Evidence map›Paper›PMID 31766600›Full record

ReviewCancers2019

A Review of the Potential Role of Human Cytomegalovirus (HCMV) Infections in Breast Cancer Carcinogenesis and Abnormal Immunity.

Jürgen Geisler, Joel Touma, Afsar Rahbar, Cecilia Söderberg-Nauclér, Katja Vetvik

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  4. Review
  5. A vaccine against cytomegalovirus: how close are we?The Journal of clinical investigation · 2025
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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

5 authors at 2 institutions in 3 countries.

Jürgen GeislerDepartment of Oncology, Akershus University Hospital (AHUS), 1478 Lørenskog, Norway.ORCID 0000-0001-6239-3856
Joel ToumaDepartment of Oncology, Akershus University Hospital (AHUS), 1478 Lørenskog, Norway.
Afsar RahbarDepartment of Medicine, Division of Microbial Pathogenesis, Bioclinicum, Karolinska Institutet, 17176 Stockholm, Sweden.ORCID 0000-0003-1158-2512
Cecilia Söderberg-NauclérDepartment of Medicine, Division of Microbial Pathogenesis, Bioclinicum, Karolinska Institutet, 17176 Stockholm, Sweden.
Katja VetvikInstitute of Clinical Medicine, University of Oslo, Campus Akershus University Hospital (AHUS), 1478 Lørenskog, Norway.ORCID 0000-0003-2454-5585
University of Oslo · NOKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously recognized classical human onco-viruses can regulate complex neoplastic events, and are estimated to play a role during carcinogenesis in 15-20% of cancer cases. Although the DNA and gene products of several viruses have been found in breast tumors, none of the classical onco-viruses have definitely been linked to the initiation of breast cancer. However, recent evidence shows that human cytomegalovirus (HCMV) gene products are found in >90% of tumors and metastases of breast cancers, and their increased expression can be correlated to a more aggressive breast cancer phenotype. Supporting the active role of HCMV in breast cancer, a specific HCMV strain, HCMV-DB, was recently shown to exert oncogenic transformational activity in breast epithelial cells in vitro, and to give rise to fast-growing, triple-negative breast tumors when injected into immune deficient mice. The same observation holds true for clinical studies implying increased HCMV protein expression in triple negative breast cancer biopsies. In addition to functionally being able to hijack tumor-promoting cellular events, HCMV is known to exhibit a wide range of immunosuppressive effects, which can have radical impact on the tumor microenvironment. HCMV infected cells can avoid recognition and elimination by the immune system by orchestrating polarization of immunosuppressive type II macrophages, preventing antigen presentation, by expressing T cell inhibitory molecules, and possibly, by the induction of regulatory T (Treg) cell responses. These actions would be especially deleterious for the antigenic activation and proliferation of tumor specific CD8

Indexed as

antiviral treatmentbreast cancercancercheck-point inhibitorsdendritic cellshuman cytomegalovirusT cellstriple negative breast cancertumor associated macrophagestumor immunology

Identifiers

PMID31766600
PMCPMC6966479
OpenAlexW2990350731

What OpenQuestion holds

Textmetadata
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.