Evidence map›Paper›PMID 12886234›Full record

ReviewLeukemia2003

Recent advances in the development of anticancer agents targeting cell death inhibitors in the Bcl-2 protein family.

S Shangary, D E Johnson

Abstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–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

25 citing papers in PubMed.

  1. Dual mTORC1/2 Inhibition Synergistically Enhances AML Cell Death in Combination with the BCL2 Antagonist Venetoclax.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  2. Roles and Regulation of BCL-xL in Hematological Malignancies.International journal of molecular sciences · 2022
    Review
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  14. Therapeutic cancer vaccines in combination with conventional therapy.Journal of biomedicine & biotechnology · 2010
    Review
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  19. BH3 mimetics to improve cancer therapy; mechanisms and examples.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2007
    Review
  20. Article
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.

S ShangaryDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
D E Johnson

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematopoietic malignancies frequently are characterized by defects in apoptosis signaling. This renders the malignant cells resistant to endogenous apoptotic stimuli, as well as exogenous stimuli, such as chemotherapy drugs and radiation. The defective apoptosis seen in human cancers often results from overexpression of antiapoptotic proteins in the Bcl-2 protein family, particularly Bcl-2 and Bcl-X(L). A great deal of effort is currently aimed at developing novel agents to inhibit the expression or function of these proteins. Antisense agents directed against Bcl-2 mRNA are showing considerable promise in clinical trials. In addition, detailed knowledge of the structures of Bcl-2 and Bcl-X(L), coupled with high-throughput and computer-assisted screening of chemical libraries, has led to the identification of a number of short peptides and small organic molecules capable of inhibiting Bcl-2 and Bcl-X(L) function. These newly described agents hold considerable promise for enhancing the chemo- and radiation sensitivities of Bcl-2- and Bcl-X(L)-overexpressing cancers. This review will highlight recent advances in the development and testing of agents targeting cell death inhibitors in the Bcl-2 protein family.

Indexed as

Antineoplastic AgentsApoptosisHematologic NeoplasmsHumansProto-Oncogene Proteins c-bcl-2Structure-Activity RelationshipAntineoplastic AgentsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID12886234

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.