Burkitt lymphoma: much more than MYC.
Chromosomal translocations causing deregulated c-MYC expression are detectable in most Burkitt lymphoma cases. However, little is known about the additional lesions necessary for lymphomagenesis. Now, two independent studies, one of which was performed by Sander et al. in this issue of Cancer Cell, identify constitutive PI3K signaling and CyclinD3 mutations as cooperating lesions in both mice and humans. The results have directly actionable therapeutic implications.
Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
David
D
Dominguez-Sola
Riccardo
R
Dalla-Favera
D000818:Animals; D002051:Burkitt Lymphoma / Q000201:enzymology* / Q000473:pathology*; D002471:Cell Transformation, Neoplastic / Q000378:metabolism*; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism*; D015398:Signal Transduction
D016271:Proto-Oncogene Proteins c-myc; D019869:Phosphatidylinositol 3-Kinases