Evidence map›Paper›PMID 24358335›Full record

ArticlePloS one2013

Mice lacking NCF1 exhibit reduced growth of implanted melanoma and carcinoma tumors.

Tiina Kelkka, Angela Pizzolla, Juha Petteri Laurila, Tomas Friman, Renata Gustafsson, Eva Källberg, Olof Olsson, Tomas Leanderson, Kristofer Rubin, Marko Salmi and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

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  11. Frontiers in immunology · 2021
    Article
  12. Article
  13. NOX2-Derived Reactive Oxygen Species in Cancer.Oxidative medicine and cellular longevity · 2020
    Review
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  15. Article
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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

12 authors at 4 institutions in 2 countries.

Tiina KelkkaMedicity Research Laboratory, Turku, Finland ; Turku Doctoral Programme of Biomedical Sciences, Turku, Finland.
Angela PizzollaMedical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Juha Petteri LaurilaMedicity Research Laboratory, Turku, Finland.
Tomas FrimanDepartment of Medical Biochemistry and Microbiology, Uppsala University, Uppsala.
Renata GustafssonDepartment of Medical Biochemistry and Microbiology, Uppsala University, Uppsala.
Eva KällbergImmunology Group, Biomedical Center, Lund University, Lund, Sweden.
Olof OlssonDepartment of Medical Biochemistry and Microbiology, Uppsala University, Uppsala.
Tomas LeandersonImmunology Group, Biomedical Center, Lund University, Lund, Sweden.
Kristofer RubinDepartment of Medical Biochemistry and Microbiology, Uppsala University, Uppsala.
Marko SalmiMedicity Research Laboratory, Turku, Finland.
Sirpa JalkanenMedicity Research Laboratory, Turku, Finland.
Rikard HolmdahlMedicity Research Laboratory, Turku, Finland ; Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Uppsala University · SEKarolinska Institutet · SELund University · SEUniversity of Turku · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NADPH oxidase 2 (NOX2) complex is a professional producer of reactive oxygen species (ROS) and is mainly expressed in phagocytes. While the activity of the NOX2 complex is essential for immunity against pathogens and protection against autoimmunity, its role in the development of malignant tumors remains unclear. We compared wild type and Ncf1 (m1J) mutated mice, which lack functional NOX2 complex, in four different tumor models. Ncf1 (m1J) mutated mice developed significantly smaller tumors in two melanoma models in which B16 melanoma cells expressing a hematopoietic growth factor FLT3L or luciferase reporter were used. Ncf1 (m1J) mutated mice developed significantly fewer Lewis Lung Carcinoma (LLC) tumors, but the tumors that did develop, grew at a pace that was similar to the wild type mice. In the spontaneously arising prostate carcinoma model (TRAMP), tumor growth was not affected. The lack of ROS-mediated protection against tumor growth was associated with increased production of immunity-associated cytokines. A significant increase in Th2 associated cytokines was observed in the LLC model. Our present data show that ROS regulate rejection of the antigenic B16-luc and LLC tumors, whereas the data do not support a role for ROS in growth of intrinsically generated tumors.

Indexed as

AnimalsCarcinomaCarcinoma, Lewis LungDisease Models, AnimalInflammationMelanomaMelanoma, ExperimentalMembrane ProteinsMiceMutationNADPH OxidasesNeoplasmsReactive Oxygen SpeciesTumor Burdenflt3 ligand proteinMembrane ProteinsNADPH Oxidasesneutrophil cytosolic factor 1Reactive Oxygen Species

Identifiers

PMID24358335
PMCPMC3865299
OpenAlexW2049334162

What OpenQuestion holds

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LicenceCC BY
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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.