ArticleLeukemia2007
ABT-737, an inhibitor of Bcl-2 family proteins, is a potent inducer of apoptosis in multiple myeloma cells.
Article in Leukemia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed, 162 citations in OpenAlex.
- Tumor gasdermin E acts as a rheostat to limit apoptotic cell survival and mutagenesis in anticancer immune environments.Science advances · 2026Article
- Retinal organoid screening reveals ABT-737 and luminespib as potential agents against a cone- precursor-derived subtype of retinoblastoma.Molecular therapy. Oncology · 2026Article
- Cytochrome c Oxidase Subunit COX4-1 Reprograms Erastin-Induced Cell Death from Ferroptosis to Apoptosis: A Transmitochondrial Study.Antioxidants (Basel, Switzerland) · 2025Article
- Antiproliferative Activity Screening inACS omega · 2025Article
- MCL1 modulates mTORC1 signaling to promote bioenergetics and tumorigenesis.Nature communications · 2025Article
- RB loss sensitizes triple-negative breast cancer to apoptosis induced by cellular stress.Cell death discovery · 2025Article
- Gigaxonin Potentiates Antiviral Innate Immune Responses by Targeting cGAS and TREX1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The formation of the 'footprint of death' as a mechanism for generating large substrate-bound extracellular vesicles that mark the site of cell death.Nature communications · 2025Article
- Review
- MetaQ: fast, scalable and accurate metacell inference via single-cell quantization.Nature communications · 2025Article
- Mitochondria of T Lymphocytes Promote Anti-Pulmonary Tumor Immune Response.World journal of oncology · 2024Article
- Clinical pharmacokinetics and pharmacodynamics of venetoclax, a selective B-cell lymphoma-2 inhibitor.Clinical and translational science · 2024Review
- Rational Formulation of targeted ABT-737 nanoparticles by self-assembled polypeptides and designed peptides.Heliyon · 2024Article
- Regulation of Cellular Senescence in Type 2 Diabetes Mellitus: From Mechanisms to Clinical Applications.Diabetes & metabolism journal · 2023Review
- Single-molecule fingerprinting of protein-drug interaction using a funneled biological nanopore.Nature communications · 2023Article
- Involvement of Bcl-2 Family Proteins in Tetraploidization-Related Senescence.International journal of molecular sciences · 2023Review
- Roles and Regulation of BCL-xL in Hematological Malignancies.International journal of molecular sciences · 2022Review
- Machine Learning and Deep Learning Applications in Multiple Myeloma Diagnosis, Prognosis, and Treatment Selection.Cancers · 2022Review
- Transcript-Level Dysregulation ofCancers · 2021Article
- Therapeutics Targeting the Core Apoptotic Machinery.Cancers · 2021Review
10 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
Disruption of pathways leading to programmed cell death plays a major role in most malignancies, including multiple myeloma (MM). ABT-737 is a BH3 mimetic small-molecule inhibitor that binds with high affinity to Bcl-2 and Bcl-xL, preventing the sequestration of proapoptotic molecules and shifting the cell survival/apoptosis balance toward apoptosis induction. In this study, we show that ABT-737 is cytotoxic to MM cell lines, including those resistant to conventional therapies, and primary tumor cells. Flow cytometric analysis of intracellular levels of Bcl-2 family proteins demonstrates a clear inversion of the Bax/Bcl-2 ratio leading to induction of apoptosis. Activation of the mitochondrial apoptosis pathway was indicated by mitochondrial membrane depolarization and caspase cleavage. Additionally, several signaling pathways known to be important for MM cell survival are disrupted following treatment with ABT-737. The impact of ABT-737 on survival could not be overcome by the addition of interleukin-6, vascular endothelial growth factor or insulin-like growth factor, suggesting that ABT-737 may be effective in preventing the growth and survival signals provided by the microenvironment. These data indicate that therapies targeting apoptotic pathways may be effective in MM treatment and warrant clinical evaluation of ABT-737 and similar drugs alone or in combination with other agents in the setting of MM.
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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.