Evidence map›Paper›PMID 40119362›Full record

ArticleBreast cancer research : BCR2025

B cells and energy metabolism in HER2-positive DCIS: insights into breast cancer progression from spatial-omics analyses.

Helga Bergholtz, Jens Henrik Norum, Tonje Gulbrandsen Lien, Martina Landschoof Skrede, Øystein Garred, Therese Sørlie

Abstract read
In one paragraph

Article in Breast cancer research : BCR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

6 authors.

Helga BergholtzDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway. helgbe@ous-hf.no.ORCID http://orcid.org/0000-0003-0999-1106
Jens Henrik NorumDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID http://orcid.org/0000-0003-2689-7154
Tonje Gulbrandsen LienDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Martina Landschoof SkredeDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Øystein GarredDepartment of Pathology, Oslo University Hospital, Oslo, Norway.
Therese SørlieDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway. tsorlie@ous-hf.no.ORCID http://orcid.org/0000-0002-5995-2319

Funding

Kreftforeningen,Norway 214924Nanostring Technologies CosMx Protein GrantWellcome Trust 223197
6 · The paper itself

Abstract

During breast tumor progression, the transition from ductal carcinoma in situ (DCIS) to invasive breast cancer is a critical step with large implications for prognosis. However, the mechanisms of invasion are still largely unknown. At the DCIS stage, there is an over-representation of HER2-positive lesions compared with invasive breast cancer. In this study, we investigated the associations between gene expression profiles in cancer cells and the immune microenvironment of HER2-positive DCIS and invasive breast tumors with concurrent DCIS using spatial transcriptomics. We found distinctly more B cells in the vicinity of DCIS ducts than in invasive tumor areas. There was higher expression of genes involved in energy metabolism in DCIS cancer cells than in invasive cancer cells and a positive correlation between expression of metabolic genes and B-cell abundance in DCIS. In contrast were processes related to epithelial to mesenchymal transition negatively correlated with B-cell abundance in DCIS. We also found significant correlation between expression of the B-cell-attracting chemokines CCL19, CCL21 and CXCL13 in stromal cells and B cell abundance in DCIS. This study indicates that B cells may play a protective role in the progression of HER2-positive DCIS to invasive breast cancer and that increased metabolic activity in intraductal cancer cells in combination with chemokines produced by stromal cells may influence the immune microenvironment of DCIS. These findings have implications for understanding HER2-positive breast cancer progression.

Indexed as

B-LymphocytesBreast NeoplasmsCarcinoma, Intraductal, NoninfiltratingEnergy MetabolismErb-b2 Receptor Tyrosine KinasesBiomarkers, TumorDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansPrognosisTranscriptomeTumor MicroenvironmentBiomarkers, TumorERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesB cellsBreast cancer progressionDCISEnergy metabolismImmune microenvironmentSpatial-omics

Identifiers

PMID40119362
PMCPMC11929220

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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.