Evidence map›Paper›PMID 20919637›Full record

ReviewAdvances in experimental medicine and biology2010

BH3-only proteins and their effects on cancer.

Thanh-Trang Vo, Anthony Letai

Abstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

26 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Tumor biomarkers for diagnosis, prognosis and targeted therapy.Signal transduction and targeted therapy · 2024
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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

2 authors.

Thanh-Trang VoAnthony Letai-Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
Anthony Letai

Funding

Probing mitochondria and personalizing leukemia therapy with BH3 profilingR01CA129974 · NCI · DANA-FARBER CANCER INST · PI LETAI, ANTHONY G · 2007 to 2016
$3.2M
NCI NIH HHS R01 CA129974
6 · The paper itself

Abstract

Apoptosis, a form of cellular suicide is a key mechanism involved in the clearance of cells that are dysfunctional, superfluous or infected. For this reason, the cell needs mechanisms o sense death cues and relay death signals to the apoptotic machinery involved in cellular execution. In the intrinsic apoptotic pathway, a subclass of BCL-2 family proteins called the BH3-onlyproteins are responsible for triggering apoptosis in response to varied cellular stress cues. The mechanisms by which they are regulated are tied to the type of cellular stress they sense. Once triggered, they interact with other BCL-2 family proteins to cause mitochondrial outer membrane permeabilization which in turn results in the activation ofserine proteases necessary for cell killing. Failure to properly sense death cues and relay the death signal can have a major impact on cancer. This chapter will discuss our current models of how BH3-only proteins function as well as their impact on carcinogenesis and cancer treatment.

Indexed as

AnimalsApoptosisHumansNeoplasmsProtein Structure, TertiaryProto-Oncogene Proteins c-bcl-2Signal TransductionStress, PhysiologicalProto-Oncogene Proteins c-bcl-2

Identifiers

PMID20919637
PMCPMC3733261

What OpenQuestion holds

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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.