Evidence map›Paper›PMID 11516099›Full record

ArticleLeukemia2001

Proteasome inhibitor-induced apoptosis of B-chronic lymphocytic leukaemia cells involves cytochrome c release and caspase activation, accompanied by formation of an approximately 700 kDa Apaf-1 containing apoptosome complex.

J B Almond, R T Snowden, A Hunter, D Dinsdale, K Cain, G M Cohen

Abstract read
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In one paragraph

Article in Leukemia, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.3field-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

20 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. The integrated stress response and proteotoxicity in cancer therapy.Biochemical and biophysical research communications · 2017
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Bortezomib induces different apoptotic rates in B-CLL cells according to IgVH and BCL-6 mutations.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2006
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

6 authors at 3 institutions in 1 country.

J B AlmondMRC Toxicology Unit, University of Leicester, UK.
R T Snowden
A Hunter
D Dinsdale
K Cain
G M Cohen
University of Leicester · GBMRC Toxicology Unit · GBLeicester Royal Infirmary · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteasome inhibitors, including lactacystin and MG132 (carbobenzoxyl-leucinyl-leucinyl-leucinal), potently induce apoptosis in leukaemic B cells from patients with B cell chronic lymphocytic leukaemia (B-CLL). This pro-apoptotic effect occurs in cells from patients at all stages of the disease, including those resistant to conventional chemotherapy, suggesting that proteasome inhibitors may be useful for treatment of B-CLL. Following initial inhibition of proteasomal activity, these agents induce mitochondrial cytochrome c release and caspase-dependent apoptosis, involving cleavage/activation of caspases -2, -3, -7, -8 and -9. Pre-treatment with the cell permeable caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe)fluoromethyl ketone (Z-VAD.fmk), did not prevent the release of cytochrome c or partial processing of caspase-9 but prevented activation of effector caspases and the induction of apoptosis. These results suggest that the release of cytochrome c is caspase independent and that caspase-9 is the initiator caspase in proteasome inhibitor-induced apoptosis of B-CLL cells. Activation of B-CLL lysates with dATP results in the formation of an approximately 700 kDa caspase-activating apoptosome complex containing Apaf-1. We describe for the first time the formation of a similar approximately 700 kDa caspase-activating apoptosome complex in B-CLL cells induced to undergo apoptosis by proteasome inhibitors.

Indexed as

Protein BiosynthesisProteinsAcetylcysteineAmino Acid Chloromethyl KetonesApoptosisApoptotic Protease-Activating Factor 1Blotting, WesternCaspase 9CaspasesCysteine EndopeptidasesCytochrome c GroupCytosolEnzyme ActivationHumansLeukemia, Lymphocytic, Chronic, B-CellLeupeptinsAcetylcysteineAmino Acid Chloromethyl KetonesAPAF1 protein, humanApoptotic Protease-Activating Factor 1benzyloxycarbonylleucyl-leucyl-leucine aldehydebenzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketoneCASP9 protein, humanCaspase 9CaspasesCysteine EndopeptidasesCytochrome c GrouplactacystinLeupeptinsMultienzyme ComplexesProteasome Endopeptidase ComplexProteins

Identifiers

PMID11516099
OpenAlexW1974796270

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.