Evidence map›Paper›PMID 22431925›Full record

ReviewTheScientificWorldJournal2012

The role of Bcl-2 family proteins in therapy responses of malignant astrocytic gliomas: Bcl2L12 and beyond.

Fotini M Kouri, Samuel A Jensen, Alexander H Stegh

Open access · goldAbstract readReview
In one paragraph

Review in TheScientificWorldJournal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Pleiotropic Effects of 3-International journal of molecular sciences · 2026
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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

3 authors at 1 institution.

Fotini M KouriKen and Ruth Davee Department of Neurology, The Northwestern Brain Tumor Institute, The Robert H. Lurie Comprehensive Cancer Center, Chicago, IL 60611, USA.
Samuel A Jensen
Alexander H Stegh
Robert H. Lurie Comprehensive Cancer Center of Northwestern University

Funding

Theranostic Magnetic Nanostructures for the Molecular Imaging of CancerU54CA151880 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MIRKIN, CHAD A. · 2010 to 2014
$11.5M
CARCINOGENESIS TRAINING PROGRAMT32CA009560 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Kathleen Janee Green · 1986 to 2026
$8.4M
The Role of Bcl2L12 in the Genesis of Malignant GliomaR00CA129172 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI STEGH, ALEXANDER H. · 2009 to 2011
$740k
NCI NIH HHS 5R00CA129172-05NCI NIH HHS R00 CA129172NCI NIH HHS T32 CA009560NCI NIH HHS T32CA09560NCI NIH HHS U54 CA151880NCI NIH HHS U54CA151880
6 · The paper itself

Abstract

Glioblastoma (GBM) is a highly aggressive and lethal brain cancer with a median survival of less than two years after diagnosis. Hallmarks of GBM tumors include soaring proliferative indices, high levels of angiogenesis, diffuse invasion into normal brain parenchyma, resistance toward therapy-induced apoptosis, and pseudopallisading necrosis. Despite the recent advances in neurosurgery, radiation therapy, and the development of targeted chemotherapeutic regimes, GBM remains one of the deadliest types of cancer. Particularly, the alkylating agent temozolomide (TMZ) in combination with radiation therapy prolonged patient survival only marginally, and clinical studies assessing efficacies of targeted therapies, foremost ATP mimetics inhibiting the activity of receptor tyrosine kinases (RTKs), revealed only few initial responders; tumor recurrence is nearly universal, and salvage therapies to combat such progression remain ineffective. Consequently, myriad preclinical and clinical studies began to define the molecular mechanisms underlying therapy resistance of GBM tumors, and pointed to the Bcl-2 protein family, in particular the atypical member Bcl2-Like 12 (Bcl2L12), as important regulators of therapy-induced cell death. This review will discuss the multi-faceted modi operandi of Bcl-2 family proteins, describe their roles in therapy resistance of malignant glioma, and outline current and future drug development efforts to therapeutically target Bcl-2 proteins.

Indexed as

Antineoplastic AgentsBrain NeoplasmsCaspasesCell NucleusCombined Modality TherapyDacarbazineGliomaHumansProto-Oncogene Proteins c-bcl-2Signal TransductionTemozolomideTumor Suppressor Protein p53Antineoplastic AgentsCaspasesDacarbazineProto-Oncogene Proteins c-bcl-2TemozolomideTumor Suppressor Protein p53

Identifiers

PMID22431925
PMCPMC3289992
OpenAlexW2001755595

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.