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Background: Since the outbreak of COVID-19 in 2020, routine CT examination was recommended to hospitalized patients at some hospitals and discovered lung cancer patients at an early stage. This study aimed to investigate the detection efficacy of routine CT examination on early diagnosis of lung cancer, especially on pathological characteristics. Methods: The epidemic of COVID-19 outbreak in January 2020 in China, and routine CT examination was recommended to hospitalized patients in June 2020 and ended in July 2021. Based on the time points, we compared the diagnosis efficacy between three periods: pre-period, peri-period, and the period of routine CT examination. Results: During the period of routine CT examination, more early stages of lung cancer were detected and the tumor size was reduced to 2.14 cm from 3.21 cm at pre-period (p = 0.03). The proportion of lung adenocarcinoma and early stage adenocarcinoma was increased by 12% and 30% in the period of routine CT examination, with referral to the pre-period of CT examination (p < 0.05). A total of 61% of diagnosed patients had the wild type of TP53 gene during the period of routine CT examination, compared to 45% of patients at the pre-period of CT examination (p = 0.001). The median Ki-67 index was 15% among patients diagnosed at the period of routine CT examination and increased to 35% at the pre-period of CT examination (p < 0.001). The period of routine CT examination was associated with a 78% higher probability of detecting an early stage of adenocarcinoma (OR = 1.78, 95%CI 1.03, 3.08) but no significant association was observed for squamous cell carcinoma. From the pre-period to the period of routine CT examination, the proportion of female patients and non-smoking patients increased by 57% and 44%, respectively (p < 0.001). Conclusion: Routine CT examination could detect more lung cancer at an early stage, especially for adenocarcinoma, and detect patients with less aggressive features. Further studies were warranted to confirm the findings. [ABSTRACT FROM AUTHOR]

Background Germline mutations play an important role in the pathogenesis of lung cancer. Nonetheless, research on malignant ground glass opacity (GGO) nodules is limited. Methods A total of 13 participants with malignant GGO nodules were recruited in this study. Peripheral blood was used for exome sequencing, and germline mutations were analyzed using InterVar. The whole exome sequencing dataset was analyzed using a filtering strategy. KOBAS 3.0 was used to analyze KEGG pathway to further identify possible deleterious mutations. Results There were seven potentially deleterious germline mutations. NM_001184790:exon8: c.C1070T in PARD3, NM_001170721:exon4:c.C392T in BCAR1 and NM_001127221:exon46: c.G6587A in CACNA1A were present in three cases each; rs756875895 frameshift in MAX, NM_005732: exon13:c.2165_2166insT in RAD50 and NM_001142316:exon2:c.G203C in LMO2, were present in two cases each; one variant was present in NOTCH3. Conclusions Our results expand the germline mutation spectrum in malignant GGO nodules. Importantly, these findings will potentially help screen the high-risk population, guide their health management, and contribute to their clinical treatment and determination of prognosis. [ABSTRACT FROM AUTHOR]

Numerous efforts have been made to elucidate the etiology and improve the treatment of lung cancer, but the overall five-year survival rate is still only 15%. Although cigarette smoking is the primary risk factor for lung cancer, only 7% of female lung cancer patients in Taiwan have a history of smoking. Since cancer results from progressive accumulation of genetic aberrations, genomic rearrangements may be early events in carcinogenesis. Results In order to identify biomarkers of early-stage adenocarcinoma, the genome-wide DNA aberrations of 60 pairs of lung adenocarcinoma and adjacent normal lung tissue in nonsmoking women were examined using Affymetrix Genome-Wide Human SNP 6.0 arrays. Common copy number variation (CNV) regions were identified by ⩾30% of patients with copy number beyond 2 ± 0.5 of copy numbers for each single nucleotide polymorphism (SNP) and at least 100 continuous SNP variant loci. SNPs associated with lung adenocarcinoma were identified by McNemar's test. Loss of heterozygosity (LOH) SNPs were identified in ⩾18% of patients with LOH in the locus. Aberration of SNP rs10248565 at HDAC9 in chromosome 7p21.1 was identified from concurrent analyses of CNVs, SNPs, and LOH. Conclusion The results elucidate the genetic etiology of lung adenocarcinoma by demonstrating that SNP rs10248565 may be a potential biomarker of cancer susceptibility. [ABSTRACT FROM AUTHOR]