Year: 2005
Type: article
Abstract: The inv(16) is one of the most frequent chromosomal translocations associated with acute myeloid leukemia (AML) and creates a chimeric fusion protein consisting of most of the runt-related X1 co-factor, core binding factor beta fused to the smooth muscle myosin heavy chain MYH11. Expression of the ARF tumor suppressor is regulated by runt-related X1, suggesting that the inv(16) fusion protein (IFP) may repress ARF expression. We established a murine bone marrow transplant model of the inv(16) in which wild type, Arf+/-, and Arf-/- bone marrow were engineered to express the IFP. IFP expression was sufficient to induce a myelomonocytic AML even when expressed in wild type bone marrow, yet removal of only a single allele of Arf greatly accelerated the disease, indicating that Arf is haploinsufficient for the induction of AML in the presence of the inv(16).
Source: Journal of Biological Chemistry
Language: English
Subfield: Hematology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $3,430
Awards: G1619565388, G275963511, G4513176822, Interplay of Myc, Tumor Supressors and Regulators of Differentiation in Lymphoma, Role of TEL and the t(12;21) in B cell ALL, G566162414, G5853943267, Role of AML1-ETO in Acute Leukemia, Mechanism of inv(16) mediated leukemogenesis, G9000081609, Cancer Center Support Grant, G963484308, G99742736
OpenAlex ID: W2000597219