Evidence map›Paper›PMID 33672955›Full record

ArticleToxins2021

ERK and mTORC1 Inhibitors Enhance the Anti-Cancer Capacity of the Octpep-1 Venom-Derived Peptide in Melanoma BRAF(V600E) Mutations.

Javier Moral-Sanz, Manuel A Fernandez-Rojo, Jeremy Potriquet, Pamela Mukhopadhyay, Andreas Brust, Patrick Wilhelm, Taylor B Smallwood, Richard J Clark, Bryan G Fry, Paul F Alewood and 4 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Toxins, 2021. 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
0.6field-weighted citation impact, top 34% 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, 11 citations in OpenAlex.

  1. Review
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  7. Pharmacological Characterisation ofInternational journal of molecular sciences · 2021
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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

14 authors at 3 institutions in 2 countries.

Javier Moral-SanzTranslational Venomics Group, Madrid Institute for Advanced Studies in Food, E28049 Madrid, Spain.ORCID 0000-0001-8602-8554
Manuel A Fernandez-RojoHepatic Regenerative Medicine Group, Madrid Institute for Advanced Studies in Food, E28049 Madrid, Spain.
Jeremy PotriquetInfectious Diseases Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD 4006, Australia.
Pamela MukhopadhyayDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD 4006, Australia.
Andreas BrustInstitute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia.
Patrick WilhelmInstitute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia.
Taylor B SmallwoodSchool of Biomedical Sciences, The University of Queensland, Brisbane, QLD 4072, Australia.ORCID 0000-0002-2211-0265
Richard J ClarkInstitute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia.ORCID 0000-0002-6807-5426
Bryan G FrySchool of Biological Sciences, The University of Queensland, Brisbane, QLD 4072, Australia.ORCID 0000-0001-6661-1283
Paul F AlewoodInstitute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia.
Nicola WaddellDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD 4006, Australia.
John J MilesDepartment of Immunology, QIMR Berghofer Medical Research Institute, Brisbane, QLD 4006, Australia.ORCID 0000-0001-5506-6304
Jason P MulvennaInfectious Diseases Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD 4006, Australia.
Maria P IkonomopoulouTranslational Venomics Group, Madrid Institute for Advanced Studies in Food, E28049 Madrid, Spain.ORCID 0000-0001-7739-080X
The University of Queensland · AUQIMR Berghofer Medical Research Institute · AUMadrid Institute for Advanced Studies · ES

Funding

FP7 People: Marie-Curie Actions N 291803-AMAROUT IIRegional Madrid Government 2018-T1/BIO-11262
6 · The paper itself

Abstract

Melanoma is the main cause of skin cancer deaths, with special emphasis in those cases carrying BRAF mutations that trigger the mitogen-activated protein kinases (MAPK) signaling and unrestrained cell proliferation in the absence of mitogens. Current therapies targeting MAPK are hindered by drug resistance and relapse that rely on metabolic rewiring and Akt activation. To identify new drug candidates against melanoma, we investigated the molecular mechanism of action of the

Indexed as

MutationAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorCell ProliferationEnergy MetabolismExtracellular Signal-Regulated MAP KinasesHumansMechanistic Target of Rapamycin Complex 1MelanomaProtein Kinase InhibitorsProto-Oncogene Proteins B-rafSignal TransductionSirolimusSkin NeoplasmsBRAF protein, humanExtracellular Signal-Regulated MAP KinasesMechanistic Target of Rapamycin Complex 1Protein Kinase InhibitorsProto-Oncogene Proteins B-rafSirolimuscancercombination-therapiesmelanoma BRAF mutationoctopus-peptidevenom-peptide

Identifiers

PMID33672955
PMCPMC7918145
OpenAlexW3130397276

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.