Abstract
Repair of DNA strand breaks induced during lymphoid antigen receptor rearrangement involves non-homologous end-joining (NHEJ). We investigated NHEJ in the aetiology of lymphoproliferative disorders (LPDs) and the disease subtypes therein through real-time quantitative RT-PCR gene expression analysis. Lower expression of XRCC6 and MRE11A was observed in all tumours, with higher expression of both XRCC4 and RAD50 observed only in multiple myeloma (MM). Hierarchical clustering enabled tumours to be clearly distinguished from controls, and by morphological sub-type. We postulate this identifies targets worthy of investigation in the genetic predisposition, pathogenesis and prognosis of lymphoid malignancies.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Acid Anhydride Hydrolases
-
Antigens, Nuclear / biosynthesis
-
Antigens, Nuclear / genetics
-
DNA Repair Enzymes / biosynthesis*
-
DNA Repair Enzymes / genetics
-
DNA Repair*
-
DNA, Neoplasm / genetics
-
DNA-Binding Proteins / biosynthesis*
-
DNA-Binding Proteins / genetics
-
Gene Expression Profiling / methods
-
Genetic Predisposition to Disease
-
Humans
-
Ku Autoantigen
-
Lymphoma, Non-Hodgkin / genetics
-
Lymphoma, Non-Hodgkin / metabolism*
-
MRE11 Homologue Protein
-
Multiple Myeloma / genetics
-
Multiple Myeloma / metabolism*
-
Neoplasm Proteins / biosynthesis*
-
Neoplasm Proteins / genetics
-
Reverse Transcriptase Polymerase Chain Reaction / methods
Substances
-
Antigens, Nuclear
-
DNA, Neoplasm
-
DNA-Binding Proteins
-
MRE11 protein, human
-
Neoplasm Proteins
-
XRCC4 protein, human
-
MRE11 Homologue Protein
-
Acid Anhydride Hydrolases
-
RAD50 protein, human
-
Xrcc6 protein, human
-
Ku Autoantigen
-
DNA Repair Enzymes