Evidence map›Paper›PMID 36774358›Full record

ArticleNature communications2023

Genomic and microenvironmental heterogeneity shaping epithelial-to-mesenchymal trajectories in cancer.

Guidantonio Malagoli Tagliazucchi, Anna J Wiecek, Eloise Withnell, Maria Secrier

Abstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing 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

61 citing papers in PubMed.

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  16. Spatial architecture of development and disease.Nature reviews. Genetics · 2026
    Review
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1 more citing papers are in PubMed but not listed here.

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

4 authors.

Guidantonio Malagoli Tagliazucchi *UCL Genetics Institute, Department of Genetics, Evolution and Environment, University College London, London, WC1E 6BT, UK.
Anna J Wiecek *UCL Genetics Institute, Department of Genetics, Evolution and Environment, University College London, London, WC1E 6BT, UK.
Eloise WithnellUCL Genetics Institute, Department of Genetics, Evolution and Environment, University College London, London, WC1E 6BT, UK.
Maria SecrierUCL Genetics Institute, Department of Genetics, Evolution and Environment, University College London, London, WC1E 6BT, UK. m.secrier@ucl.ac.uk.ORCID 0000-0003-2758-1741

Funding

Biotechnology and Biological Sciences Research Council BB/R01356X/1Medical Research Council MR/T042184/1Wellcome Trust
6 · The paper itself

Abstract

The epithelial to mesenchymal transition (EMT) is a key cellular process underlying cancer progression, with multiple intermediate states whose molecular hallmarks remain poorly characterised. To fill this gap, we present a method to robustly evaluate EMT transformation in individual tumours based on transcriptomic signals. We apply this approach to explore EMT trajectories in 7180 tumours of epithelial origin and identify three macro-states with prognostic and therapeutic value, attributable to epithelial, hybrid E/M and mesenchymal phenotypes. We show that the hybrid state is relatively stable and linked with increased aneuploidy. We further employ spatial transcriptomics and single cell datasets to explore the spatial heterogeneity of EMT transformation and distinct interaction patterns with cytotoxic, NK cells and fibroblasts in the tumour microenvironment. Additionally, we provide a catalogue of genomic events underlying distinct evolutionary constraints on EMT transformation. This study sheds light on the aetiology of distinct stages along the EMT trajectory, and highlights broader genomic and environmental hallmarks shaping the mesenchymal transformation of primary tumours.

Indexed as

Antineoplastic AgentsNeoplasmsEpithelial-Mesenchymal TransitionGenomicsHumansPhenotypeTumor MicroenvironmentAntineoplastic Agents

Identifiers

PMID36774358
PMCPMC9922305

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Registered trials

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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.