Nature reviews. Immunology · 2026Review
- Fate Bifurcation of Cellular Senescence: Dynamic Regulation from Tumor Suppression to Recurrence Risk.Cells · 2026Review
- Article
- Electrophilic compound screening identifies GPX4-dependent ferroptosis as a senescence vulnerability.Nature cell biology · 2026Article
- Review
- RPA hyperphosphorylation hinders the resolution of R-loops and G-quadruplex-associated R-loops during RAS-driven senescence.Nucleic acids research · 2026Article
- Evolution of Cancer Metastases via Lineage Trans-Differentiation.Research (Washington, D.C.) · 2026Article
- Cellular senescence in liver diseases: From molecular drivers to therapeutic targeting.Journal of hepatology · 2026Review
- Employing RNA editing to engineer personalized tumor-specific neoantigens (editopes).bioRxiv : the preprint server for biology · 2025Article
- Oncogenic KRAS mutations drive immune suppression through immune-related regulatory network and metabolic reprogramming.Cell death & disease · 2025Review
- Regulatory Interplay of p53, AMPK, and mTOR in Decidualization: Implications for Reproductive Competence and Cancer Biology.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Targeting Senescence in Oncology: An Emerging Therapeutic Avenue for Cancer.Current oncology (Toronto, Ont.) · 2025Review
- The rise of RAS: how gradual oncogene activation shapes the OIS spectrum.Genes & development · 2025Review
- The Inositol-5-Phosphatase SHIP1: Expression, Regulation and Role in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2025Review
- Regulation of cellular senescence in tumor progression and therapeutic targeting: mechanisms and pathways.Molecular cancer · 2025Review
- Cellular senescence offers distinct immunological vulnerabilities in cancer.Trends in cancer · 2025Review
- Unveiling the cell-type-specific landscape of cellular senescence through single-cell transcriptomics using SenePy.Nature communications · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Adelyne S L Chan *Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0003-2214-0306
Haoran Zhu *Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0003-3879-0389
Masako NaritaCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-9774-4908
Liam D CassidyCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.
Andrew R J YoungCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-7522-5525
Camino Bermejo-RodriguezDepartment of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, UK.ORCID http://orcid.org/0000-0002-7554-1640
Aleksandra T JanowskaCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0009-0005-3104-3542
Hung-Chang ChenCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.
Sarah GoughCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0001-8697-9659
Naoki OshimoriDepartment of Cell, Developmental and Cancer Biology, Knight Cancer Institute, Oregon Health and Science University, Portland, OR, USA.
Lars ZenderDepartment of Medical Oncology and Pneumology, University Hospital Tuebingen, Tuebingen, Germany.ORCID http://orcid.org/0000-0001-7626-2849
Sarah J AitkenCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-1897-4140
Matthew HoareCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0001-5990-9604
Masashi NaritaCancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK. Masashi.Narita@cruk.cam.ac.uk.ORCID http://orcid.org/0000-0001-7764-577X
Funding
Mechanisms of cellular crosstalk in tumor-promoting niche formationR01CA245535 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI OSHIMORI, NAOKI · 2021 to 2025
$2.1MCancer Research UK 19159Medical Research Council MR/X00970X/1NCI NIH HHS R01 CA245535
Abstract
Oncogenic RAS-induced senescence (OIS) is an autonomous tumour suppressor mechanism associated with premalignancy
Indexed as
CarcinogenesisCellular SenescenceHepatocytesLiver NeoplasmsOncogene Protein p21(ras)AnimalsCarcinoma, HepatocellularFemaleGTP PhosphohydrolasesHumansMaleMembrane ProteinsMiceMonomeric GTP-Binding ProteinsPhenotypeSingle-Cell Gene Expression AnalysisGTP PhosphohydrolasesMembrane ProteinsMonomeric GTP-Binding ProteinsNRAS protein, humanNras protein, mouseOncogene Protein p21(ras)
Identifiers
What OpenQuestion holds
Textmetadata
LicenceCC BY
Read underepoch 390
Registered trials
None linked
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.