Abstract
Burkitt's lymphoma (BL), one of the most aggressive tumors affecting humans, characterized by the constitutive activation of the Myc oncogene together with the alteration of many other genetic and epigenetic factors. Among them, the INK4a/ARF locus has been well documented to play a central role in BL. Recently, we have discovered that simultaneous deregulation of both DNA methylation patterns and the ubiquitin-dependent proteolysis system is required to completely inactive the INK4/ARF locus, opening new possibilities for treating Burkitt's lymphoma. In this review, we integrate our discovery with the general view of BL and propose a new comprehensive approach to analyze and manage this aggressive disease.
Copyright © 2012 Wiley Periodicals, Inc.
MeSH terms
-
ADP-Ribosylation Factors / genetics*
-
ADP-Ribosylation Factors / metabolism
-
Burkitt Lymphoma / genetics*
-
Burkitt Lymphoma / metabolism
-
Burkitt Lymphoma / pathology
-
Cyclin-Dependent Kinase Inhibitor p16 / genetics*
-
Cyclin-Dependent Kinase Inhibitor p16 / metabolism
-
DNA Methylation
-
Gene Expression Regulation, Neoplastic*
-
Genetic Loci
-
Humans
-
MicroRNAs / genetics
-
MicroRNAs / metabolism
-
Proteasome Endopeptidase Complex / genetics
-
Proteasome Endopeptidase Complex / metabolism
-
Proteolysis
-
Proto-Oncogene Proteins c-myc / genetics*
-
Proto-Oncogene Proteins c-myc / metabolism
-
Signal Transduction
-
Ubiquitin / genetics
-
Ubiquitin / metabolism
Substances
-
Cyclin-Dependent Kinase Inhibitor p16
-
MYC protein, human
-
MicroRNAs
-
Proto-Oncogene Proteins c-myc
-
Ubiquitin
-
Proteasome Endopeptidase Complex
-
ADP-Ribosylation Factors