Evidence map›Paper›PMID 27406745›Full record

ArticleNature communications2016

Decreased NK-cell tumour immunosurveillance consequent to JAK inhibition enhances metastasis in breast cancer models.

Alessia Bottos, Dagmar Gotthardt, Jason W Gill, Albana Gattelli, Anna Frei, Alexandar Tzankov, Veronika Sexl, Aleksandra Wodnar-Filipowicz, Nancy E Hynes

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 102 citations in OpenAlex.

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  6. Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026
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  19. Advances in Immunocompetent Mouse and Rat Models.Cold Spring Harbor perspectives in medicine · 2024
    Review
  20. Article

6 more citing papers are in PubMed but not listed here.

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 at 4 institutions in 2 countries.

Alessia BottosFriedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.
Dagmar GotthardtInstitute of Pharmacology and Toxicology, Department for Biomedical Sciences, University of Veterinary Medicine, 1210 Vienna, Austria.
Jason W GillFriedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.ORCID 0000-0003-0955-6470
Albana GattelliFriedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.
Anna FreiFriedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.
Alexandar TzankovInstitute of Pathology, University Hospital Basel, CH-4031 Basel, Switzerland.ORCID 0000-0002-1100-3819
Veronika SexlInstitute of Pharmacology and Toxicology, Department for Biomedical Sciences, University of Veterinary Medicine, 1210 Vienna, Austria.
Aleksandra Wodnar-FilipowiczStem Cell Center of Competence, University of Basel, CH-4002 Basel, Switzerland.
Nancy E HynesFriedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.
Friedrich Miescher Institute · CHUniversity of Basel · CHUniversity of Veterinary Medicine Vienna · ATUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The JAK/STAT pathway is an attractive target for breast cancer therapy due to its frequent activation, and clinical trials evaluating JAK inhibitors (JAKi) in advanced breast cancer are ongoing. Using patient biopsies and preclinical models of breast cancer, we demonstrate that the JAK/STAT pathway is active in metastasis. Unexpectedly, blocking the pathway with JAKi enhances the metastatic burden in experimental and orthotopic models of breast cancer metastasis. We demonstrate that this prometastatic effect is due to the immunosuppressive activity of JAKi with ensuing impairment of NK-cell-mediated anti-tumour immunity. Furthermore, we show that immunostimulation with IL-15 overcomes the enhancing effect of JAKi on metastasis formation. Our findings highlight the importance of evaluating the effect of targeted therapy on the tumour environment. The impact of JAKi on NK cells and the potential value of immunostimulators to overcome the weakened tumour immunosurveillance, are worthwhile considering in the clinical setting of breast cancer.

Indexed as

Immunologic SurveillanceModels, BiologicalAnimalsBone NeoplasmsBreast NeoplasmsCell DifferentiationCell ProliferationCytotoxicity, ImmunologicEnzyme ActivationFemaleHumansImmunomodulationInterleukin-15Janus Kinase InhibitorsJanus KinasesKiller Cells, NaturalInterleukin-15Janus Kinase InhibitorsJanus KinasesSTAT Transcription Factors

Identifiers

PMID27406745
PMCPMC4947169
OpenAlexW2469534996

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.