Evidence map›Paper›PMID 26898917›Full record

ArticleScientific reports2016

Host kinin B1 receptor plays a protective role against melanoma progression.

Andrea G Maria, Patrícia Dillenburg-Pilla, Rosana I Reis, Elaine M Floriano, Cristiane Tefé-Silva, Simone G Ramos, João B Pesquero, Clara Nahmias, Claudio M Costa-Neto

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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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

9 authors at 4 institutions in 2 countries.

Andrea G MariaDepartment of Biochemistry and Immunology; Ribeirão Preto Medical School - University of São Paulo, 14049-900, Ribeirão Preto, Brazil.
Patrícia Dillenburg-PillaDepartment of Biochemistry and Immunology; Ribeirão Preto Medical School - University of São Paulo, 14049-900, Ribeirão Preto, Brazil.
Rosana I ReisDepartment of Biochemistry and Immunology; Ribeirão Preto Medical School - University of São Paulo, 14049-900, Ribeirão Preto, Brazil.
Elaine M FlorianoDepartament of Pathology, Ribeirão Preto Medical School - University of São Paulo, 14049-900, Ribeirão Preto, Brazil.
Cristiane Tefé-SilvaDepartament of Pathology, Ribeirão Preto Medical School - University of São Paulo, 14049-900, Ribeirão Preto, Brazil.
Simone G RamosDepartament of Pathology, Ribeirão Preto Medical School - University of São Paulo, 14049-900, Ribeirão Preto, Brazil.
João B PesqueroDepartment of Biophysics, Federal University of São Paulo, 04039-032, São Paulo, Brazil.
Clara NahmiasInserm U981,Institut Gustave Roussy, 94800, Villejuif, France.
Claudio M Costa-NetoDepartment of Biochemistry and Immunology; Ribeirão Preto Medical School - University of São Paulo, 14049-900, Ribeirão Preto, Brazil.
Universidade de São Paulo · BRBipar · FRInstitut Gustave Roussy · FRUniversidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma is a very aggressive tumor that arises from melanocytes. Late stage and widely spread diseases do not respond to standard therapeutic approaches. The kallikrein-kinin system (KKS) participates in biological processes such as vasodilatation, pain and inflammatory response. However, the role of KKS in tumor formation and progression is not completely understood. The role of the host kinin B1 receptor in melanoma development was evaluated using a syngeneic melanoma model. Primary tumors and metastasis were respectively induced by injecting B16F10 melanoma cells, which are derived from C57BL/6 mice, subcutaneously or in the tail vein in wild type C57BL/6 and B1 receptor knockout mice (B1(-/-)). Tumors developed in B1(-/-) mice presented unfavorable prognostic factors such as increased incidence of ulceration, higher levels of IL-10, higher activation of proliferative pathways such as ERK1/2 and Akt, and increased mitotic index. Furthermore, in the metastasis model, B1(-/-) mice developed larger metastatic colonies in the lung and lower CD8(+)immune effector cells when compared with WT animals. Altogether, our results provide evidences that B1(-/-) animals developed primary tumors with multiple features associated with poor prognosis and unfavorable metastatic onset, indicating that the B1 receptor may contribute to improve the host response against melanoma progression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsDisease ProgressionFemaleInterleukin-10Kallikrein-Kinin SystemLung NeoplasmsMelanoma, ExperimentalMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitotic IndexProto-Oncogene Proteins c-aktReceptor, Bradykinin B1IL10 protein, mouseInterleukin-10Mapk1 protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktReceptor, Bradykinin B1

Identifiers

PMID26898917
PMCPMC4761993
OpenAlexW2409387322

What OpenQuestion holds

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Registered trials

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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.