Evidence map›Paper›PMID 31152164›Full record

ArticleNature genetics2019

High-throughput single-cell ChIP-seq identifies heterogeneity of chromatin states in breast cancer.

Kevin Grosselin, Adeline Durand, Justine Marsolier, Adeline Poitou, Elisabetta Marangoni, Fariba Nemati, Ahmed Dahmani, Sonia Lameiras, Fabien Reyal, Olivia Frenoy and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 265 papers.

0numbers the graph read from it
0cells of the map it votes in
265citing papers in PubMed
23.8field-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

265 citing papers in PubMed, 469 citations in OpenAlex.

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  15. The role of epigenetic alterations in canine mammary cancer.The Journal of reproduction and development · 2026
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205 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 7 institutions in 3 countries.

Kevin GrosselinHiFiBiO SAS, Paris, France.ORCID http://orcid.org/0000-0001-6189-3197
Adeline DurandCNRS UMR3244, Institut Curie, PSL University, Paris, France.ORCID http://orcid.org/0000-0002-7423-2504
Justine MarsolierCNRS UMR3244, Institut Curie, PSL University, Paris, France.
Adeline PoitouHiFiBiO SAS, Paris, France.
Elisabetta MarangoniTranslational Research Department Institut Curie, PSL University, Paris, France.
Fariba NematiTranslational Research Department Institut Curie, PSL University, Paris, France.
Ahmed DahmaniTranslational Research Department Institut Curie, PSL University, Paris, France.
Sonia LameirasInstitut Curie Genomics of Excellence Platform, PSL University, Paris, France.
Fabien ReyalTranslational Research Department Institut Curie, PSL University, Paris, France.
Olivia FrenoyHiFiBiO SAS, Paris, France.
Yannick PousseHiFiBiO SAS, Paris, France.
Marcel ReichenHiFiBiO SAS, Paris, France.
Adam WoolfeHiFiBiO SAS, Paris, France.
Colin BrenanHiFiBiO SAS, Paris, France.
Andrew D GriffithsLaboratoire de Biochimie, CNRS UMR8231, ESPCI Paris, PSL University, Paris, France. andrew.griffiths@espci.fr.ORCID http://orcid.org/0000-0002-0808-3539
Céline VallotCNRS UMR3244, Institut Curie, PSL University, Paris, France. celine.vallot@curie.fr.ORCID http://orcid.org/0000-0003-1601-2359
Annabelle GérardHiFiBiO SAS, Paris, France. a.gerard@hifibio.com.ORCID http://orcid.org/0000-0003-0411-768X
HiFiBiO Therapeutics (France) · FRCentre National de la Recherche Scientifique · FRUniversité Paris Sciences et Lettres · FRBroad Institute · USHiFiBiO Therapeutics (United States) · USInserm · FRInstitut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Modulation of chromatin structure via histone modification is a major epigenetic mechanism and regulator of gene expression. However, the contribution of chromatin features to tumor heterogeneity and evolution remains unknown. Here we describe a high-throughput droplet microfluidics platform to profile chromatin landscapes of thousands of cells at single-cell resolution. Using patient-derived xenograft models of acquired resistance to chemotherapy and targeted therapy in breast cancer, we found that a subset of cells within untreated drug-sensitive tumors share a common chromatin signature with resistant cells, undetectable using bulk approaches. These cells, and cells from the resistant tumors, have lost chromatin marks-H3K27me3, which is associated with stable transcriptional repression-for genes known to promote resistance to treatment. This single-cell chromatin immunoprecipitation followed by sequencing approach paves the way to study the role of chromatin heterogeneity, not just in cancer but in other diseases and healthy systems, notably during cellular differentiation and development.

Indexed as

Chromatin ImmunoprecipitationGenetic HeterogeneityHigh-Throughput Nucleotide SequencingSingle-Cell AnalysisBreast NeoplasmsChromatinComputational BiologyEpigenesis, GeneticFemaleHistonesHumansMicrofluidic Analytical TechniquesStromal CellsWorkflowChromatinHistones

Identifiers

PMID31152164
OpenAlexW2947608130

What OpenQuestion holds

Textmetadata
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.