Evidence map›Paper›PMID 39218912›Full record

ArticleNature communications2024

Multi-omic lineage tracing predicts the transcriptional, epigenetic and genetic determinants of cancer evolution.

F Nadalin, M J Marzi, M Pirra Piscazzi, P Fuentes-Bravo, S Procaccia, M Climent, P Bonetti, C Rubolino, B Giuliani, I Papatheodorou and 2 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Multiplexed enrichment and tracking of lineages with CloneSweeper.bioRxiv : the preprint server for biology · 2026
    Article
  13. Review
  14. Targeting tumor transition windows.Exploration of targeted anti-tumor therapy · 2026
    Review
  15. Article
  16. How cancer arises: Genetics releases, plasticity creates, genetics stabilizes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

F Nadalin *Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy. francesca@ebi.ac.uk.ORCID 0000-0002-3886-0896
M J Marzi *Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.
M Pirra Piscazzi *Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.ORCID 0009-0001-9355-4285
P Fuentes-Bravo *Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.ORCID 0000-0003-0278-3494
S ProcacciaCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.ORCID 0000-0001-5791-3079
M ClimentCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.
P BonettiCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.
C RubolinoCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.
B GiulianiCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.
I PapatheodorouEuropean Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, Cambridge, UK.ORCID 0000-0001-7270-5470
J C MarioniEuropean Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, Cambridge, UK.ORCID 0000-0001-9092-0852
F NicassioCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy. francesco.nicassio@iit.it.ORCID 0000-0002-5954-5318

Funding

Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) IG22851Fondazione Cariplo (Cariplo Foundation) 2015-0590National Center for Gene Therapy and Drugs based on RNA Technology
6 · The paper itself

Abstract

Cancer is a highly heterogeneous disease, where phenotypically distinct subpopulations coexist and can be primed to different fates. Both genetic and epigenetic factors may drive cancer evolution, however little is known about whether and how such a process is pre-encoded in cancer clones. Using single-cell multi-omic lineage tracing and phenotypic assays, we investigate the predictive features of either tumour initiation or drug tolerance within the same cancer population. Clones primed to tumour initiation in vivo display two distinct transcriptional states at baseline. Remarkably, these states share a distinctive DNA accessibility profile, highlighting an epigenetic basis for tumour initiation. The drug tolerant niche is also largely pre-encoded, but only partially overlaps the tumour-initiating one and evolves following two genetically and transcriptionally distinct trajectories. Our study highlights coexisting genetic, epigenetic and transcriptional determinants of cancer evolution, unravelling the molecular complexity of pre-encoded tumour phenotypes.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticNeoplasmsAnimalsCell LineageCell Line, TumorHumansMiceMultiomicsPhenotypeSingle-Cell AnalysisTranscription, Genetic

Identifiers

PMID39218912
PMCPMC11366763

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.