Evidence map›Paper›PMID 19138742›Full record

ReviewSeminars in cancer biology2009

Bcl-2 family proteins as regulators of oxidative stress.

Nathan Susnow, Liyun Zeng, Daciana Margineantu, David M Hockenbery

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.

  1. Relationship Between Human mutL Homolog 1 (hMLH1) Hypermethylation and Colorectal Cancer: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Pooled it
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  16. Exploring the antioxidant potential of prolactin.Frontiers in pharmacology · 2025
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  19. Review
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22 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

4 authors at 1 institution in 1 country.

Nathan SusnowDepartment of Medicine, University of Washington, Seattle, 98195-6424, United States.
Liyun Zeng
Daciana Margineantu
David M Hockenbery
Fred Hutch Cancer Center · US

Funding

UNIVERSITY OF WASHINGTON GI TRAINING GRANTT32DK007742 · NIDDK · UNIVERSITY OF WASHINGTON · PI GRADY, WILLIAM MALLORY · 1996 to 2022
$4.7M
Small Molecule Inhibitors of BcI xL Survival ProteinU01CA091310 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HOCKENBERY, DAVID MARK · 2001 to 2004
$1.8M
Regulation of substrate-linked mitochondrial ROS generationR21CA127347 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HOCKENBERY, DAVID M. · 2006 to 2007
$354k
NCI NIH HHS R21 CA127347NCI NIH HHS U01 CA91310NIDDK NIH HHS T32DK007742-12
6 · The paper itself

Abstract

The Bcl-2 family of proteins includes pro- and anti-apoptotic factors acting at mitochondrial and microsomal membranes. An impressive body of published studies, using genetic and physical reconstitution experiments in model organisms and cell lines, supports a view of Bcl-2 proteins as the critical arbiters of apoptotic cell death decisions in most circumstances (excepting CD95 death receptor signaling in Type I cells). Evasion of apoptosis is one of the hallmarks of cancer [Hanahan D, Weinberg RA. The hallmarks of cancer. Cell 2000;100:57-70], relevant to tumorigenesis as well as resistance to cytotoxic drugs, and deregulation of Bcl-2 proteins is observed in many cancers [Manion MK, Hockenbery DM. Targeting BCL-2-related proteins in cancer therapy. Cancer Biol Ther. 2003;2:S105-14; Olejniczak ET, Van Sant C, Anderson MG, Wang G, Tahir SK, Sauter G, et al. Integrative genomic analysis of small-cell lung carcinoma reveals correlates of sensitivity to bcl-2 antagonists and uncovers novel chromosomal gains. Mol Cancer Res. 2007;5:331-9]. The rekindled interest in aerobic glycolysis as a cancer trait raises interesting questions as to how metabolic changes in cancer cells are integrated with other essential alterations in cancer, e.g. promotion of angiogenesis and unbridled growth signals. Apoptosis induced by multiple different signals involves loss of mitochondrial homeostasis, in particular, outer mitochondrial membrane integrity, releasing cytochrome c and other proteins from the intermembrane space. This integrative process, controlled by Bcl-2 family proteins, is also influenced by the metabolic state of the cell. In this review, we consider the role of reactive oxygen species, a metabolic by-product, in the mitochondrial pathway of apoptosis, and the relationships between Bcl-2 functions and oxidative stress.

Indexed as

AnimalsApoptosisCaspasesEndoplasmic ReticulumHumansMitochondriaOxidative StressProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesCaspasesProto-Oncogene Proteins c-bcl-2Reactive Oxygen Species

Identifiers

PMID19138742
PMCPMC4770790
OpenAlexW2013842624

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.