ArticleLeukemia2016
Re-activation of mitochondrial apoptosis inhibits T-cell lymphoma survival and treatment resistance.
Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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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
17 citing papers in PubMed, 32 citations in OpenAlex.
- Understanding the Functional Dependence and Inhibition of the Bcl‑2 Pro-Survival Proteins in a Wide Spectrum of Cancers toward Precision Medicine.ACS pharmacology & translational science · 2025Article
- Discovery of Macrocyclic Myeloid Cell Leukemia 1 (Mcl-1) Inhibitors that Demonstrate Potent Cellular Efficacy and In Vivo Activity in a Mouse Solid Tumor Xenograft Model.Journal of medicinal chemistry · 2025Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Challenges in nodal peripheral T-cell lymphomas: from biological advances to clinical applicability.Frontiers in oncology · 2023Review
- Sensitivity of Cutaneous T-Cell Lymphoma Cells to the Mcl-1 Inhibitor S63845 Correlates with the Lack of Bcl-w Expression.International journal of molecular sciences · 2022Article
- The mitochondrial anti-apoptotic dependencies of hematologic malignancies: from disease biology to advances in precision medicine.Haematologica · 2022Review
- Design and optimisation of a small-molecule TLR2/4 antagonist for anti-tumour therapy.RSC medicinal chemistry · 2021Article
- Molecularly targeted therapies for relapsed and refractory peripheral T-cell lymphomas.Seminars in hematology · 2021Article
- Updates in the Treatment of Peripheral T-Cell Lymphomas.Journal of experimental pharmacology · 2021Review
- Physiological Functions of Mcl-1: Insights From Genetic Mouse Models.Frontiers in cell and developmental biology · 2021Review
- MCL-1 inhibitors, fast-lane development of a new class of anti-cancer agents.Journal of hematology & oncology · 2020Review
- Enhancing venetoclax activity in hematological malignancies.Expert opinion on investigational drugs · 2020Review
- High activation of STAT5A drives peripheral T-cell lymphoma and leukemia.Haematologica · 2020Article
- Article
- Discovery of novel drug sensitivities in T-PLL by high-throughput ex vivo drug testing and mutation profiling.Leukemia · 2018Article
- The prognostic significance ofOncotarget · 2017Article
- Review
Corrections and comments
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Authors and funding
23 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T lymphocyte non-Hodgkin's lymphoma (T-NHL) represents an aggressive and largely therapy-resistant subtype of lymphoid malignancies. As deregulated apoptosis is a frequent hallmark of lymphomagenesis, we analyzed gene expression profiles and protein levels of primary human T-NHL samples for various apoptotic regulators. We identified the apoptotic regulator MCL-1 as the only pro-survival BCL-2 family member to be highly expressed throughout all human T-NHL subtypes. Functional validation of pro-survival protein members of the BCL-2 family in two independent T-NHL mouse models identified that the partial loss of Mcl-1 significantly delayed T-NHL development in vivo. Moreover, the inducible reduction of MCL-1 protein levels in lymphoma-burdened mice severely impaired the continued survival of T-NHL cells, increased their susceptibility to chemotherapeutics and delayed lymphoma progression. Lymphoma viability remained unaffected by the genetic deletion or pharmacological inhibition of all alternative BCL-2 family members. Consistent with a therapeutic window for MCL-1 treatment within the context of the whole organism, we observed an only minimal toxicity after systemic heterozygous loss of Mcl-1 in vivo. We conclude that re-activation of mitochondrial apoptosis by blockade of MCL-1 represents a promising therapeutic strategy to treat T-cell lymphoma.
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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.