Evidence map›Paper›PMID 31744894›Full record

ArticleMolecular cancer therapeutics2020

Rational Combination Therapy for Melanoma with Dinaciclib by Targeting BAK-Dependent Cell Death.

Xiaoou Xu, Shizuka Eshima, Shinichiro Kato, David E Fisher, Hiroaki Sakurai, Yoshihiro Hayakawa, Satoru Yokoyama

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2020. 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 28% 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, 14 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

7 authors at 2 institutions in 2 countries.

Xiaoou XuDivision of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama, Toyama, Japan.
Shizuka EshimaDivision of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama, Toyama, Japan.
Shinichiro KatoDivision of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama, Toyama, Japan.
David E FisherDepartment of Dermatology, Cutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Massachusetts.
Hiroaki SakuraiDepartment of Cancer Cell Biology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.ORCID 0000-0003-0657-9570
Yoshihiro HayakawaDivision of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama, Toyama, Japan.
Satoru YokoyamaDivision of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama, Toyama, Japan. yokoyama@pha.u-toyama.ac.jp.
University of Toyama · JPMassachusetts General Hospital · US

Funding

Transcriptional mechanisms and melanomaP01CA163222 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DAVID E FISHER · 2013 to 2026
$25.3M
The MITF transcriptional network: melanoma risk and carcinogenesisR01AR043369 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DAVID E FISHER · 1996 to 2026
$9.4M
Therapeutic strategies for treatment of giant congenital melanocytic neviR01AR072304 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DAVID E FISHER · 2017 to 2026
$3.9M
A druggable dependency in low-MITF/high-AXL melanoma: preclinical efficacy and mechanism of action in a key treatment-resistant subclass.R01CA222871 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI FISHER, DAVID E · 2018 to 2022
$1.8M
NCI NIH HHS P01 CA163222NCI NIH HHS R01 CA222871NIAMS NIH HHS R01 AR043369NIAMS NIH HHS R01 AR072304
6 · The paper itself

Abstract

Mutation of the oncogene BRAF is among the most common genetic alterations in melanoma. BRAF inhibitors alone or in combination with MEK inhibitors fail to eradicate the tumor in most patients due to combinations of intrinsic or acquired resistance. Therefore, novel strategies are needed to improve the therapeutic efficacy of BRAF inhibition. We demonstrated that dinaciclib has potent antimelanoma effects by inducing BAK-dependent apoptosis through MCL1 reduction. Contrary to dinaciclib, the inhibitors of BRAF/MEK/CDK4/6 induced apoptosis dominantly through a BAX-dependent mechanism. Although the combination of BRAF and MEK inhibitors did not exhibit additive antimelanoma effects, their combination with dinaciclib synergistically inhibited melanoma growth both

Indexed as

Cell DeathCell Line, TumorCyclic N-OxidesCyclin-Dependent KinasesDrug Therapy, CombinationHumansIndolizinesMelanomaPyridinium CompoundsCyclic N-OxidesCyclin-Dependent KinasesdinaciclibIndolizinesPyridinium Compounds

Identifiers

PMID31744894
PMCPMC7007861
OpenAlexW2990321273

What OpenQuestion holds

Textmetadata
LicenceTDM
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.