Background and aim: Non-melanoma skin Cancers (NMSC) are one of the most prevalent malignancies of the human. Although the morality rate is not high for these Cancers, they may cause high morbility for the patients. In addition to the skin type, factors such as sun exposure, head and neck radiotherapy, inappropriate use of sunscreen and cultural changes may increase the incidence of these Cancers. The objective of this study was to determine NMSC in Isfahan.Materials and Methods: We used data of the Cancer resistery center for performing this study and the incidence of NMSC per 100,000 populations was determined. Results: Overall 1681 cases were registered. The incidence of NMSC was calculated to be 10.67/100,000population. The most common site for BCC and SCC was middle face. Conclusion: NMSC incidence in Isfahan is lower than west countries although this incidence is 10.67/100,000in a year. It means that 5-6 thousand cases of NMSC occur in Iran each year. We can prevent its morbidity and mortality by early correct diagnosis.

Context: One of the most important achievements in Cancer research is the development of Cancer immunotherapy. However, only a subset of patients respond to immunotherapy modalities, and few patients respond for a durable time. Here, we review the possible genomic mechanisms of response and resistance to these therapies, which can lead to the selection of responders, who may benefit most from immunotherapy. Evidence Acquisition: We searched PubMed, Scopus, and Web of Science Core Collection with the following keywords: "Immunotherapy, Resistance, Response, Programmed cell death 1 receptor, CTLA-4, Cancer immunity, Tumor Genomics, and Somatic Mutations". Results: T cells that specifically recognize Cancer-associated antigens, are responsible for the immune system response against Cancer. Nonsynonymous mutations, which are transcribed and translated into polypeptides, may generate new epitopes (neoepitopes), which can lead to their presentation on major histocompatibility (MHC) class I molecules and subsequently recognized by the adaptive immune system. Despite the unprecedented durable responses, the majority of patients treated with Cancer immunotherapies do not respond to the therapy (primary resistance), and some patients relapse after an initial response (acquired resistance). Resistance to immunotherapy can be a result of tumor cell intrinsic or extrinsic factors. There is correlation between tumor mutation burden (TMB) and response to immunotherapy. In addition, mismatch repair deficient tumors harbor considerably more somatic mutations compared to mismatch repair proficient tumors and respond better to anti-programmed cell death protein 1 (anti-PD1) therapy. Mutations in other DNA repair genes may also affect immunotherapy response. Conclusions: Neoantigen specific T cells constitute a major "active component" for the success of Cancer immunotherapies. The genetic damage that confers tumorigenic growth, can also be targeted by the immune machinery to inhibit Cancer development and progression. With further validation of experiments, Genomics-based approaches can allow to select patients most likely to achieve durable responses to immunotherapy modalities.