Evidence map›Paper›PMID 27366944›Full record

ArticleOncotarget2016

Basal autophagy is pivotal for Hodgkin and Reed-Sternberg cells' survival and growth revealing a new strategy for Hodgkin lymphoma treatment.

Katrin Birkenmeier, Katharina Moll, Sebastian Newrzela, Sylvia Hartmann, Stefan Dröse, Martin-Leo Hansmann

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. [Mechanism by which mycobacterial antigen 85B inhibits autophagy and promotes apoptosis in Hodgkin lymphoma cells].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
    Article
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  12. Targeting autophagy in lymphomas: a double-edged sword?International journal of hematology · 2018
    Review
  13. Autophagy and Tumor Metabolism.Cell metabolism · 2017
    Review
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

6 authors at 2 institutions in 1 country.

Katrin BirkenmeierDr. Senckenberg Institute of Pathology, University Hospital of Frankfurt, 60596 Frankfurt am Main, Germany.
Katharina MollDr. Senckenberg Institute of Pathology, University Hospital of Frankfurt, 60596 Frankfurt am Main, Germany.
Sebastian NewrzelaDr. Senckenberg Institute of Pathology, University Hospital of Frankfurt, 60596 Frankfurt am Main, Germany.
Sylvia HartmannDr. Senckenberg Institute of Pathology, University Hospital of Frankfurt, 60596 Frankfurt am Main, Germany.
Stefan DröseClinic of Anesthesiology, Intensive-Care Medicine and Pain Therapy, Goethe-University Hospital, 60596 Frankfurt am Main, Germany.
Martin-Leo HansmannDr. Senckenberg Institute of Pathology, University Hospital of Frankfurt, 60596 Frankfurt am Main, Germany.
Goethe University Frankfurt · DEUniversity Hospital Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As current classical Hodgkin lymphoma (cHL) treatment strategies have pronounced side-effects, specific inhibition of signaling pathways may offer novel strategies in cHL therapy. Basal autophagy, a regulated catabolic pathway to degrade cell's own components, is in cancer linked with both, tumor suppression or promotion. The finding that basal autophagy enhances tumor cell survival would thus lead to immediately testable strategies for novel therapies. Thus, we studied its contribution in cHL.We found constitutive activation of autophagy in cHL cell lines and primary tissue. The expression of key autophagy-relevant proteins (e.g. Beclin-1, ULK1) and LC3 processing was increased in cHL cells, even in lymphoma cases. Consistently, cHL cells exhibited elevated numbers of autophagic vacuoles and intact autophagic flux. Autophagy inhibition with chloroquine or inactivation of ATG5 induced apoptosis and reduced proliferation of cHL cells. Chloroquine-mediated inhibition of basal autophagy significantly impaired HL growth in-vivo in NOD SCID γc-/- (NSG) mice. We found that basal autophagy plays a pivotal role in sustaining mitochondrial function.We conclude that cHL cells require basal autophagy for growth, survival and sustained metabolism making them sensitive to autophagy inhibition. This suggests basal autophagy as useful target for new strategies in cHL treatment.

Indexed as

AnimalsAutophagyAutophagy-Related Protein 5Cell Line, TumorCell ProliferationCell SurvivalChloroquineHodgkin DiseaseHumansMiceMice, SCIDMitochondriaOxidative PhosphorylationReed-Sternberg CellsAutophagy-Related Protein 5ChloroquineautophagyB-cell lymphomaHodgkin lymphomalymphoma pathogenesistargeted therapy

Identifiers

PMID27366944
PMCPMC5216819
OpenAlexW2473117328

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.