Introduction: Cytochrome P4502C19 (CYP2C19) is well-known to be one of the determinants responsible for the pronounced interethnic and individual differences in response and character of clinically important drugs. CYP2C19*3 arises from a G to A transition at position 636 in exon 4 of CYP2C19. These individuals be situated poor metabolizers (PMs) of a wide range of medications including omeprazole (OMP). In this study, we determined genotypes of CYP2C19*3 in Iranian Azeri Turkish population to compare allele frequencies with previous findings in other ethnic groups. Methods: CYP2C19*3 allelic variant was determined in 200 unrelated healthy Iranian volunteers by polymerase chain reaction-restriction fragment length polymorphism assays (PCR-RFLP). Results: The frequencies of CYP2C19*3 in healthy volunteers reported in this study (P = 0.569, χ 2 = 2.35). This is not higher than that would be predicted from the genotypic status of these cases in CYP2C19*3 allelic variants. Our results revealed that 95.46% had wild type allele, they did not carry any of the tested mutations and 9 (4.54%) had mutant alleles. Conclusion: Our data recommend that genotyping for CYP2C19*3 is interest in using pharmacokinetics to individualize medicine, but results of this study demonstrated that CYP2C19*3 genetic polymorphism is not important determinant of the efficacy of PM of drugs, such as OMP, which may be metabolized by this enzyme.

It is estimated that there were 18.1 million cancer cases worldwide in 2018, with about 9 million deaths. Proper diagnosis of cancer is essential for its effective treatment because each type of cancer requires a specific treatment procedure. Cancer therapy includes one or more approaches such as surgery, radiotherapy, chemotherapy, and immunotherapy. In recent years, immunotherapy has received much attention and immune checkpoint molecules have been used to treat several cancers. These molecules are involved in regulating the activity of T lymphocytes. Accumulated evidence shows that targeting immune checkpoint regulators like PD-1/PD-L1 and CTLA-4 are significantly useful in treating cancers. According to studies, these molecules also have pivotal roles in the chemoresistance of cancer cells. Considering these findings, the combination of immunotherapy and chemotherapy can help to treat cancer with a more efficient approach. Among immune checkpoint molecules, the B7 family checkpoints have been studied in various cancer types such as breast cancer, myeloma, and lymphoma. In these cancers, they cause the cells to become resistant to the chemotherapeutic agents. Discovering the exact signaling pathways and selective targeting of these checkpoint molecules may provide a promising avenue to overcome cancer development and therapy resistance. Highlights: (1) The development of resistance to cancer chemotherapy or immunotherapy is the main obstacle to improving the outcome of these anti-cancer therapies. (2) Recent investigations have described the involvement of immune checkpoint molecules in the development of cancer therapy resistance. (3) In the present study, the molecular participation of the B7 immune checkpoint family in anticancer therapies has been highlighted. (4) Targeting these immune checkpoint molecules may be considered an efficient approach to overcoming this obstacle.