Abstract
The transcriptional repressor Gfi1 can be a so-called "oncorequisite" factor that is required for the development and maintenance of lymphoid neoplasia, such as Acute Lymphoblastic Leukemia (ALL), but does not have a direct role in the ontogeny of the disease. The study supporting this role of Gfi1 (Khandanpour C, Phelan J, et al., Cancer Cell, 2013, 23:200-214) shows that inhibition of Gfi1 cannot only cure mice from ALL but also blocks the expansion of human primary ALL cells. The study concludes that this feature of Gfi1 can be exploited to improve current ALL therapies.
MeSH terms
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Animals
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Apoptosis / drug effects
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Apoptosis / genetics
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Cell Proliferation / drug effects
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DNA Damage
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DNA-Binding Proteins / genetics*
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DNA-Binding Proteins / metabolism
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Gene Expression Regulation, Leukemic
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Histone Demethylases / genetics
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Histone Demethylases / metabolism
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Humans
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Interleukin Receptor Common gamma Subunit / deficiency
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Interleukin Receptor Common gamma Subunit / genetics
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Mice
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Mice, Inbred NOD
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Mice, Knockout
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Mice, SCID
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Models, Genetic
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Morpholinos / genetics
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Morpholinos / pharmacology
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Oligonucleotides, Antisense / genetics
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Oligonucleotides, Antisense / pharmacology
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics*
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy
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Transcription Factors / genetics*
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Transcription Factors / metabolism
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Tumor Suppressor Protein p53 / genetics*
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Tumor Suppressor Protein p53 / metabolism
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Xenograft Model Antitumor Assays
Substances
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DNA-Binding Proteins
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GFI1 protein, human
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Il2rg protein, mouse
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Interleukin Receptor Common gamma Subunit
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Morpholinos
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Oligonucleotides, Antisense
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Transcription Factors
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Tumor Suppressor Protein p53
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Histone Demethylases
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KDM1A protein, human