Evidence map›Paper›PMID 22150924›Full record

ReviewBrain pathology (Zurich, Switzerland)2012

Autophagy in brain tumors: a new target for therapeutic intervention.

Niroop Kaza, Latika Kohli, Kevin A Roth

Open access · greenAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Guanabenz Sensitizes Glioblastoma Cells to Sunitinib by Inhibiting GADD34-Mediated Autophagic Signaling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Autophagy as a Potential Therapy for Malignant Glioma.Pharmaceuticals (Basel, Switzerland) · 2020
    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

3 authors at 1 institution in 1 country.

Niroop KazaDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294-0017, USA.
Latika Kohli
Kevin A Roth
University of Alabama at Birmingham · US

Funding

Viral and molecular chemotherapy of malignant CNS tumorsP50CA097247 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GILLESPIE, G. YANCEY · 2002 to 2009
$13.5M
Alabama Neuroscience Blueprint Core CenterP30NS057098 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SWEATT, JOHN DAVID · 2006 to 2010
$9.5M
UAB Neuroscience Core CenterP30NS047466 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STANDAERT, DAVID G. · 2005 to 2019
$8.5M
Molecular Characterization of Neural Stem Cell ApoptosisR01NS041962 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ROTH, KEVIN A · 2003 to 2012
$3.0M
BCL-X DEPENDENT NEUROPATHOLOGYR01NS035107 · NINDS · WASHINGTON UNIVERSITY · PI ROTH, KEVIN A · 1996 to 2010
$2.8M
Novel Treatment of NF-1 Associated Malignant Peripheral Nerve Sheath TumorsR01CA122804 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CARROLL, STEVEN L. · 2008 to 2012
$1.5M
Role of Neuregulin-1 in Schwann Cell NeoplasiaR01NS048353 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CARROLL, STEVEN L. · 2004 to 2008
$1.3M
Multi-Modal Lysosomotropic Death Therapy for Malignant Peripheral Nerve Sheath TuR01CA134773 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ROTH, KEVIN A · 2009 to 2011
$722k
NCI NIH HHS CA134773NCI NIH HHS P50CA097247NCI NIH HHS R01 CA134773NINDS NIH HHS NS41962NINDS NIH HHS P30 NS047466NINDS NIH HHS P30 NS057098NINDS NIH HHS R01 NS035107NINDS NIH HHS R01 NS041962
6 · The paper itself

Abstract

The role of autophagy, traditionally considered a cellular homeostatic and recycling mechanism, has expanded dramatically to include an involvement in discrete stages of tumor initiation and development. Gliomas are the most aggressive and also the most common brain malignancies. Current treatment modalities have only a modest effect on patient outcomes. Resistance to apoptosis, a hallmark of most cancers, has driven the search for novel targets in cancer therapy. The autophagy lysosomal pathway is one such target that is being explored in multiple cancers including gliomas and is a promising avenue for further therapeutic development. This review summarizes our current understanding of the autophagic process and its potential utility as a target for glioma therapy.

Indexed as

AnimalsAntineoplastic AgentsAutophagyBrain NeoplasmsCell Transformation, NeoplasticDrug DesignGliomaHumansMutationAntineoplastic Agents

Identifiers

PMID22150924
PMCPMC3243074
OpenAlexW1931182390

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.