Evidence map›Paper›PMID 34581776›Full record

ReviewBiochemical Society transactions2021

Targeting the BCL-2-regulated apoptotic pathway for the treatment of solid cancers.

W Douglas Fairlie, Erinna F Lee

Abstract readReview
In one paragraph

Review in Biochemical Society transactions, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
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  5. Review
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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.

W Douglas FairlieCell Death and Survival Laboratory, Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria 3084, Australia.ORCID 0000-0002-2498-1160
Erinna F LeeCell Death and Survival Laboratory, Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria 3084, Australia.ORCID 0000-0003-1255-9808

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The deregulation of apoptosis is a key contributor to tumourigenesis as it can lead to the unwanted survival of rogue cells. Drugs known as the BH3-mimetics targeting the pro-survival members of the BCL-2 protein family to induce apoptosis in cancer cells have achieved clinical success for the treatment of haematological malignancies. However, despite our increasing knowledge of the pro-survival factors mediating the unwanted survival of solid tumour cells, and our growing BH3-mimetics armamentarium, the application of BH3-mimetic therapy in solid cancers has not reached its full potential. This is mainly attributed to the need to identify clinically safe, yet effective, combination strategies to target the multiple pro-survival proteins that typically mediate the survival of solid tumours. In this review, we discuss current and exciting new developments in the field that has the potential to unleash the full power of BH3-mimetic therapy to treat currently recalcitrant solid malignancies.

Indexed as

ApoptosisAntineoplastic AgentsCell Line, TumorHumansNeoplasmsProto-Oncogene Proteins c-bcl-2Antineoplastic AgentsProto-Oncogene Proteins c-bcl-2apoptosisBCL-2BH3-mimeticscancer

Identifiers

PMID34581776
PMCPMC8589438

What OpenQuestion holds

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Registered trials

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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.