Evidence map›Paper›PMID 27635472›Full record

ArticleOncotarget2016

The mitochondrial translation machinery as a therapeutic target in Myc-driven lymphomas.

Aleco D'Andrea, Ilaria Gritti, Paola Nicoli, Marco Giorgio, Mirko Doni, Annalisa Conti, Valerio Bianchi, Lucia Casoli, Arianna Sabò, Alexandre Mironov and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 69 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

12 authors at 5 institutions in 2 countries.

Aleco D'AndreaDepartment of Experimental Oncology, European Institute of Oncology, Milan, Italy.
Ilaria GrittiDepartment of Experimental Oncology, European Institute of Oncology, Milan, Italy.
Paola NicoliDepartment of Experimental Oncology, European Institute of Oncology, Milan, Italy.
Marco GiorgioDepartment of Experimental Oncology, European Institute of Oncology, Milan, Italy.
Mirko DoniDepartment of Experimental Oncology, European Institute of Oncology, Milan, Italy.
Annalisa ContiCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia, Milan, Italy.
Valerio BianchiCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia, Milan, Italy.
Lucia CasoliCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia, Milan, Italy.
Arianna SabòCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia, Milan, Italy.
Alexandre MironovThe Institute of Molecular Oncology of the Italian Foundation for Cancer Research, Milan, Italy.
Galina V BeznoussenkoThe Institute of Molecular Oncology of the Italian Foundation for Cancer Research, Milan, Italy.
Bruno AmatiDepartment of Experimental Oncology, European Institute of Oncology, Milan, Italy.
European Institute of Oncology · ITCenter for Genomic Science · ITFIRC Institute of Molecular Oncology · ITItalian Institute of Technology · ITUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The oncogenic transcription factor Myc is required for the progression and maintenance of diverse tumors. This has led to the concept that Myc itself, Myc-activated gene products, or associated biological processes might constitute prime targets for cancer therapy. Here, we present an in vivo reverse-genetic screen targeting a set of 241 Myc-activated mRNAs in mouse B-cell lymphomas, unraveling a critical role for the mitochondrial ribosomal protein (MRP) Ptcd3 in tumor maintenance. Other MRP-coding genes were also up regulated in Myc-induced lymphoma, pointing to a coordinate activation of the mitochondrial translation machinery. Inhibition of mitochondrial translation with the antibiotic Tigecycline was synthetic-lethal with Myc activation, impaired respiratory activity and tumor cell survival in vitro, and significantly extended lifespan in lymphoma-bearing mice. We have thus identified a novel Myc-induced metabolic dependency that can be targeted by common antibiotics, opening new therapeutic perspectives in Myc-overexpressing tumors.

Indexed as

AnimalsArabidopsis ProteinsBurkitt LymphomaCell Line, TumorHumansMiceMice, TransgenicMinocyclineMitochondriaMitochondrial ProteinsProtein BiosynthesisProto-Oncogene Proteins c-mycRNA-Binding ProteinsTigecyclineXenograft Model Antitumor AssaysArabidopsis ProteinsMinocyclineMitochondrial ProteinsMYC protein, humanMyc protein, mouseProto-Oncogene Proteins c-mycPTCD3 protein, humanRNA-Binding ProteinsTigecyclinelymphomamitochondriamitochondrial translationMycTigecycline

Identifiers

PMID27635472
PMCPMC5341918
OpenAlexW2517286776

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.