Evidence map›Paper›PMID 41535941›Full record

ArticleCell communication and signaling : CCS2026

A pro-carcinogenic oral microbe internalized by breast cancer cells promotes mammary tumorigenesis.

Sheetal Parida, Deeptashree Nandi, Deepak Verma, Mingyang Yi, Ashutosh Yende, Jessica Queen, Kathleen L Gabrielson, Cynthia L Sears, Dipali Sharma

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Medicina (Kaunas, Lithuania) · 2026
    Article
  3. Article
  4. The Role of Selected Bacteria in Breast Cancer Initiation and Development.International journal of molecular sciences · 2026
    Review
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

9 authors.

Sheetal ParidaDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Deeptashree NandiDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Deepak VermaDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Mingyang YiDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Ashutosh YendeDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Jessica QueenDepartment of Medicine, Infectious Disease, Johns Hopkins University School of Medicine, Maryland, Baltimore, USA.
Kathleen L GabrielsonDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Cynthia L SearsDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Dipali SharmaDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. dsharma7@jhmi.edu.

Funding

Breast Cancer Research Foundation 90047965Congressionally Directed Medical Research Programs BC191572
6 · The paper itself

Abstract

The intricate relationship between microbiota and breast cancer presents an additional risk factor that can have a profound impact on disease progression. Focusing on dysbiosis, our metagenomic analysis shows overabundance of an oral pathogenic microbe F. nucleatum and co-habitation of associated biofilm forming oral microbes in cancerous breast. Mammary gland colonization with F. nucleatum results in the development of metaplastic lesions accompanied with inflammation, DNA damage and hyper-proliferation in healthy mice. Exhibiting the impact of circulating F. nucleatum introduced via hematogenous route, breast tumor bearing mice show accelerated tumor growth and metastatic progression. Increased proliferation, migration, self-renewal and chemoresistance in breast cancer cells as well as non-tumorigenic breast epithelial cells bearing pathogenic BRCA1 mutation is observed upon F. nucleatum exposure which is internalized by the cells in a Gal-GalNAc dependent manner. Of interest, cells harboring BRCA1 mutations exhibit greater cell surface accumulation of Gal-GalNAc sugar residue. This work sheds light on the oncogenic impact of a pro-carcinogenic oral bacterium, F. nucleatum, on normal mammary epithelium and breast cancer, implicates the impairment of DNA damage and repair pathways as its functional mediators, and proposes the concept of increased vulnerability of BRCA1 mutant breast cancer cells owing to their preferential internalization of F. nucleatum.

Indexed as

Breast NeoplasmsCarcinogenesisFusobacterium nucleatumMouthAnimalsBRCA1 ProteinCell Line, TumorCell ProliferationDNA DamageFemaleHumansMiceBRCA1 ProteinBRCA mutant cellsBreast cancerDNA damageF. nucleatumOral dysbiosis

Identifiers

PMID41535941
PMCPMC13154579

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.