ArticleOncotarget2016
Defining specificity and on-target activity of BH3-mimetics using engineered B-ALL cell lines.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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.
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
22 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Conventional chemotherapy: millions of cures, unresolved therapeutic index.Nature reviews. Cancer · 2025Review
- BH3 profiling as pharmacodynamic biomarker for the activity of BH3 mimetics.Haematologica · 2024Article
- Targeting MCL-1 triggers DNA damage and an anti-proliferative response independent from apoptosis induction.Cell reports · 2023Article
- Selective MCL-1 inhibitor ABBV-467 is efficacious in tumor models but is associated with cardiac troponin increases in patients.Communications medicine · 2023Article
- Novel BCL-2 Inhibitor Lisaftoclax in Relapsed or Refractory Chronic Lymphocytic Leukemia and Other Hematologic Malignancies: First-in-Human Open-Label Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Quantifying requirements for mitochondrial apoptosis in CAR T killing of cancer cells.Cell death & disease · 2023Article
- Venetoclax Drug Increases the Apoptosis of T and B Acute Lymphoblastic Leukemia Cells by Reducing the Expression ofInternational journal of molecular and cellular medicine · 2023Article
- MCL-1 is a master regulator of cancer dependency on fatty acid oxidation.Cell reports · 2022Article
- Targeting mitochondrial respiration and the BCL2 family in high-grade MYC-associated B-cell lymphoma.Molecular oncology · 2022Article
- Mcl-1 Inhibition: Managing Malignancy in Multiple Myeloma.Frontiers in pharmacology · 2021Review
- Peptide design by optimization on a data-parameterized protein interaction landscape.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Discovery of Mcl-1 inhibitors from integrated high throughput and virtual screening.Scientific reports · 2018Article
- Iterative optimization yields Mcl-1-targeting stapled peptides with selective cytotoxicity to Mcl-1-dependent cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Modulation of Navitoclax Sensitivity by Dihydroartemisinin-Mediated MCL-1 Repression in BCR-ABLClinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Pathways and mechanisms of venetoclax resistance.Leukemia & lymphoma · 2017Review
- Structure of a Myeloid cell leukemia-1 (Mcl-1) inhibitor bound to drug site 3 of Human Serum Albumin.Bioorganic & medicinal chemistry · 2017Article
- Article
- From basic apoptosis discoveries to advanced selective BCL-2 family inhibitors.Nature reviews. Drug discovery · 2017Review
- Development of venetoclax for therapy of lymphoid malignancies.Drug design, development and therapy · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
One of the hallmarks of cancer is a resistance to the induction of programmed cell death that is mediated by selection of cells with elevated expression of anti-apoptotic members of the BCL-2 family. To counter this resistance, new therapeutic agents known as BH3-mimetic small molecules are in development with the goal of antagonizing the function of anti-apoptotic molecules and promoting the induction of apoptosis. To facilitate the testing and modeling of BH3-mimetic agents, we have developed a powerful system for evaluation and screening of agents both in culture and in immune competent animal models by engineering mouse leukemic cells and re-programming them to be dependent on exogenously expressed human anti-apoptotic BCL-2 family members. Here we demonstrate that this panel of cell lines can determine the specificity of BH3-mimetics to individual anti-apoptotic BCL-2 family members (BCL-2, BCL-XL, BCL-W, BFL-1, and MCL-1), demonstrate whether cell death is due to the induction of apoptosis (BAX and BAK-dependent), and faithfully assess the efficacy of BH3-mimetic small molecules in pre-clinical mouse models. These cells represent a robust and valuable pre-clinical screening tool for validating the efficacy, selectivity, and on-target action of BH3-mimetic agents.
Indexed as
Identifiers
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.