Evidence map›Paper›PMID 40101158›Full record

ArticleCancer research2025

Single-Cell Expression Analysis of Ductal Carcinoma In Situ Identifies Complex Genotypic-Phenotypic Relationships Altering Epithelial Composition.

Xiaodi Qin, Siri H Strand, Marissa R Lee, Aashrith Saraswathibhatla, David G P van IJzendoorn, ChunFang Zhu, Sujay Vennam, Sushama Varma, Allison Hall, Rachel E Factor and 10 more

Abstract read
In one paragraph

Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Denoising image-based spatial transcriptomics data with DenoIST.bioRxiv : the preprint server for biology · 2025
    Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors.

Xiaodi QinDuke Cancer Institute, Duke University School of Medicine, Durham, North Carolina.ORCID 0000-0001-7066-8151
Siri H StrandDepartment of Pathology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0001-6596-9945
Marissa R LeeDuke Cancer Institute, Duke University School of Medicine, Durham, North Carolina.ORCID 0000-0001-7188-9933
Aashrith SaraswathibhatlaDepartment of Mechanical Engineering, Stanford University, Stanford, California.ORCID 0000-0002-0971-8065
David G P van IJzendoornDepartment of Pathology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0002-2249-5919
ChunFang ZhuDepartment of Pathology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0002-6773-0820
Sujay VennamDepartment of Pathology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0001-6312-1238
Sushama VarmaDepartment of Pathology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0001-8137-0641
Allison HallDepartment of Pathology, Duke University School of Medicine, Durham, North Carolina.ORCID 0000-0003-3413-603X
Rachel E FactorDepartment of Pathology, Duke University School of Medicine, Durham, North Carolina.ORCID 0009-0009-5715-4098
Lorraine KingDepartment of Surgery, Duke University School of Medicine, Durham, North Carolina.ORCID 0009-0004-4617-7458
Lunden SimpsonDepartment of Surgery, Duke University School of Medicine, Durham, North Carolina.ORCID 0000-0002-7556-1078
Xiaoke LuoDepartment of Surgery, Washington University School of Medicine, St. Louis, Missouri.ORCID 0009-0006-8028-3822
Graham A ColditzDepartment of Surgery, Washington University School of Medicine, St. Louis, Missouri.ORCID 0000-0002-7307-0291
Shu JiangDepartment of Surgery, Washington University School of Medicine, St. Louis, Missouri.ORCID 0000-0003-1464-4838
Ovijit ChaudhuriDepartment of Mechanical Engineering, Stanford University, Stanford, California.ORCID 0000-0002-9287-3401
E Shelley HwangDepartment of Surgery, Duke University School of Medicine, Durham, North Carolina.ORCID 0000-0002-8571-1148
Jeffrey R MarksDepartment of Surgery, Duke University School of Medicine, Durham, North Carolina.ORCID 0000-0002-2054-5468
Kouros OwzarDuke Cancer Institute, Duke University School of Medicine, Durham, North Carolina.ORCID 0000-0002-3340-1287
Robert B WestDepartment of Pathology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0002-8330-8283

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI JOHN N. NORTON · 1985 to 2026
$174.8M
National Cancer Institute (NCI) CA014236National Cancer Institute (NCI) CA-17-035NCI NIH HHS P30 CA014236
6 · The paper itself

Abstract

Ductal carcinoma in situ (DCIS) is a risk factor for subsequent invasive breast cancer (IBC). To identify events in DCIS that lead to invasive cancer, we performed single-cell RNA sequencing on DCIS lesions and matched normal breast tissue. Inferred copy-number variation was used to identify neoplastic epithelial cells from clinical specimens, which contained a mixture of DCIS and normal ducts. Phylogenetic analysis demonstrated intratumoral clonal heterogeneity that was associated with significant gene expression differences. Classification of epithelial cells into mammary cell states revealed that subclones contained a mixture of cell states, suggesting an ongoing pattern of differentiation after neoplastic transformation. Cell state proportions were significantly different based on estrogen receptor expression, with estrogen receptor-negative DCIS more closely resembling the distribution in the normal breast, particularly with respect to cells with basal characteristics. Specific alterations in cell state proportions were associated with progression to invasive cancer in a cohort of DCIS with longitudinal outcome. Ongoing transcription of key basement membrane (BM) genes occurred in specific subsets of epithelial cell states, including basal/myoepithelial, which are diminished in DCIS. In the transition to IBC, the BM protein laminin, but not COL4, was altered in DCIS adjacent to invasion. Loss of COL4, but not laminin, in an in vitro DCIS model led to an invasive phenotype. These findings suggest that the process of invasion is a loss-of-function event due to an imbalance in critical cell populations essential for BM integrity rather than a gain of an invasive phenotype by neoplastic cells. SIGNIFICANCE: Single-cell analyses reveal ductal carcinoma in situ comprises multiple genetic clones with significant phenotypic diversity and link alterations in epithelial cell states and basement membrane integrity with invasive breast cancer progression.

Indexed as

Breast NeoplasmsCarcinoma, Intraductal, NoninfiltratingEpithelial CellsSingle-Cell AnalysisDNA Copy Number VariationsFemaleGene Expression Regulation, NeoplasticGenotypeHumansPhenotype

Identifiers

PMID40101158
PMCPMC12167932

What OpenQuestion holds

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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.