Evidence map›Paper›PMID 33917524›Full record

ArticleCancers2021

Modulated Electro-Hyperthermia Induces a Prominent Local Stress Response and Growth Inhibition in Mouse Breast Cancer Isografts.

Csaba András Schvarcz, Lea Danics, Tibor Krenács, Pedro Viana, Rita Béres, Tamás Vancsik, Ákos Nagy, Attila Gyenesei, József Kun, Marko Fonović and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. 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

14 authors at 3 institutions in 2 countries.

Csaba András SchvarczInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.
Lea DanicsInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.
Tibor Krenács1st Department of Pathology and Experimental Cancer Research, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0001-9164-065X
Pedro VianaInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.
Rita BéresInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.
Tamás VancsikInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.
Ákos NagyMolecular Oncohematology Research Group, 1st Department of Pathology and Experimental Cancer Research, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0001-6118-0365
Attila GyeneseiBioinformatics Research Group, Genomics and Bioinformatics Core Facility, János Szentágothai Research Centre, University of Pécs, H-7624 Pécs, Hungary.
József KunBioinformatics Research Group, Genomics and Bioinformatics Core Facility, János Szentágothai Research Centre, University of Pécs, H-7624 Pécs, Hungary.
Marko FonovićDepartment of Biochemistry and Molecular and Structural Biology, Jožef Stefan Institute, 1000 Ljubljana, Slovenia.
Robert VidmarDepartment of Biochemistry and Molecular and Structural Biology, Jožef Stefan Institute, 1000 Ljubljana, Slovenia.
Zoltán BenyóInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.ORCID 0000-0001-6015-0359
Tamás KaucsárInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.
Péter HamarInstitute of Translational Medicine, Semmelweis University, 1094 Budapest, Hungary.
Semmelweis University · HUJožef Stefan Institute · SIUniversity of Pecs · HU

Funding

András Korányi Foundation Dr. Schvarcz Csaba 2019-2021Educating Experts of the Future: Developing Bioinformatics and Biostatistics competencies of European Biomedical Students BECOMING, 2019-1-HU01-KA203-061251Ministry of Human Capacities EFOP-3.6.3-VEKOP-16-2017-00009Ministry of Human Capacities Insitutional Excellence Program for the Higher Education within the framework of the Molecular Biology Thematic Program of the Semmelweis UniversityMinistry of Innovation and Technology Cooperative Doctoral ProgramNational Research, Development and Innovation Office ANN-110810National Research, Development and Innovation Office GINOP-2.3.1-20-2020-00001National Research, Development and Innovation Office GINOP-2.3.4-15-2020-00010National Research, Development and Innovation Office K-112964National Research, Development and Innovation Office K-125174National Research, Development and Innovation Office NVKP_16-1-2016-0042National Research, Development and Innovation Office SNN-114619Semmelweis Fund for Science and Innovation 139610/TMI/2020
6 · The paper itself

Abstract

Modulated electro-hyperthermia (mEHT) is a selective cancer treatment used in human oncology complementing other therapies. During mEHT, a focused electromagnetic field (EMF) is generated within the tumor inducing cell death by thermal and nonthermal effects. Here we investigated molecular changes elicited by mEHT using multiplex methods in an aggressive, therapy-resistant triple negative breast cancer (TNBC) model. 4T1/4T07 isografts inoculated orthotopically into female BALB/c mice were treated with mEHT three to five times. mEHT induced the upregulation of the stress-related Hsp70 and cleaved caspase-3 proteins, resulting in effective inhibition of tumor growth and proliferation. Several acute stress response proteins, including protease inhibitors, coagulation and heat shock factors, and complement family members, were among the most upregulated treatment-related genes/proteins as revealed by next-generation sequencing (NGS), Nanostring and mass spectrometry (MS). pathway analysis demonstrated that several of these proteins belong to the response to stimulus pathway. Cell culture treatments confirmed that the source of these proteins was the tumor cells. The heat-shock factor inhibitor KRIBB11 reduced mEHT-induced complement factor 4 (C4) mRNA increase. In conclusion, mEHT monotherapy induced tumor growth inhibition and a complex stress response. Inhibition of this stress response is likely to enhance the effectiveness of mEHT and other cancer treatments.

Indexed as

antiproliferative effectmodulated electro-hyperthermiastress responsetriple negative breast cancer isografttumor growth inhibition

Identifiers

PMID33917524
PMCPMC8038813
OpenAlexW3150277333

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.