Evidence map›Paper›PMID 31930708›Full record

ArticleEMBO molecular medicine2020

Macrophages induce malignant traits in mammary epithelium via IKKε/TBK1 kinases and the serine biosynthesis pathway.

Ewa Wilcz-Villega, Edward Carter, Alastair Ironside, Ruoyan Xu, Isabella Mataloni, Julie Holdsworth, William Jones, Rocío Moreno Béjar, Lukas Uhlik, Robert B Bentham and 7 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. The Microenvironment in DCIS and Its Role in Disease Progression.Advances in experimental medicine and biology · 2025
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
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

17 authors at 3 institutions in 2 countries.

Ewa Wilcz-VillegaCentre for Molecular Oncology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Edward CarterCentre for Tumour Biology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Alastair IronsideCentre for Tumour Biology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Ruoyan XuCentre for Molecular Oncology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Isabella MataloniCentre for Molecular Oncology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Julie HoldsworthCentre for Tumour Biology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
William JonesCentre for Molecular Oncology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Rocío Moreno BéjarCentre for Molecular Oncology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Lukas UhlikCentre for Molecular Oncology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Robert B BenthamDepartment of Cell and Developmental Biology, Consortium for Mitochondrial Research, University College London, London, UK.
Susana A GodinhoCentre for Molecular Oncology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Jesmond DalliLipid Mediator Unit, Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine, Queen Mary University of London, London, UK.
Richard GroseCentre for Tumour Biology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Gyorgy SzabadkaiDepartment of Cell and Developmental Biology, Consortium for Mitochondrial Research, University College London, London, UK.ORCID 0000-0002-3006-3577
Louise JonesCentre for Tumour Biology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.
Kairbaan Hodivala-DilkeCentre for Tumour Biology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.ORCID 0000-0002-2859-749X
Katiuscia BianchiCentre for Molecular Oncology, Barts Cancer Institute, John Vane Science Centre, Queen Mary University of London, London, UK.ORCID 0000-0002-4549-4476
Queen Mary University of London · GBUniversity College London · GBUniversity of Padua · IT

Funding

ATHEROGENIC &ANTIATHEROGENIC LIPOPROTEINS IN CADF32HL008004 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI WILSON, PAUL R · 1989 to 1990
–
Barts and The London School of Medicine and Dentistry 467/2053Biotechnology and Biological Sciences Research Council BB/L020874/1Breast Cancer Now 2017NovPR988Cancer Research UK (CRUK) C8218/A21453Italian Association for Cancer Research AIRC, IG13447Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society 107613/Z/15/ZUK Research and Innovation|Biotechnology and Biological Sciences Research Council (BBSRC) BB/L020874/1University College London COMPleX/British Heart Foundation Fund SP/08/004Wellcome TrustWellcome Trust (WT) 097815/Z/11/Z
6 · The paper itself

Abstract

During obesity, macrophages infiltrate the breast tissue leading to low-grade chronic inflammation, a factor considered responsible for the higher risk of breast cancer associated with obesity. Here, we formally demonstrate that breast epithelial cells acquire malignant properties when exposed to medium conditioned by macrophages derived from human healthy donors. These effects were mediated by the breast cancer oncogene IKKε and its downstream target-the serine biosynthesis pathway as demonstrated by genetic or pharmacological tools. Furthermore, amlexanox, an FDA-approved drug targeting IKKε and its homologue TBK1, delayed in vivo tumour formation in a combined genetic mouse model of breast cancer and high-fat diet-induced obesity/inflammation. Finally, in human breast cancer tissues, we validated the link between inflammation-IKKε and alteration of cellular metabolism. Altogether, we identified a pathway connecting obesity-driven inflammation to breast cancer and a potential therapeutic strategy to reduce the risk of breast cancer associated with obesity.

Indexed as

I-kappa B KinaseSerineAminopyridinesAnimalsBreast NeoplasmsCulture Media, ConditionedEpithelial CellsFemaleHumansInflammationMacrophagesMammary Glands, HumanMiceObesityProtein Serine-Threonine KinasesAminopyridinesamlexanoxCulture Media, ConditionedI-kappa B KinaseProtein Serine-Threonine KinasesSerineTBK1 protein, humanTbk1 protein, mouseinflammationmacrophagesmalignant transformationobesitytumour metabolism

Identifiers

PMID31930708
PMCPMC7005540
OpenAlexW3000333037

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.