ArticleBlood2010
Senescence induction in human fibroblasts and hematopoietic progenitors by leukemogenic fusion proteins.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- A direct comparison between AML1-ETO and ETO2-GLIS2 leukemia fusion proteins reveals context-dependent binding and regulation of target genes and opposite functions in cell differentiation.Frontiers in cell and developmental biology · 2022Article
- Drug Resistance Mechanisms of Acute Myeloid Leukemia Stem Cells.Frontiers in oncology · 2022Review
- Expansion of senescent megakaryocyte-lineage cells maintains CML cell leukemogenesis.Blood advances · 2020Article
- Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place.Cancer discovery · 2018Review
- Article
- RUNX-mediated growth arrest and senescence are attenuated by diverse mechanisms in cells expressing RUNX1 fusion oncoproteins.Journal of cellular biochemistry · 2018Article
- Senescence is a Spi1-induced anti-proliferative mechanism in primary hematopoietic cells.Haematologica · 2017Article
- The immune receptor Trem1 cooperates with diminished DNA damage response to induce preleukemic stem cell expansion.Leukemia · 2017Article
- The Regulation of Cellular Functions by the p53 Protein: Cellular Senescence.Cold Spring Harbor perspectives in medicine · 2017Review
- ASPL-TFE3 Oncoprotein Regulates Cell Cycle Progression and Induces Cellular Senescence by Up-Regulating p21.Neoplasia (New York, N.Y.) · 2016Article
- Regulation of AKT signaling by Id1 controls t(8;21) leukemia initiation and progression.Blood · 2015Article
- Cooperativity of imprinted genes inactivated by acquired chromosome 20q deletions.The Journal of clinical investigation · 2013Article
- Monoubiquitinated Fanconi anemia D2 (FANCD2-Ub) is required for BCR-ABL1 kinase-induced leukemogenesis.Leukemia · 2011Article
- Never-ageing cellular senescence.European journal of cancer (Oxford, England : 1990) · 2011Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Hematologic malignancies are typically associated with leukemogenic fusion proteins, which are required to maintain the oncogenic state. Previous studies have shown that certain oncogenes that promote solid tumors, such as RAS and BRAF, can induce senescence in primary cells, which is thought to provide a barrier to tumorigenesis. In these cases, the activated oncogene elicits a DNA damage response (DDR), which is essential for the senescence program. Here we show that 3 leukemogenic fusion proteins, BCR-ABL, CBFB-MYH11, and RUNX1-ETO, can induce senescence in primary fibroblasts and hematopoietic progenitors. Unexpectedly, we find that senescence induction by BCR-ABL and CBFB-MYH11 occurs through a DDR-independent pathway, whereas RUNX1-ETO induces senescence in a DDR-dependent manner. All 3 fusion proteins activate the p38 MAPK pathway, which is required for senescence induction. Our results reveal diverse pathways for oncogene-induced senescence and further suggest that leukemias harbor genetic or epigenetic alterations that inactivate senescence induction genes.
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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.