Evidence map›Paper›PMID 30171377›Full record

SynthesisApoptosis : an international journal on programmed cell death2018

Targeting autophagy for combating chemoresistance and radioresistance in glioblastoma.

Matthew A Taylor, Bhaskar C Das, Swapan K Ray

Abstract readSystematic Review
In one paragraph

Synthesis in Apoptosis : an international journal on programmed cell death, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
9.9field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 144 citations in OpenAlex.

  1. Article
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  3. The CHI3L1 protein plays role as a protecting factor against autophagy in glioblastoma cells.Apoptosis : an international journal on programmed cell death · 2026
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16 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Matthew A TaylorDepartment of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, Building 2, Room C11, 6439 Garners Ferry Road, Columbia, SC, 29209, USA.ORCID 0000-0001-7503-4094
Bhaskar C DasDepartments of Medicine and Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.ORCID 0000-0002-5837-027X
Swapan K RayDepartment of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, Building 2, Room C11, 6439 Garners Ferry Road, Columbia, SC, 29209, USA. swapan.ray@uscmed.sc.edu.ORCID 0000-0003-1734-542X
University of South Carolina · USIcahn School of Medicine at Mount Sinai · US

Funding

DIFFERENTIATION AND APOPTOSIS IN MALIGNANT NEUROBLASTOMAR01NS057811 · NINDS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RAY, SWAPAN K. · 2006 to 2009
$1.3M
PROTEOLYTIC CONTROL OF GLIOBLASTOMAR01CA091460 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RAY, SWAPAN K · 2003 to 2007
$1.1M
NCI NIH HHS CA91460NCI NIH HHS R01 CA091460NINDS NIH HHS NS57811NINDS NIH HHS R01 NS057811
6 · The paper itself

Abstract

Autophagy is an evolutionarily conserved catabolic process that plays an essential role in maintaining cellular homeostasis by degrading unneeded cell components. When exposed to hostile environments, such as hypoxia or nutrient starvation, cells hyperactivate autophagy in an effort to maintain their longevity. In densely packed solid tumors, such as glioblastoma, autophagy has been found to run rampant due to a lack of oxygen and nutrients. In recent years, targeting autophagy as a way to strengthen current glioblastoma treatment has shown promising results. However, that protective autophagy inhibition or autophagy overactivation is more beneficial, is still being debated. Protective autophagy inhibition would lower a cell's previously activated defense mechanism, thereby increasing its sensitivity to treatment. Autophagy overactivation would cause cell death through lysosomal overactivation, thus introducing another cell death pathway in addition to apoptosis. Both methods have been proven effective in the treatment of solid tumors. This systematic review article highlights scenarios where both autophagy inhibition and activation have proven effective in combating chemoresistance and radioresistance in glioblastoma, and how autophagy may be best utilized for glioblastoma therapy in clinical settings.

Indexed as

AutophagyDrug Resistance, NeoplasmAntineoplastic AgentsAutophagosomesBrain NeoplasmsCell DeathGlioblastomaHumansRadiation-Sensitizing AgentsTemozolomideAntineoplastic AgentsRadiation-Sensitizing AgentsTemozolomideAutophagyCell deathChemoresistanceGlioblastomaRadioresistance

Identifiers

PMID30171377
PMCPMC6193815
OpenAlexW2889148842

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.