Personalized and Precision Medicine Journal

Abstract IntroductionLung cancer is the prevailing form of cancer globally, with a significant fatality rate among both males and females. Lung cancer is the third most frequent type of cancer in Iran, and it is becoming more common all the time. Patients are frequently diagnosed in the advanced stages of the disease, which contributes to the high death rate. Therefore, the ability to identify molecular markers is essential for both early diagnosis and the choice of conventional treatment for lung cancer. Numerous genetic variations have been found to be strongly linked to the development of lung cancer, according to studies. The aim of this work is to look into the genes that contribute to the development of lung cancer.
Materials and methods: The present review was authored using search terms related to lung cancer, key genes, clinical biomarkers, and early diagnosis that were found on PubMed, NCBI, Scopus, Science Direct, and Google Scholar.
Findings: Since the EGFR, KRAS, BRAF, and TP53 genes are the most significant and involved in the development of lung cancer, finding mutations in these genes can be a valuable clinical diagnostic for lung cancer diagnosis and therapy.
Discussion and conclusion: With an emphasis on personalized medicine, the identification of genes linked to lung cancer may be utilized as clinical biomarkers for the disease's early diagnosis and effective treatment. The state of targeted lung cancer therapy and early detection techniques may be enhanced by molecular biomarkers. In the field of personalized medicine, identifying the genes linked to lung cancer as clinical biomarkers for early diagnosis and assessing treatment response to select a targeted treatment can be crucial in streamlining the therapeutic process, improving treatment response, lowering mortality, and lessening the material and spiritual harm this illness causes.

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 Lung cancer is still the most common cancer worldwide in terms of the number of newly diagnosed cases and mortality rate. The expression of miR-146a was reduced in mesenchymal-like lung cancer cell lines. The overexpression of miR-146a induced a marked reduction of the mesenchymal marker and increase in the epithelial marker in lung cancer cell lines. The current study investigated the association of miR-146a genotypes and lung susceptibility in a Tehran population to determine the visibility of using RFLP-PCR genotype. The results revealed a significantly higher frequency of miR-146a CG and CC genotypes (p =0.01 and p=0.008, respectively) in patients compared with the control group. Those with the miR-146a GC and CC genotypes had an increased risk for developing lung cancer (OR=1.9; 95% CI: 1.1-3.3 and OR=4.1; 95% CI: 1.5-12.3, respectively). Moreover, the frequency rates of miR-146a CC genotype and C allele were significantly higher in patients than in the controls (p =0.006 and p=0.000, respectively).

Abstract Lung cancer is the leading cause of cancer deaths worldwide. Approximately 25% of nonsmall-cell lung cancers have mutations in the EGFR gene, most of which occur in hotspot regions in exons 18, 19, 20, and 21. In-frame deletions in exon 19 (~50%) and the L858R point mutation in exon 21 (~40%) are associated with a favorable response to EGFR tyrosine kinase inhibitors. In this study, mutations of two exons of 19 and 21 in 50 lung cancer tumor samples were investigated by the sequence method. From 50 lung cancer patients, 8 (16%) patients had an L858R (c.2573T>G) mutation, 6 (12%) patients had deletion type 1a mutation, and one patient had deletion type 1b mutation. Examining the sequence of candidate genes associated with lung cancer can be very important in choosing the right treatment approach.