ArticleBlood2012
Inhibition of apoptosis by BCL2 prevents leukemic transformation of a murine myelodysplastic syndrome.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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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
26 citing papers in PubMed, 45 citations in OpenAlex.
- Celastrol induces apoptosis of myelodysplastic syndrome cells through a ROS-dependent pro-apoptotic endoplasmic-reticulum stress pathway.Cancer cell international · 2026Article
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- RSL3 enhances ROS-mediated cell apoptosis of myelodysplastic syndrome cells through MYB/Bcl-2 signaling pathway.Cell death & disease · 2024Article
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- The BH3-only protein NOXA serves as an independent predictor of breast cancer patient survival and defines susceptibility to microtubule targeting agents.Cell death & disease · 2021Article
- Mechanistic insights and potential therapeutic approaches for NUP98-rearranged hematologic malignancies.Blood · 2020Review
- TLR2/6 signaling promotes the expansion of premalignant hematopoietic stem and progenitor cells in the NUP98-HOXD13 mouse model of MDS.Experimental hematology · 2020Article
- BOK promotes erythropoiesis in a mouse model of myelodysplastic syndrome.Annals of hematology · 2019Article
- Impact of elevated anti-apoptotic MCL-1 and BCL-2 on the development and treatment of MLL-AF9 AML in mice.Cell death and differentiation · 2019Article
- Effects of cobalt chloride on the stem cell marker expression and osteogenic differentiation of stem cells from human exfoliated deciduous teeth.Cell stress & chaperones · 2019Article
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- High-fat-diet impaired mitochondrial function of cumulus cells but improved the efficiency of parthenogenetic embryonic quality in mice.Animal cells and systems · 2018Article
- Combined venetoclax and alvocidib in acute myeloid leukemia.Oncotarget · 2017Article
- Epigenetically Aberrant Stroma in MDS Propagates Disease via Wnt/β-Catenin Activation.Cancer research · 2017Article
- A fate worse than death: apoptosis as an oncogenic process.Nature reviews. Cancer · 2016Review
- PUMA promotes apoptosis of hematopoietic progenitors driving leukemic progression in a mouse model of myelodysplasia.Cell death and differentiation · 2016Article
- Molecular and Cellular Mechanisms of Myelodysplastic Syndrome: Implications on Targeted Therapy.International journal of molecular sciences · 2016Review
- Article
- Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
Abstract
Programmed cell death or apoptosis is a prominent feature of low-risk myelodysplastic syndromes (MDS), although the underlying mechanism remains controversial. High-risk MDS have less apoptosis associated with increased expression of the prosurvival BCL2-related proteins. To address the mechanism and pathogenic role of apoptosis and BCL2 expression in MDS, we used a mouse model resembling human MDS, in which the fusion protein NUP98-HOXD13 (NHD13) of the chromosomal translocation t(2;11)(q31;p15) is expressed in hematopoietic cells. Hematopoietic stem and progenitor cells from 3-month-old mice had increased rates of apoptosis associated with increased cell cycling and DNA damage. Gene expression profiling of these MDS progenitors revealed a specific reduction in Bcl2. Restoration of Bcl2 expression by a BCL2 transgene blocked apoptosis of the MDS progenitors, which corrected the macrocytic anemia. Blocking apoptosis also restored cell-cycle quiescence and reduced DNA damage in the MDS progenitors. We expected that preventing apoptosis would accelerate malignant transformation to acute myeloid leukemia (AML). However, contrary to expectations, preventing apoptosis of premalignant cells abrogated transformation to AML. In contrast to the current dogma that overcoming apoptosis is an important step toward cancer, this work demonstrates that gaining a survival advantage of premalignant cells may delay or prevent leukemic progression.
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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.