Cancer cell line derived from a relapsed pediatric patient with early B-cell precursor (Pre-B) acute lymphoblastic leukemia.
- Well-characterized to have a point mutation of the p53 gene at codon 273.
- Expresses wild-type Bax, Bcl-xl, and Bcl-2.
- Well used tool for p53 studies in leukemia.
p53 is a tumor suppressor protein that in humans is encoded by the TP53 gene. p53 regulates the cell cycle and thereby functions as a tumor suppressor that is involved in preventing cancer. Mutation or inactivation of the p53 gene has been implicated in a wide range of human malignancies, however most cases of acute lymphoblastic leukemia express normal p53. The MDM2 oncoprotein is the human homolog of the mouse double minute 2 (MDM2) gene product and acts as an important negative regulator of the p53 tumor suppressor by binding to the N-terminal trans-activation domain of p53 and inhibiting transcriptional activation of the p53 gene.
Emory researchers have established a cell line from a pediatric patient with relapsed, early B cell precursor (Pre-B) acute lymphoblastic leukemia (ALL) with myeloid phenotype. This cell line has been characterized to contain a loss-of-function point mutation of the p53 gene at codon 273 and to express wild-type levels of the MDM2 oncoprotein. The mutation at codon 273 in p53 has been shown to diminish the tumor-repression activity of p53 in the EU-6 cell line. This cell line provides a useful tool for studies of the role of p53 mutations in the pathogenesis of leukemia.
Cell line is available for out-license.
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Findley et al. 1997. Blood 89:2986-2993.