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.
Highlights
The transcriptional repressor Gfi1 can be a socalled “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 deletion of Gfi1 delayed T-ALL progression, and abrogated the ability of the leukemic cells to grow in transplanted hosts
The inhibition of Gfi1 was achieved with a morpholino that was applied to the transplanted NSG mice and could significantly inhibit the expansion of the human T-ALL cells
Summary
The transcriptional repressor Gfi1 can be a socalled “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(2):200-214) shows that inhibition of Gfi1 cannot only cure mice from ALL and blocks the expansion of human primary ALL cells.
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