OBJECTIVE: To investigate the expression and clinical significance of Rad52, a homologous recombination repair gene, in tissues of nasopharyngeal carcinoma (NPC). METHOD: The expression of Rad52 was detected with three-step immunohistochemistry technique in tissues of 38 NPC patients and which have the corresponding paracancerous tissues. All of the Rad52 expression and clinical data (gender, age, clinical stage ) were compared and analyzed to conclude the relationship between them. RESULT: The Rad52 expressions were significantly different from NPC tissues to peri-NPC tissues (P < 0.05). It was found by Spearman analysis method that the Rad52 expression decreased with patients'clinical stages (P < 0.05), but has no significant relationship with gender, age, recurrence, and lymphonode metastasis (P > 0.05). The expression of Rad52 influenced the survival time of NPC patients significantly (P < 0.05). CONCLUSION The Rad52 expression can be a useful prognostic and treatment factor for NPC patients.
Adult ; Carcinoma ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Middle Aged ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms ; metabolism ; Neoplasm Staging ; Rad52 DNA Repair and Recombination Protein ; metabolism ; Survival Rate ; Young Adult

Tumors often have DNA repair defects, suggesting additional inhibition of other DNA repair pathways in tumors may lead to synthetic lethality. Accumulating data demonstrate that DNA repair-defective tumors, in particular homologous recombination (HR), are highly sensitive to DNA-damaging agents. Thus, HR-defective tumors exhibit potential vulnerability to the synthetic lethality approach, which may lead to new therapeutic strategies. It is well known that poly (adenosine diphosphate (ADP)-ribose) polymerase (PARP) inhibitors show the synthetically lethal effect in tumors defective in BRCA1 or BRCA2 genes encoded proteins that are required for efficient HR. In this review, we summarize the strategies of targeting DNA repair pathways and other DNA metabolic functions to cause synthetic lethality in HR-defective tumor cells.
Animals ; Antineoplastic Agents ; pharmacology ; Breast Neoplasms ; genetics ; DNA Repair ; drug effects ; genetics ; Gene Expression Regulation, Neoplastic ; drug effects ; Genes, Lethal ; genetics ; Genes, Tumor Suppressor ; drug effects ; Genes, cdc ; drug effects ; Humans ; Mutagenesis ; Poly(ADP-ribose) Polymerase Inhibitors ; Rad52 DNA Repair and Recombination Protein ; antagonists & inhibitors ; Recombination, Genetic ; drug effects ; genetics