Evidence map›Paper›PMID 32046105›Full record

ArticleInternational journal of molecular sciences2020

Knockdown of Atg7 Induces Nuclear-LC3 Dependent Apoptosis and Augments Chemotherapy in Colorectal Cancer Cells.

Anna-Lena Scherr, Adam Jassowicz, Anna Pató, Christin Elssner, Lars Ismail, Nathalie Schmitt, Paula Hoffmeister, Lasse Neukirch, Georg Gdynia, Benjamin Goeppert and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 30 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

13 authors at 5 institutions in 1 country.

Anna-Lena ScherrNational Center for Tumor Diseases, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Adam JassowiczNational Center for Tumor Diseases, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Anna PatóNational Center for Tumor Diseases, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Christin ElssnerNational Center for Tumor Diseases, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Lars IsmailNational Center for Tumor Diseases, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Nathalie SchmittNational Center for Tumor Diseases, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Paula HoffmeisterNational Center for Tumor Diseases, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Lasse NeukirchClinical Cooperation Unit Applied Tumor Immunity, National Center for Tumor Diseases and German Cancer Research Center, Heidelberg 69120, Germany.
Georg GdyniaInstitute of Pathology, University Hospital Heidelberg, Heidelberg 69120, Germany.
Benjamin GoeppertInstitute of Pathology, University Hospital Heidelberg, Heidelberg 69120, Germany.
Henning Schulze-BergkamenDepartment of internal Medicine II, Marien Hospital, Wesel46483, Germany.
Dirk JägerNational Center for Tumor Diseases, University Hospital Heidelberg, 69120 Heidelberg, Germany.
Bruno Christian KöhlerNational Center for Tumor Diseases, University Hospital Heidelberg, 69120 Heidelberg, Germany.
University Hospital Heidelberg · DEHeidelberg University · DENational Center for Tumor Diseases · DEGerman Cancer Research Center · DEMarien Hospital Wesel · DE

Funding

the German Cancer Aid No. 70113593the Medical Faculty of the University Heidelberg to ALS (Rahel-Goitein-Strauss Program) and by research grants of the Brigitte and Dr. Konstanze Wegener foundation, the German Research Foundation No. KO5205/1-1
6 · The paper itself

Abstract

Autophagy is a catabolic process that enables cells to degrade obsolete content and refuel energy depots. In colorectal cancer (CRC) autophagy has been shown to promote tumorigenesis through energy delivery in the condition of uncontrolled proliferation. With this study, we aimed at evaluating whether autophagy sustains CRC cell viability and if it impacts therapy resistance. Initially, a colorectal cancer tissue micro array, containing mucosa (

Indexed as

ApoptosisDrug Resistance, NeoplasmAdenocarcinomaAntineoplastic AgentsAutophagyAutophagy-Related Protein 7Beclin-1Cells, CulturedCell SurvivalColorectal NeoplasmsFluorouracilHT29 CellsHumansIrinotecanMicrotubule-Associated ProteinsAntineoplastic AgentsATG7 protein, humanAutophagy-Related Protein 7Beclin-1FluorouracilIrinotecanMAP1LC3B protein, humanMicrotubule-Associated ProteinsapoptosisAtg7autophagycolorectal cancerLC3

Identifiers

PMID32046105
PMCPMC7038172
OpenAlexW3004897179

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.