Personalized and Precision Medicine Journal

Abstract Cancer is largely a disease of older people; the median age for cancer diagnosis in industrialised countries is approaching 70 years of age and is expected to increase. The morbidity and mortality rates of various tumors increase with age, and thus, malignant tumors are generally defined as aging diseases. The immune system has an ambiguous role in cancer, as it plays an important immune surveillance role in the antitumor response but is also closely associated with the initiation and progression of tumors. With aging we assist to the erosion of the immune response called immunosenescence. This deregulation particularly affects the T cell compartment of the adaptive immune response. In addition to the accumulation of genetic mutations, many researchers believe that immunosenescence may also play an important role in
the tumoral process. In the future, targeting immune senescent cells may be a novel interventional opportunity in cancer patients.

Abstract Lung cancer is the leading cause of cancer death in men and the second leading cause of cancer death in women worldwide. FGFR is involved in a variety of cellular processes including angiogenesis, wound healing, tissue repair, and tumorigenesis. Recently, a common polymorphism in the transmembrane domain of the FGFR4 gene, Gly388Arg, has been reported to correlate with alteration of cell migration in vitro and with disease progression and/or survival in breast, colon, prostate and lung cancer. To evaluate the prognostic significance of the FGFR4 Gly388Arg polymorphism in lung cancer, we analyzed a case-control study of 110 lung cancer patients and 90 healthy control. Genomic DNA from whole-blood specimens was extracted using Salting-out method. Quality of DNA was evaluated by electrophoresis. To determine the distribution of FGFR4 Arg388 and FGFR4 Gly388 alleles in lung carcinoma patients, RFLP-PCR was used. In this study demonstrated that there was no relationship between polymorphism of FGFR4 Gly388Arg gene and lung cancer. Also, no significant relationship was observed between this polymorphism and clinical and pathological features of patients. It is suggested that the large casecontrol studies are needed to detect genetic determinants affecting patients’ prognosis, with the promise of targeting these putative genetic determinants to provide new therapeutic tools for patients with lung cancer.

Abstract Colorectal cancer (CRC) is the third most common type of cancer worldwide. It develops through a gradual accumulation of genetic and epigenetic changes, leading to the transformation of normal colonic mucosa into invasive cancer. Approximately 90% of colorectal cancer cases are sporadic without family history or genetic predisposition, while in less than 10% a causative genetic event has been identified. Since personalized medicine works on three subjects of determining disease indices in people, choosing the best therapeutic method and predicting disease relapse, it seems that regarding colorectal cancer, more researches are required in order to achieve favorable results. The recent advances in molecular biology and the genetic classification of CRC are essential to individualize these therapies and will be basic for improving the treatment in the next years. We are optimistic about the success of personalized medicine for this disease.

Abstract Humans are continuously exposed to a wide of carcinogenic and mutagenic stimuli, including environmental toxins, radiation and viruses as well as other infections. Tumor metastasis is responsible for approximately 9% of all cancer related deaths. The tumor microenvironment (TME) contains many distinct cell types, including endothelial cells and their precursors, pericytes, smooth muscle cells, fibroblasts, carcinoma-associated fibroblasts, myofibroblasts, neutrophils, eosinophils, basophils, mast cells, T and B lymphocytes, natural killer cells and antigen presenting cells (APC) such as macrophages and dendritic cells. Recent evidence has shown that stromal tissue is much more than a passive bystander in the development and progression of cancers. None the lese,the clinical therapy for many types of human cancers has mainly focused on the malignant cancer cell itself, and have made great achievements, yet cancer therapy still remains a great challenge. This review highlights the evidence for the crucial role of the tumor microenvironment in tumor progression and metastasis.

Abstract We present a Non-Small Cell Lung Cancer Grade IV patient, diagnosed at 46 years of age, with multiple relapse from the diagnosis and demonstrating a poor prognosis after 3 cycles of treatments. A clinical comprehensive genomic profile was performed with the goal of finding potential actionable molecular alterations. The patient showed significant symptomatic and laboratory improvement with a combination chemotherapy determined by the molecular profiling, which would otherwise not have been considered. The mentioned approach was conducted since no other targeted therapies seemed actionable for him.

Abstract Mitochondria are the extra-nuclear source of DNA in cells and play an important role in cell death susceptibility,  oxidative stress regulation, metabolism, and signaling in normal cells. Because of this, its dysfunction can contribute to the progression of cancer and metastasis. Also, mtDNA mutations have been reported in many cancers, followed by altered mitochondrial activity and cellular signaling . This increase in mtDNA mutation is due to the proximity of the genome to the OXPHOS system which are thought to be more in extent than mutation nuclear. These mutations do not inactivate energy metabolism but change its state. Therefore, it is not surprising that the function of mitochondria is vital for cancer cells, in addition to understanding the mechanisms of mitochondrial function in the process of tumor formation and cancer progression is essential for cancer treatments.