Evidence map›Paper›PMID 34288272›Full record

ArticleCancer science2021

Novel RAF/MEK inhibitor CH5126766/VS-6766 has efficacy in combination with eribulin for the treatment of triple-negative breast cancer.

Hisako Ono, Mano Horinaka, Mamiko Sukeno, Mie Morita, Shusuke Yasuda, Emi Nishimoto, Eiichi Konishi, Toshiyuki Sakai

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Hisako OnoDepartment of Molecular Diagnostics and Therapeutics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.ORCID https://orcid.org/0000-0003-1192-683X
Mano HorinakaDepartment of Drug Discovery Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.ORCID https://orcid.org/0000-0001-8168-1802
Mamiko SukenoDepartment of Drug Discovery Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Mie MoritaDepartment of Drug Discovery Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Shusuke YasudaDepartment of Drug Discovery Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Emi NishimotoDepartment of Drug Discovery Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Eiichi KonishiDepartment of Surgical Pathology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Toshiyuki SakaiDepartment of Drug Discovery Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Various molecular-targeting drugs have markedly improved the treatment of patients with breast cancer. As yet, therapies for triple-negative breast cancer are mainly cytotoxic agents. To investigate the novel therapy for triple-negative breast cancer, we herein examined the effects of a new combination therapy comprising a RAF/MEK inhibitor CH5126766, also known as VS-6766, which we originally discovered, and eribulin. The combination of CH5126766 and eribulin potently inhibited cell growth in the triple-negative breast cancer cell lines tested. The underlying mechanism in the efficacy of this combination treatment in vitro and in vivo was due to enhanced apoptosis through the suppression of survivin and Bcl-2 family proteins. We also showed the suppressed expression of programmed cell death ligand 1 (PD-L1) in combination therapy in vivo. We found that combination therapy with eribulin and CH5126766 for triple-negative breast cancer inhibited cell growth by apoptosis and raised a possibility that immune responses through suppression of PD-L1 might partially contribute to inhibition of tumor growth, indicating the potential of this combination as a novel strategy for triple-negative breast cancer.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisB7-H1 AntigenCell CycleCell Line, TumorCell ProliferationCoumarinsFemaleFuransKetonesMiceMice, Inbred BALB CMitogen-Activated Protein Kinase KinasesOncogene Protein v-aktPolyether PolyketidesB7-H1 AntigenCoumarinseribulinFuransKetonesMitogen-Activated Protein Kinase KinasesOncogene Protein v-aktPolyether PolyketidesProtein Kinase InhibitorsProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-rafRO5126766SurvivinapoptosisCH5126766/VS-6766eribulinPD-L1TNBC

Identifiers

PMID34288272
PMCPMC8486178
OpenAlexW3184366846

What OpenQuestion holds

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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.