ArticleBlood2013
Requirement for antiapoptotic MCL-1 in the survival of BCR-ABL B-lineage acute lymphoblastic leukemia.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 94 citations in OpenAlex.
- A triple-action PROTAC for wild-type p53 cancer therapy.Cell reports. Medicine · 2025Article
- Anti-apoptotic MCL-1 promotes long-chain fatty acid oxidation through interaction with ACSL1.Molecular cell · 2024Article
- Targeting MCL-1 triggers DNA damage and an anti-proliferative response independent from apoptosis induction.Cell reports · 2023Article
- Macrocyclic Carbon-Linked Pyrazoles As Novel Inhibitors of MCL-1.ACS medicinal chemistry letters · 2023Article
- Article
- 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
- The Emerging Role of Venetoclax-Based Treatments in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2022Review
- Adapted to Survive: Targeting Cancer Cells with BH3 Mimetics.Cancer discovery · 2022Review
- SFPQ-ABL1 and BCR-ABL1 use different signaling networks to drive B-cell acute lymphoblastic leukemia.Blood advances · 2022Article
- Synergistic apoptotic effect of Mcl-1 inhibition and doxorubicin on B-cell precursor acute lymphoblastic leukemia cells.Molecular biology reports · 2022Article
- Inhibition of MCL1 induces apoptosis in anaplastic large cell lymphoma and in primary effusion lymphoma.Scientific reports · 2022Article
- Inhibiting casein kinase 2 sensitizes acute lymphoblastic leukemia cells to venetoclax via MCL1 degradation.Blood advances · 2021Article
- BH3 Mimetics in Hematologic Malignancies.International journal of molecular sciences · 2021Review
- Combination Therapy of Navitoclax with Chemotherapeutic Agents in Solid Tumors and Blood Cancer: A Review of Current Evidence.Pharmaceutics · 2021Review
- Targeting MCL-1 in cancer: current status and perspectives.Journal of hematology & oncology · 2021Review
- Article
- The Heme-Regulated Inhibitor Pathway Modulates Susceptibility of Poor Prognosis B-Lineage Acute Leukemia to BH3-Mimetics.Molecular cancer research : MCR · 2021Article
- BH3 Mimetics for the Treatment of B-Cell Malignancies-Insights and Lessons from the Clinic.Cancers · 2020Review
- Enhancing venetoclax activity in hematological malignancies.Expert opinion on investigational drugs · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The response of Philadelphia chromosome (Ph(+)) acute lymphoblastic leukemia (ALL) to treatment by BCR-ABL tyrosine kinase inhibitors (TKIs) has been disappointing, often resulting in short remissions typified by rapid outgrowth of drug-resistant clones. Therefore, new treatments are needed to improve outcomes for Ph(+) ALL patients. In a mouse model of Ph(+) B-lineage ALL, MCL-1 expression is dysregulated by the BCR-ABL oncofusion protein, and TKI treatment results in loss of MCL-1 expression prior to the induction of apoptosis, suggesting that MCL-1 may be an essential prosurvival molecule. To test this hypothesis, we developed a mouse model in which conditional allele(s) of Mcl-1 can be deleted either during leukemia transformation or later after the establishment of leukemia. We report that endogenous MCL-1's antiapoptotic activity promotes survival during BCR-ABL transformation and in established BCR-ABL(+) leukemia. This requirement for MCL-1 can be overcome by overexpression of other antiapoptotic molecules. We further demonstrate that strategies to inhibit MCL-1 expression potentiate the proapoptotic action of BCL-2 inhibitors in both mouse and human BCR-ABL(+) leukemia cell lines. Thus, strategies focused on antagonizing MCL-1 function and expression would be predicted to be effective therapeutic strategies.
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.