Four additional mutations were identified in MDA-PCa2b and one mutation in LAPC4 cell line located in 39-UTR of GRM1 gene and these mutations have been reported in NCBI data base in different populations. These mutations occurred as germline alterations in tumor samples investigated and we observed that the Concanamycin A frequency of these mutations is high in AA tumor samples as compared to CAs. High frequency of these mutations observed in AA samples may associate with differential GRM1 expression and function, which may result in the progression or more severity of the disease. AA population has shown a high incidence and mortality rate and presents a clinically more aggressive disease than CAs. The functional role of these mutations has not been reported in literature. A missense polymorphism identified in exon- 9 of GRM1 gene in PCa cell lines and tumors resulted in serine to proline change at 993 amino acid position at cytoplasmic end of receptor. Previous study using 1000 breast cancer patients showed association of this SNP in ER+/PR+ ductal carcinoma in TTgenotype carrier with later age at diagnosis as compared to either TC- and CC-genotype carriers. However, no association was found with melanoma susceptibility. A larger tumor samples study is required to confirm the association of this SNP with susceptibility to prostate carcinogenesis, aggressiveness and progression. Chronic hepatitis C virus infection is a major cause of mortality and morbidity throughout the world infecting around 3.1% of the world��s population. The development of much needed specific antiviral therapies and an effective vaccine has been hampered by the lack of a suitable small animal model. The determinants restricting HCV tropism to human and chimpanzee hosts are unknown. Replication of HCV strain JFH1 has been demonstrated in mouse cells only upon antibody selection, highlighting the very limited replication efficiency. Human CD81 and occludin have been implicated as important entry receptors for retrovirus particles bearing HCV glycoproteins, HCV pseudoparticles, into NIH3T3 murine cells. However, HCV infection, spontaneous replication and particle production by mouse cells have not yet been reported. In mammalian cells, the host detects and responds to infection by RNA-viruses, including HCV, by primarily recognizing viral RNA 6-Hydroxydopamine hydrobromide through several distinct pathogen recognition receptors, including the cell surface and endosomal RNA sensors Toll-like receptors 3 and 7, and the cytoplasmic RNA sensors retinoic acid-inducible gene I and melanoma differentiation associated gene 5.