Studies reporting the Indian prevalence of Epidermal Growth Factor Receptor (EGFR) mutation are mostly single centers with small sample sizes. This systematic review and meta-analysis summarized the available evidence of EGFR mutation epidemiology in Indian patients with adenocarcinoma (ADC) Non-Small Cell Lung Cancer (NSCLC). We conducted a structured literature search in PubMed, and EMBASE databases from January 2004 through October 2019. The primary outcome of interest was prevalence of EGFR mutation by gender, smoking status, and mutation subtype. The review included 34 studies. EGFR mutation prevalence was 39.5% in patients with ADC, and significantly higher in females, non-smokers, and patients with exon 19 deletions. The EGFR mutation frequency in Indian patients with ADC was higher than reported in Caucasians but at a lower range of that reported in East Asians. These findings support the use of EGFR mutation testing to guide choice of treatment.
Background: A latest Meta-analysis on TP53 Arg72Pro polymorphism with gastric cancer (GC) risk was published in 2015 including 20 literatures, while our study included 43 studies.Moreover, the results of previously published original studies were inconsistent and the credibility of the significant correlation between the statistical results has been ignored.Therefore, an updated Meta-analysis was conducted to further explore these associations.Objective: To explore whether these two gene polymorphisms are related to the risk, clinical manifestations, and pathological features of GC.Methods: We searched several Chinese and English databases.The crude odds ratio (OR) with 95% confidence interval (CI) was used to evaluate the correlation.In addition, false positive reporting probability (FPRP), bayesian false discovery probability (BFDP), and Venice criteria were used to assess the reliability of statistically significant correlation.Results: Overall, the TP53 Arg72Pro polymorphism was related to a significantly increased GC risk (AP vs. AA: OR = 1.12, 95% CI = 1.02 -1.24; PP + AP vs. AA: OR = 1.12, 95% CI = 1.02 -1.24; P vs. A: OR = 1.07, 95% CI = 1.00 -1.15).However, after excluding the low quality and Hardy-Weinberg Disequilibrium (HWD) studies, significant changes were found on the TP53 Arg72Pro polymorphism with GC risk in Caucasians (PP vs. AA: OR = 1.48, 95% CI = 1.01 -2.16) and non-gastric cancer control groups (PP vs. AP + AA: OR = 1.33, 95% CI = 1.07 -1.64)).However, the above significant results were considered unreliable after being adjusted with Bayesian error detection probability (BFDP) and false positive
Introduction: DNA repair enzymes continuously monitor DNA to correct damaged nucleotide residues generated by exposure to environmental mutagenic and cytotoxic compounds or carcinogens. Our objective was to investigate the association among XRCC1 (Arg399Gln and Arg194Trp), XRCC3 (Thr241Met), XPD-ERCC2 (Lys751Gln), APE1 (Asp241Glu), PARP-ADPRT (Val762Ala) DNA repair gene polymorphisms and lung cancer in Turkish population. Materials and Methods: Our patient group consists of 90 patients with lung cancer and the control group had 100 healthy individuals all of those smoking. DNA was extracted using the whole blood samples. PCR- RFLP technique was used to investigate the polymorphisms on target genes. Results: There was no significant difference in the genotype distributions of XPD Lys751Gln, XRCC1 Arg194Trp, XRCC3 Thr241Met, APE1 Asp241Glu between lung cancer patients and controls for each polymorphism (p > 0.05). However, there was a significant difference between the genotype distributions of XRCC1 Arg399Gln, and PARP Val762Ala in patients and the control group (p > 0.05). Discussion: Only the polymorphisms of XRCC1 codon 399 and PARP Val762Ala alleles are associated with the risk of lung cancer. Other genotypes were not related to lung cancer.
Non-small cell lung cancers (NSCLCs) represent over 80% of all malignant lung tumours and are one of the leading causes of cancer death throughout the world.First-and second-line treatment of advanced or metastatic NSCLCs has changed dramatically during the last two decades with the development of novel immunotherapies (e.g., checkpoint inhibitors targeting PD-1, PD-L1, and CTLA-4) sparing NSCLC patients from the toxic effects of chemotherapy.However, only 15% -20% of all patients respond to treatment.In order to improve response rates, experimental and clinical evidence has provided the basis for further evaluating the combination of co-stimulatory and inhibitory monoclonal antibodies to improve the anti-tumour immune response.Innovative second-and third-generation immuno-oncology drugs are currently evaluated in ongoing phase I-III trials (either alone or in combination) including the new checkpoint inhibitor target TIGIT (T cell immunoreceptor with Ig and ITIM domains).TIGIT functions as an inhibitory immunoglobin receptor which is overexpressed by different immune cells including effector and memory CD4 + T and CD8 + T cells, regulatory T cells (T regs ), follicular T helper cells (T fh ), and natural killer cells.Targeting the interaction between the receptors of the TIGIT receptors (e.g., CD96, CD112R, CD226, TIGIT and their corresponding binding partners) has become an innovative strategy for the next concepts of cancer immunotherapy that has the potential to synergize with PD-1/PD-L1checkpoint inhibition.Currently, four anti-TIGIT monoclonal antibodies are currently being studied in phase III trials in NSCLCs: 1) tiragolumab (SKYSCRAPER programme); 2) vibostolimab (KEYVIVE programme); 3) domvanalimab (ARC programme), and 4) ociperlimab (Ad-vanTIG programme).The vast majority of these studies are ongoing; however, the SKYSCRAPER-01 trial (tiragolumab in NSCLC) and the SKYSCRAPER-02 trial (tiragolumab in SCLC) were negative and did not meet their primary endpoint.The underlying preclinical and clinical mechanisms of these unexpectedly negative studies are currently far from being clear and the results How to cite this paper:
