ArticleOncogene2006
p16Ink4a or p19Arf loss contributes to Tal1-induced leukemogenesis in mice.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 27 citations in OpenAlex.
- Overexpression of Lmo2 initiates T-lymphoblastic leukemia via impaired thymocyte competition.The Journal of experimental medicine · 2023Article
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- PRDM14 promotes RAG-dependent Notch1 driver mutations in mouse T-ALL.Biology open · 2016Article
- Dynamic interaction between TAL1 oncoprotein and LSD1 regulates TAL1 function in hematopoiesis and leukemogenesis.Oncogene · 2012Article
- Induction of histiocytic sarcoma in mouse skeletal muscle.PloS one · 2012Article
- Acute lymphoblastic leukemia cells that survive combination chemotherapy in vivo remain sensitive to allogeneic immune effects.Leukemia research · 2011Article
- Functional interactions between Lmo2, the Arf tumor suppressor, and Notch1 in murine T-cell malignancies.Blood · 2011Article
- Stage-specific Arf tumor suppression in Notch1-induced T-cell acute lymphoblastic leukemia.Blood · 2009Article
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- Article
- High-risk acute lymphoblastic leukemia cells with bcr-abl and INK4A/ARF mutations retain susceptibility to alloreactive T cells.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2008Article
- Article
- Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc.Molecular and cellular biology · 2006Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Analysis of the INK4A/ARF locus in human T-ALL patients revealed frequent deletions in exon 2, the exon common to both p16(INK4A) and p14(ARF). Other studies have described selective deletion of exon 1beta of p14(ARF) or methylation of the p16(INK4A) promoter. Therefore, it is unclear from these studies whether loss of p16(INK4A) and/or p14(ARF) contributes to the development of T-ALL. To elucidate the relative contribution of the ink4a/arf locus to T-cell leukemogenesis, we mated our tal1 transgenic mice to ink4a/arf-/-, p16(ink4a)-/-, and p19(arf)-/- mice and generated tal1/ink4a/arf+/-, tal1/p16(ink4a)+/-, and tal1/p19(arf)+/- mice. Each of these mice developed T-cell leukemia rapidly, indicating that loss of either p16(ink4a) or p19(arf) cooperates with Tal1 to induce leukemia in mice. Preleukemic studies reveal that Tal1 expression stimulates entry into the cell cycle and thymocyte apoptosis in vivo. Interestingly, mice expressing a DNA-binding mutant of Tal1 do not exhibit increases in S phase cells. The S phase induction is accompanied by an increase in thymocyte apoptosis in tal1 transgenic mice. Whereas apoptosis is reduced to wild-type levels in tal1/ink4a/arf-/- mice, S phase induction remains unaffected. Thus, Tal1 stimulates cell cycle entry independent of the ink4a/arf locus, but its ability to induce apoptosis is Ink4a/Arf-dependent.
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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.