Association of Caspase 8 and Caspase 10 Genetic Polymorphisms with B-cell Non Hodgkin's Lymphoma in Egypt: A Case-Control StudyHanaa Hamed Arnaout1, Mervat Mamdooh Khorshied1, Ola M. Reda Khorshid2* and Mona Hazem El-Nagdy1
- *Corresponding Author:
- Dr. Satya P. Singh
Department of Biosciences
E-mail: [email protected]
Received date: July 10, 2012; Accepted date: August 08, 2012; Published date: August 10, 2012
Citation: Arnaout HH, Khorshied MM, Khorshid OMR, El-Nagdy MH (2012) Association of Caspase 8 and Caspase 10 Genetic Polymorphisms with B-cell Non Hodgkin’s Lymphoma in Egypt: A Case-Control Study. J Cancer Sci Ther 4: 249-253. doi:10.4172/1948-5956.1000150
Copyright: © 2012 Arnaout HH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background and purpose: Non-Hodgkin lymphomas are closely related diseases with distinctive morphologic, immunophenotypic, genetic, and clinical features. Genetic susceptibility studies of NHL are mandatory to identify at risk populations and to clarify important disease mechanisms. Caspase genes play a key role in regulation of apoptotic cell death, and dysregulation of this signaling pathway has been shown to participate in tumorigenesis. The current study aimed at defining the role of Caspase 8-D302H, Caspase 8-652 6N ins/del and Caspase 10-I522L genetic polymorphisms as risk factors for NHL and their possible role as genetic prognostic markers. Methods: The present study included 100 Egyptian B-cell NHL patients and 100 healthy controls. Genotyping of the studied genes was performed by polymerase chain reaction-restriction fragment length polymorphism (PCRRFLP) technique. Data was analyzed using SPSS statistical package version 15. Results: The study revealed that CASP8-D302H mutant genotypes were significantly higher in NHL patients when compared to the controls and conferred increased risk of NHL. For CASP8-652 6N ins/del and Casp10- I522L, there was no statistical difference in the distribution of the different genotypes between NHL cases and the controls. Furthermore, there were no statistical differences between NHL patients harboring the wild or mutant genotypes of the studied genes as regards their response to therapy. Conclusions: CASP8-D302H genetic polymorphism represents a genetic risk factor for NHL in Egyptian population. Hopefully, better understanding of the functional consequences of caspase genes polymorphism would provide a foundation for future studies of the possible role of these genes in lymphomagenesis.