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Record W4406146480 · doi:10.1158/2159-8290.cd-24-0094

Chronic Viral Mimicry Induction following p53 Loss Promotes Immune Evasion

2025· article· en· W4406146480 on OpenAlexafffund
Charles A. Ishak, Sajid A. Marhon, Naïri Tchrakian, Anjelica Hodgson, Helen Loo Yau, Isabela M. Gonzaga, Melanie Peralta, Ilinca M. Lungu, Stephanie Gomez, Sheng‐Ben Liang, Shu Yi Shen, Raymond Chen, Jocelyn Chen, Biji Chatterjee, Kevin N. Wanniarachchi, Junwoo Lee, Nicholas Zehrbach, Amir Hosseini, Parinaz Mehdipour, Siyu Sun, Alexander Solovyov, Ilias Ettayebi, Kyle E. Francis, Aobo He, Taiyi Wu, Shengrui Feng, Tiago da Silva Medina, Felipe Campos de Almeida, Jane Bayani, Jason Li, Spencer MacDonald, Yadong Wang, Sarah S. Garcia, Elisa Arthofer, Noor Diab, Aneil Srivastava, Paul Tran Austin, Peter Sabatini, Benjamin D. Greenbaum, Catherine O′Brien, Trevor G. Shepherd, Ming‐Sound Tsao, Katherine B. Chiappinelli, Amit M. Oza, Blaise Clarke, Robert Rottapel, Stéphanie Lheureux, Daniel D. De Carvalho

Bibliographic record

VenueCancer Discovery · 2025
Typearticle
Languageen
FieldImmunology and Microbiology
TopicImmune cells in cancer
Canadian institutionsWestern UniversityMount Sinai HospitalOntario Institute for Cancer ResearchUniversity Health NetworkUniversity of TorontoPrincess Margaret Cancer Centre
FundersCanadian Institutes of Health ResearchNational Cancer InstituteNational Institutes of HealthUniversity of GlasgowGovernment of OntarioPrincess Margaret Cancer FoundationGeorge Washington University
KeywordsBiologyCarcinogenesisMolecular mimicryImmune systemTranscription (linguistics)Transcription factorImmunogenicityCancerHSF1ImmunologyCancer researchCell biologyGeneticsGene

Abstract

fetched live from OpenAlex

Abstract Epigenetic therapies facilitate transcription of immunogenic repetitive elements that cull cancer cells through “viral mimicry” responses. Paradoxically, cancer-initiating events also facilitate transcription of repetitive elements. Contributions of repetitive element transcription toward cancer initiation, and the mechanisms by which cancer cells evade lethal viral mimicry responses during tumor initiation remain poorly understood. In this report, we characterize premalignant lesions of the fallopian tube along with syngeneic epithelial ovarian cancer models to explore the earliest events of tumorigenesis following the loss of the p53 tumor suppressor protein. We report that p53 loss permits the transcription of immunogenic repetitive elements and chronic viral mimicry activation that increases cellular tolerance of cytosolic nucleic acids and diminishes cellular immunogenicity. This selection process can be partially attenuated pharmacologically. Altogether, these results reveal that viral mimicry conditioning following p53 loss promotes immune evasion and may represent a pharmacologic target for early cancer interception. Significance: Our landmark discovery of viral mimicry characterized repetitive elements as immunogenic stimuli that cull cancer cells. If expressed repetitive elements cull cancer cells, why does every human cancer express repetitive elements? Our report offers an exciting advancement toward understanding this paradox and how to exploit this mechanism for cancer interception. See related commentary by Murayama and Cañadas, p. 670

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesMeta-epidemiology (narrow)
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.143
Threshold uncertainty score1.000

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.001
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.009
GPT teacher head0.266
Teacher spread0.257 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations17
Published2025
Admission routes2
Has abstractyes

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