Evidence map›Paper›PMID 32290241›Full record

ReviewCancers2020

BCL-2 Proteins in Pathogenesis and Therapy of B-Cell Non-Hodgkin Lymphomas.

Magdalena Klanova, Pavel Klener

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 82 citations in OpenAlex.

  1. Exploratory biomarker analysis from a phase III study of the PI3K inhibitor, copanlisib, in combination with rituximab in patients with indolent non-Hodgkin lymphoma, a retrospective study.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Trial
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  12. The molecular landscape of AL amyloidosis.British journal of haematology · 2025
    Review
  13. The inhibitory effects ofIn silico pharmacology · 2025
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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 at 1 institution in 1 country.

Magdalena KlanovaInstitute of Pathological Physiology, First Faculty of Medicine, Charles University in Prague, 12853 Prague, Czech Republic.
Pavel KlenerInstitute of Pathological Physiology, First Faculty of Medicine, Charles University in Prague, 12853 Prague, Czech Republic.ORCID 0000-0001-7786-9378
Charles University · CZ

Funding

Grantová Agentura České Republiky GA20-25308SMinisterstvo Školství, Mládeže a Tělovýchovy PROGRES Q26/LF1Ministerstvo Školství, Mládeže a Tělovýchovy PROGRES Q28/LF1Ministerstvo Zdravotnictví Ceské Republiky AZV 17-28980AUniverzita Karlova v Praze PRIMUS 19/MED/07Univerzita Karlova v Praze UNCE/MED/016
6 · The paper itself

Abstract

The ability to inhibit mitochondrial apoptosis is a hallmark of B-cell non-Hodgkin lymphomas (B-NHL). Activation of mitochondrial apoptosis is tightly controlled by members of B-cell leukemia/lymphoma-2 (BCL-2) family proteins via protein-protein interactions. Altering the balance between anti-apoptotic and pro-apoptotic BCL-2 proteins leads to apoptosis evasion and extended survival of malignant cells. The pro-survival BCL-2 proteins: B-cell leukemia/lymphoma-2 (BCL-2/BCL2), myeloid cell leukemia-1 (MCL-1/MCL1) and B-cell lymphoma-extra large (BCL-XL/BCL2L1) are frequently (over)expressed in B-NHL, which plays a crucial role in lymphoma pathogenesis, disease progression, and drug resistance. The efforts to develop inhibitors of anti-apoptotic BCL-2 proteins have been underway for several decades and molecules targeting anti-apoptotic BCL-2 proteins are in various stages of clinical testing. Venetoclax is a highly specific BCL-2 inhibitor, which has been approved by the US Food and Drug Agency (FDA) for the treatment of patients with chronic lymphocytic leukemia (CLL) and is in advanced clinical testing in other types of B-NHL. In this review, we summarize the biology of BCL-2 proteins and the mechanisms of how these proteins are deregulated in distinct B-NHL subtypes. We describe the mechanism of action of BH3-mimetics and the status of their clinical development in B-NHL. Finally, we summarize the mechanisms of sensitivity/resistance to venetoclax.

Indexed as

apoptosisB-cell leukemia/lymphoma-2 (BCL-2)non-Hodgkin lymphomas (NHL)venetoclax

Identifiers

PMID32290241
PMCPMC7226356
OpenAlexW3016105251

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.