Evidence map›Paper›PMID 22429822›Full record

ArticleCell proliferation2012

Caspase-mediated programmed cell death pathways as potential therapeutic targets in cancer.

X Wen, Z-Q Lin, B Liu, Y-Q Wei

Abstract read
In one paragraph

Article in Cell proliferation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 138 citations in OpenAlex.

  1. Article
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  7. Methyl alcohol extract of marine green algaNutrition research and practice · 2025
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  12. Review
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  15. Article
  16. Article
  17. Article
  18. Article
  19. Orexins in apoptosis: a dual regulatory role.Frontiers in cellular neuroscience · 2024
    Review
  20. Article

3 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 2 institutions in 1 country.

X WenState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University, Chengdu, China.
Z-Q Lin
B Liu
Y-Q Wei
Sichuan University · CNState Key Laboratory of Biotherapy

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The caspase family is well characterized as playing a crucial role in modulation of programmed cell death (PCD), which is a genetically regulated, evolutionarily conserved process with numerous links to many human diseases, most notably cancer. In this review, we focus on summarizing the intricate relationships between some members of the caspase family and their key apoptotic mediators, involving tumour necrosis factor receptors, the Bcl-2 family, cytochrome c, Apaf-1 and IAPs in cancer initiation and progression. We elucidate new emerging types of cross-talk between several caspases and autophagy-related genes (Atgs) in cancer. Moreover, we focus on presenting several PCD-modulating agents that may target caspases-3, -8 and -9, and their substrates PARP-1 and Beclin-1, which may help us harness caspase-modulated PCD pathways for future drug discovery.

Indexed as

ApoptosisAntineoplastic AgentsApoptosis Regulatory ProteinsApoptotic Protease-Activating Factor 1Beclin-1Caspase InhibitorsCaspasesCytochromes cHumansInhibitor of Apoptosis ProteinsMembrane ProteinsNeoplasmsPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2Receptors, Tumor Necrosis FactorSubstrate SpecificityAntineoplastic AgentsApoptosis Regulatory ProteinsApoptotic Protease-Activating Factor 1Beclin-1BECN1 protein, humanCaspase InhibitorsCaspasesCytochromes cInhibitor of Apoptosis ProteinsMembrane ProteinsPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2Receptors, Tumor Necrosis Factor

Identifiers

PMID22429822
PMCPMC6495317
OpenAlexW1973839771

What OpenQuestion holds

Textmetadata
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.