ReviewJournal of hematology & oncology2018
BCL-2 as therapeutic target for hematological malignancies.
Review in Journal of hematology & oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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.
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Who cites it
116 citing papers in PubMed, 222 citations in OpenAlex.
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- Targeting lysosome-dependent cell death in cancer: towards therapeutic strategies.Biomarker research · 2026Review
- Beyond CD30: Dual-Targeting of Malignant and Regulatory T Cells by Brentuximab Vedotin Remodels the Lymphoma Microenvironment and Overcomes Resistance via BCL2 Inhibition in Mycosis Fungoides.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting signaling pathways in lymphoma: From molecular mechanisms to clinical breakthroughs.Chinese medical journal · 2026Review
- Review
- Streptomyces koyangensis L-asparaginase: computational prediction of dual-mechanism BCL-2 interaction in acute lymphoblastic leukemia.Scientific reports · 2026Article
- DrugBank mining with machine learning reveals novel candidates for BCL-2 inhibition.Scientific reports · 2026Article
- Drug-tolerant persister cells in lymphoid malignancies: from mechanisms to therapeutic opportunities.Frontiers in oncology · 2026Review
- Effect of Oral Posaconazole on Venetoclax Plasma Concentration and its Efficacy in Patients with Acute Myeloid Leukemia.Recent patents on anti-cancer drug discovery · 2026Article
- Evaluation of New Coumarins for Anti-Cancer Activity in HL-60 Cell Line Supported by Molecular Docking, MD Simulation, and Binding Free Energy Calculations.OncoTargets and therapy · 2026Article
- Inhibiting the pathological changes of PASMCs is an effective approach for medicinal plants or secondary metabolites in treating pulmonary hypertension.Frontiers in pharmacology · 2026Review
- Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025Review
- The role of Bcl‑2 in controlling the transition between autophagy and apoptosis (Review).Molecular medicine reports · 2025Review
- Integration of transcriptome-wide association study and gene-based association analysis identifies candidate genes for Hodgkin lymphoma.Journal of cancer research and clinical oncology · 2025Article
- Investigating additional malignancy rates and prognostic factors in multiple myeloma patients: a Surveillance, Epidemiology, and End Results (SEER) database retrospective cohort study.Translational cancer research · 2025Article
- A combination of Dihydroartemisinin and Venetoclax enhances antitumor effect in AML via C-MYC/BCL-XL/MCL-1 triple targeting.Discover oncology · 2025Article
- A phase 1 study of the combination of BH3-mimetic, navitoclax, and mTORC1/2 inhibitor, vistusertib, in patients with advanced solid tumors.Cancer chemotherapy and pharmacology · 2025Article
- Mechanism of Curcumin in Inhibiting Proliferation of Head and Neck Squamous Cell Carcinoma: A Network Pharmacology and Cellular Experimental Study.BioMed research international · 2025Article
- Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells.Scientific reports · 2024Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disruption of the physiologic balance between cell proliferation and cell death is an important step of cancer development. Increased resistance to apoptosis is a key oncogenic mechanism in several hematological malignancies and, in many cases, especially in lymphoid neoplasias, has been attributed to the upregulation of BCL-2. The BCL-2 protein is the founding member of the BCL-2 family of apoptosis regulators and was the first apoptosis modulator to be associated with cancer. The recognition of the important role played by BCL-2 for cancer development and resistance to treatment made it a relevant target for therapy for many diseases, including solid tumors and hematological neoplasias. Among the different strategies that have been developed to inhibit BCL-2, BH3-mimetics have emerged as a novel class of compounds with favorable results in different clinical settings, including chronic lymphocytic leukemia (CLL). In April 2016, the first inhibitor of BCL-2, venetoclax, was approved by the US Food and Drug Administration for the treatment of patients with CLL who have 17p deletion and had received at least one prior therapy. This review focuses on the relevance of BCL-2 for apoptosis modulation at the mitochondrial level, its potential as therapeutic target for hematological malignancies, and the results obtained with selective inhibitors belonging to the BH3-mimetics, especially venetoclax used in monotherapy or in combination with other agents.
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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.