Background: Tumor involvement of mediastinal lymph nodes is of high importance in non-small cell lung cancer (NSCLC). Invasive mediastinal staging is recommended in selected patients without evidence of mediastinal involvement on staging by imaging. In the present study we aimed to evaluate the effectiveness of invasive mediastinal staging in reducing pN2, its impact on survival and the risk factors for occult pN2. Methods: Patients with NSCLC tumors larger than 3 cm, central tumors or cN1 cases treated in our institution between 2013 and 2018 were prospectively included in the study. Incidence of pN2 and overall survival was compared among invasively staged (IS) and non-invasively staged groups (NIS). Multivariate analysis was performed to identify risk factors of pN2. Results: A total of 201 patients were included in the study, 79 (39.3%) of whom were not invasively staged (NIS group) and 122 (60.7%) were invasively staged (IS group). Incidence of cN1 and mean PET/CT uptake was different among both groups. Prevalence of pN2 was similar in both groups (7.6% in NIS vs. 12.6% in IS; P>0.05). Median survival in IS-pN2 patients was 11 months longer than in NIS-pN2 group (33.6 vs. 22.5 months; P=0.245). cN1 emerged as the only a risk factor for pN2. Conclusions: Invasive staging does not reduce the incidence of pN2. However, this finding could be biased because in our series cN1 patients were more often staged and cN1 has been detected as a risk factor for pN2. In addition patient better selection after invasive staging might have an impact on overall survival. To conclude, invasive mediastinal staging in intermediate risk patients for positive mediastinal nodes is justified.
Background: Genome-wide association studies have identified robust susceptibility loci associated with lung cancer. As part of the OncoArray-TRICL consortium, we have recently completed the largest GWAS on lung cancer including 29,266 cases and 56,450 controls of European descent. The goal of this study is to integrate the complete GWAS results with a large-scale expression quantitative trait loci (eQTL) mapping study in human lung tissues (n¼1,038) to identify candidate causal genes for lung cancer. Method: Transcriptome-wide association study (TWAS) was used to integrate GWAS and lung eQTL signals and identify genes whose levels of expression in lung tissue are causally related to lung cancer. TWAS was performed on six histological and smoking subgroups, namely overall lung cancer, adenocarcinoma, squamous cell carcinoma, small cell carcinoma, never-smokers, and ever-smokers. Result: As expected, the main TWAS signal for all histological subtypes and ever-smokers was on chromosome 15q25. The genes most strongly associated with lung cancer at this locus were IREB2(P TWAS ¼4.97E-104), and to a lower extent, CHRNA5(P TWAS ¼5.26E-20) and HYKK(P TWAS ¼2.04E-17). TWAS identified causal genes were different from those reported in GWAS including JAMLon 11q23.3 in overall lung cancer (P TWAS ¼1.39E-6) and adenocarcinoma (P TWAS ¼2.09E-8),NOTCH4on 6p21.32 in squamous cell carcinoma (P TWAS ¼1.24E-12), ZNRD1on 6p22.1 in overall lung cancer (P TWAS ¼3.41E-14) and ever-smokers (P TWAS ¼1.29E-9), HIST1H2BDon 6p22.2 for small cell carcinoma (P TWAS ¼1.54E-6), and NEXNon 1p31.1 in never-smokers (P TWAS ¼2.64E-5). In addition, a new small cell carcinoma susceptibility locus was identified on 4q32.2 and associated with the expression levels of TMA16(P TWAS ¼4.2E-6). Conclusion: In conclusion, lung tissue TWAS on lung cancer, histological subtypes and smoking subgroups revealed novel causal genes in GWAS-nominated loci. A new locus for small cell carcinoma (4q32.2-TMA16) was also identified and will require further validation.Background: Published risk estimates for diagnosis of lung cancer based on family history are typically focused on close relatives, rather than a more diverse or complete family history. This study provides relative risks (RR) for lung cancer based on comprehensive family history data obtained from a statewide Cancer Registry linked to a high quality genealogy data resource. Risk estimates presented avoid common recall, recruitment, ascertainment biases, and are based on an individual's (proband's) lung cancer family history constellation (pattern of lung cancer affected relatives). Method: A population-based genealogical resource linked to a statewide electronic SEER cancer registry estimated relative risk (RR) for lung cancer for an individual based upon their lung cancer family history. Family history data available for a proband included degree of relationship (first to thirddegree), paternal or maternal family lung cancer history, number of lung cancer affected relatives and age at diagnosis of affected...
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