Evidence map›Paper›PMID 38527495›Full record

ArticleCancer discovery2024

Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells.

Dalia Rosano, Emre Sofyali, Heena Dhiman, Chiara Ghirardi, Diana Ivanoiu, Timon Heide, Andrea Vingiani, Alessia Bertolotti, Giancarlo Pruneri, Eleonora Canale and 16 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
11.4field-weighted citation impact, top 1% of its field
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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

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  17. HES1 oscillations are required for cell cycle reentry in oestrogen receptor-positive breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  18. Review
  19. Targeting tumor transition windows.Exploration of targeted anti-tumor therapy · 2026
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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

26 authors at 10 institutions in 5 countries.

Dalia Rosano *Department of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0000-0002-7372-9535
Emre Sofyali *Department of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0000-0002-5113-4047
Heena Dhiman *Department of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0000-0001-7840-0563
Chiara GhirardiDepartment of Experimental Oncology, IEO, European Institute of Oncology IRCCS, Milan, Italy.ORCID 0009-0001-5518-9061
Diana IvanoiuDepartment of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0009-0008-3988-3871
Timon HeideHuman Technopole, Milan, Italy.ORCID 0000-0002-1386-7469
Andrea VingianiIstituto Nazionale Tumori, Milan, Italy.ORCID 0000-0002-9827-3976
Alessia BertolottiIstituto Nazionale Tumori, Milan, Italy.ORCID 0000-0002-5562-3817
Giancarlo PruneriIstituto Nazionale Tumori, Milan, Italy.ORCID 0000-0002-7963-7172
Eleonora CanaleDepartment of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0009-0002-0145-8438
Hannah F DewhurstDepartment of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0009-0006-2401-5604
Debjani SahaDepartment of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0000-0002-8190-0777
Neil SlavenDepartment of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0000-0003-4794-9806
Iros BarozziDepartment of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0000-0003-0690-3473
Tong LiDepartment of Surgery and Cancer, Imperial College London, London, United Kingdom.
Grigory ZemlyanskiyDepartment of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0009-0008-3807-9937
Henry PhillipsDepartment of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0009-0008-4966-623X
Chela JamesHuman Technopole, Milan, Italy.ORCID 0000-0003-3996-0909
Balázs GyőrffyDepartment of Bioinformatics, Semmelweis University, Budapest, Hungary.ORCID 0000-0002-5772-3766
Claire LynnCentre for Evolution and Cancer, Institute of Cancer Research, London, United Kingdom.ORCID 0000-0002-2630-4075
George D CresswellCentre for Evolution and Cancer, Institute of Cancer Research, London, United Kingdom.ORCID 0000-0003-3303-068X
Farah RehmanCharing Cross Hospital, Imperial College NHS Trust, London, United Kingdom.ORCID 0000-0003-3879-315X
Roberta NoberiniDepartment of Experimental Oncology, IEO, European Institute of Oncology IRCCS, Milan, Italy.ORCID 0000-0002-7267-1079
Tiziana BonaldiDepartment of Experimental Oncology, IEO, European Institute of Oncology IRCCS, Milan, Italy.ORCID 0000-0003-3556-1265
Andrea SottorivaHuman Technopole, Milan, Italy.ORCID 0000-0001-6709-9533
Luca MagnaniDepartment of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0000-0002-7534-0785
Imperial College London · GBInstitute of Cancer Research · GBBreast Cancer Now · GBEuropean Institute of Oncology · ITTumori Foundation · USUniversity of Milan · ITComprehensive Cancer Center Vienna · ATImperial College Healthcare NHS Trust · GBLawrence Berkeley National Laboratory · USSemmelweis University · HU

Funding

Cancer Research UK 23110Cancer Research UK (CRUK) A23110Horizon 2020 Framework Programme (H2020) 823 839
6 · The paper itself

Abstract

Patients with estrogen receptor-positive breast cancer receive adjuvant endocrine therapies (ET) that delay relapse by targeting clinically undetectable micrometastatic deposits. Yet, up to 50% of patients relapse even decades after surgery through unknown mechanisms likely involving dormancy. To investigate genetic and transcriptional changes underlying tumor awakening, we analyzed late relapse patients and longitudinally profiled a rare cohort treated with long-term neoadjuvant ETs until progression. Next, we developed an in vitro evolutionary study to record the adaptive strategies of individual lineages in unperturbed parallel experiments. Our data demonstrate that ETs induce nongenetic cell state transitions into dormancy in a stochastic subset of cells via epigenetic reprogramming. Single lineages with divergent phenotypes awaken unpredictably in the absence of recurrent genetic alterations. Targeting the dormant epigenome shows promising activity against adapting cancer cells. Overall, this study uncovers the contribution of epigenetic adaptation to the evolution of resistance to ETs. SIGNIFICANCE: This study advances the understanding of therapy-induced dormancy with potential clinical implications for breast cancer. Estrogen receptor-positive breast cancer cells adapt to endocrine treatment by entering a dormant state characterized by strong heterochromatinization with no recurrent genetic changes. Targeting the epigenetic rewiring impairs the adaptation of cancer cells to ETs. See related commentary by Llinas-Bertran et al., p. 704. This article is featured in Selected Articles from This Issue, p. 695.

Indexed as

Breast NeoplasmsEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHumansNeoplasm Recurrence, Local

Identifiers

PMID38527495
PMCPMC11061610
OpenAlexW4394764204

What OpenQuestion holds

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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.