ReviewCell death & disease2020
Targeting BCL-2 in B-cell malignancies and overcoming therapeutic resistance.
Review in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
Who cites it
141 citing papers in PubMed, 2 syntheses or guidelines pooled it, 253 citations in OpenAlex.
- Synergistic innovations of nanomedicine in lymphoma treatment: a systematic review.Journal of translational medicine · 2025Pooled it
- The role of chidamide in the treatment of B-cell non-Hodgkin lymphoma: An updated systematic review.Biomolecules & biomedicine · 2023Pooled it
- Efficacy and safety of fixed-duration venetoclax plus obinutuzumab in untreated Japanese CLL and SLL: a phase 2 study.International journal of hematology · 2026Trial
- Venetoclax treatment for chronic lymphocytic leukemia/small lymphocytic leukemia in Japan: post-marketing surveillance.International journal of hematology · 2024Trial
- Aberrant expression of MERTK activates BCR via CD79a in CLL cells: alternative therapeutic strategy for relapsed/refractory CLL.Leukemia · 2026Article
- Spectroscopic Signature of Apoptosis Induced by Venetoclax in Philadelphia-Positive Acute Lymphoblastic Leukemia.Analytical chemistry · 2026Article
- First-Line Bruton's Tyrosine Kinase Inhibitor-Based Regimens for Mantle Cell Lymphoma.Current oncology (Toronto, Ont.) · 2026Review
- Radiation induces senescence in lymphatic endothelial cells (LECs) and murine tail lymphedema tissue, contributing to lymphedema progression.Cell death & disease · 2026Article
- Targeting signaling pathways in lymphoma: From molecular mechanisms to clinical breakthroughs.Chinese medical journal · 2026Review
- Chronic lymphocytic leukemia with IGH/BCL2 fusion and clonal heterogeneity: phenotypic and molecular profiling analysis of a rare case.Annals of hematology · 2026Article
- Lineage-determining transcription factors constrain cohesin to drive multi-enhancer oncogene regulation.Nature cell biology · 2026Article
- Article
- MarkerPredict: predicting clinically relevant predictive biomarkers with machine learning.NPJ systems biology and applications · 2025Article
- Article
- A Novel Approach to Prognostic Factors and Risk Stratification in Pediatric AML: Case Report and Literature Review.International journal of molecular sciences · 2025Review
- Review
- A PP2A-mtATR-tBid axis links DNA damage-induced CIP2A degradation to apoptotic dormancy and therapeutic resistance in PDAC.Cancer letters · 2025Article
- Systems biology-enabled targeting of NF-κΒ and BCL2 overcomes microenvironment-mediated BH3-mimetic resistance in DLBCL.Cell death & disease · 2025Article
- B-Cell Lymphoma 2 Inhibition in Acute Lymphoblastic Leukemia: Mechanisms, Resistance, and Emerging Combinations With Venetoclax.Journal of hematology · 2025Review
- Integrative network toxicology, molecular dynamics and transcriptional analysis elucidate DEHP-induced cardiovascular dysfunction.Toxicology research · 2025Article
81 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Defects in apoptosis can promote tumorigenesis and impair responses of malignant B cells to chemotherapeutics. Members of the B-cell leukemia/lymphoma-2 (BCL-2) family of proteins are key regulators of the intrinsic, mitochondrial apoptotic pathway. Overexpression of antiapoptotic BCL-2 family proteins is associated with treatment resistance and poor prognosis. Thus, inhibition of BCL-2 family proteins is a rational therapeutic option for malignancies that are dependent on antiapoptotic BCL-2 family proteins. Venetoclax (ABT-199, GDC-0199) is a highly selective BCL-2 inhibitor that represents the first approved agent of this class and is currently widely used in the treatment of chronic lymphocytic leukemia (CLL) as well as acute myeloid leukemia (AML). Despite impressive clinical activity, venetoclax monotherapy for a prolonged duration can lead to drug resistance or loss of dependence on the targeted protein. In this review, we provide an overview of the mechanism of action of BCL-2 inhibition and the role of this approach in the current treatment paradigm of B-cell malignancies. We summarize the drivers of de novo and acquired resistance to venetoclax that are closely associated with complex clonal shifts, interplay of expression and interactions of BCL-2 family members, transcriptional regulators, and metabolic modulators. We also examine how tumors initially resistant to venetoclax become responsive to it following prior therapies. Here, we summarize preclinical data providing a rationale for efficacious combination strategies of venetoclax to overcome therapeutic resistance by a targeted approach directed against alternative antiapoptotic BCL-2 family proteins (MCL-1, BCL-xL), compensatory prosurvival pathways, epigenetic modifiers, and dysregulated cellular metabolism/energetics for durable clinical remissions.
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What OpenQuestion holds
Registered trials
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.