Lung Cancer In Nonsmokers Research Articles

Cuproptosis-Related Gene - SLC31A1, FDX1 and ATP7B - Polymorphisms are Associated with Risk of Lung Cancer.

BackgroundCuproptosis is a novel copper-dependent cell death, and the copper level was increased in lung cancer patients. However, few studies evaluated the association between single-nucleotide polymorphisms (SNPs) in cuproptosis-related genes and lung cancer risk.MethodsSix SNPs of the SLC31A1, FDX1 and ATP7B genes were genotyped in a case–control cohort including 650 lung cancer cases and 650 controls using the MassARRAY platform.ResultsThe minor alleles of SLC31A1-rs10981694 and FDX1-rs10488764 were associated with an increased risk of lung cancer (rs10981694: OR=1.455, 95% CI: 1.201–1.763, p<0.001; rs10488764: OR=1.483, 95% CI: 1.244–1.768, p<0.001). In contrast, the minor alleles of rs9535826 and rs9535828 in ATP7B were related to a decreased risk of the disease (rs9535826: OR=0.714, 95% CI: 0.608–0.838 p<0.001; rs9535828: OR=0.679, 95% CI: 0.579–0.796, p<0.001). The frequencies of rs10981694-TG/GG and rs10488764-GA/AA genotypes were significantly higher in lung cancer cases than that in controls, making them risk genotypes for the disease (p < 0.001); while the rs9535826-TG/GG and rs9535828-GA/AA genotypes were protective genotypes and associated with a reduced risk of the disease (p<0.001). Genetic model evaluation revealed that SLC31A1-rs10981694 and FDX1-rs10488764 were associated with a growing risk of lung cancer in dominant, recessive and log-additive models (p<0.001). Moreover, rs9535826 and rs9535828 in ATP7B were related to a declining risk of the disease in three genetic models (p<0.001). In addition, stratification analysis showed that FDX1-rs10488764 was risk variant for lung cancer in both smokers and nonsmokers, and was associated with risk of each pathological type of lung cancer (p<0.008).ConclusionThe results shed new light on the correlation between cuproptosis-related genes and risk of lung cancer.

Using geogenic radon potential to assess radon priority area designation, a case study around Castleisland, Co. Kerry, Ireland

Globally, indoor radon exposure is the leading cause of lung cancer in non-smokers and second most common cause after tobacco smoking. Soil-gas radon is the main contributor to indoor radon, but its spatial distribution is highly variable, which poses certain challenges for mapping and predicting radon anomalies. Measurement of indoor radon typically takes place over long periods of time (e.g. 3 months) and is seasonally adjusted to an annual average concentration. In this article we investigate the suitability of using soil-gas radon and soil-permeability measurements for rapid radon risk assessments at local scale. The area of Castleisland, Co. Kerry was chosen as a case study due to availability of indoor radon data and the presence of significant radon anomalies. In total, 135 soil-gas and permeability measurements were collected and complemented with 180 indoor radon measurements for an identical 6 km2 area. Both soil-gas and indoor radon concentrations ranged from very low (<10 kBqm−3, 0.1 Bqm−3) to anomalously high (>1433 kBqm−3, 65,000 Bqm−3) values. Our method classifies almost 50% of the area as a high radon potential area, and allows assessment of geogenic controls on radon distribution by including other geological variables. Cumulatively, the percentage of indoor radon variance explained by soil-gas radon concentration, bedrock geology, subsoil permeability and Quaternary geology is 34% (16%, 10%, 4% and 4% respectively). Soil-gas and indoor radon anomalies are associated with black shales, whereas the presence of karst and geological faults are other contributing factors. Sampling of radon soil-gas and soil permeability, used in conjunction with other geogenic data, can therefore facilitate rapid designation of radon priority areas. Such an approach demonstrates the usefulness of high-resolution geogenic maps in predicting indoor radon risk categories when compared to the application of indoor radon measurements alone. This method is particularly useful to assess radon potential in areas where indoor radon measurements are sparse or lacking, with particular application to rural areas, land rezoned for residential use, or for sites prior to building construction.

Radon and Lung Cancer: Current Trends and Future Perspectives.

Simple SummaryRadon represents the main risk factor of lung cancer in non-smokers and the second one in smoking patients. In Europe, there are several radon-prone areas, but regulatory policies may vary between countries. Radon causes DNA damage and high genomic tumor instability, but its exact carcinogenesis mechanism in lung cancer remains unknown. Molecular drivers in NSCLC are more often described in non-smoker patients and a potential association between radon exposure and oncogenic-driven NSCLC has been postulated. This is an updated review on indoor radon exposure and its role in lung cancer carcinogenesis, especially focusing on its potential relation with NSCLC with driver genomic alterations. We want to contribute to rising knowledge and awareness on this still silent but preventable lung cancer risk factor.Lung cancer is a public health problem and the first cause of cancer death worldwide. Radon is a radioactive gas that tends to accumulate inside homes, and it is the second lung cancer risk factor after smoking, and the first one in non-smokers. In Europe, there are several radon-prone areas, and although the 2013/59 EURATOM directive is aimed to regulate indoor radon exposition, regulating measures can vary between countries. Radon emits alpha-ionizing radiation that has been linked to a wide variety of cytotoxic and genotoxic effects; however, the link between lung cancer and radon from the genomic point of view remains poorly described. Driver molecular alterations have been recently identified in non-small lung cancer (NSCLC), such as somatic mutations (EGFR, BRAF, HER2, MET) or chromosomal rearrangements (ALK, ROS1, RET, NTRK), mainly in the non-smoking population, where no risk factor has been identified yet. An association between radon exposure and oncogenic NSCLC in non-smokers has been hypothesised. This paper provides a practical, concise and updated review on the implications of indoor radon in lung cancer carcinogenesis, and especially of its potential relation with NSCLC with driver genomic alterations.

Characteristics and immune checkpoint inhibitor effects on non-smoking non-small cell lung cancer with KRAS mutation: A single center cohort (STROBE-compliant).

Kirsten rat sarcoma (KRAS) mutation (KRASm) is associated with poor prognosis in non-small cell lung cancer (NSCLC) patients. We have aimed to survey NSCLC patients harboring KRASm in Taiwan, where never-smoking lung adenocarcinoma predominates, and analyze the immune checkpoint inhibitor effect on NSCLC harboring KRASm.NSCLC patients with KRASm were enrolled and tested on programmed death-ligand 1 (PD-L1) expression using available tissue. We analyzed their clinical features, PD-L1 status, responses to ICIs, and overall survival (OS).We studied 93 patients with a median age 66.0 years, 23.7% of whom were women, and 22.6% were never-smokers. The results showed that G12C (36.6%) was the most common KRASm. In 47 patients with available tissue for PD-L1 testing, PD-L1 expression was positive in 66.0% of patients, while PD-L1 ≥50% was higher in ever-smokers (P = .038). Among 23 patients receiving ICI treatment, those with PD-L1 ≥50% experience a 45.5% response rate to ICI. There were benefits from ICI treatment on OS compared with no ICI treatment (median OS 35.6 vs 9.8 months, P = .002) for all of our patients, and for patients with PD-L1 ≥50% (median OS not-reached vs 8.4 months, P = .008). There were no differences in survival across different KRAS subtypes (P = .666).Never-smokers composed more than one-fifth of KRASm in NSCLC in Taiwan. A high PD-L1 expression was related to smoking history and responded well to ICI. ICI treatment improved the OS in NSCLC patients with KRASm, particularly those with PD-L1 ≥50%.

Sex disparity of lung cancer risk in non-smokers: a multicenter population-based prospective study based on China National Lung Cancer Screening Program.

Background:Non-smokers account for a large proportion of lung cancer patients, especially in Asia, but the attention paid to them is limited compared with smokers. In non-smokers, males display a risk for lung cancer incidence distinct from the females—even after excluding the influence of smoking; but the knowledge regarding the factors causing the difference is sparse. Based on a large multicenter prospective cancer screening cohort in China, we aimed to elucidate the interpretable sex differences caused by known factors and provide clues for primary and secondary prevention.Methods:Risk factors including demographic characteristics, lifestyle factors, family history of cancer, and baseline comorbidity were obtained from 796,283 Chinese non-smoking participants by the baseline risk assessment completed in 2013 to 2018. Cox regression analysis was performed to assess the sex difference in the risk of lung cancer, and the hazard ratios (HRs) that were adjusted for different known factors were calculated and compared to determine the proportion of excess risk and to explain the existing risk factors.Results:With a median follow-up of 4.80 years, 3351 subjects who were diagnosed with lung cancer were selected in the analysis. The lung cancer risk of males was significantly higher than that of females; the HRs in all male non-smokers were 1.29 (95% confidence interval [CI]: 1.20–1.38) after adjusting for the age and 1.38 (95% CI: 1.28–1.50) after adjusting for all factors, which suggested that known factors could not explain the sex difference in the risk of lung cancer in non-smokers. Known factors were 7% (|1.29–1.38|/1.29) more harmful in women than in men. For adenocarcinoma, women showed excess risk higher than men, contrary to squamous cell carcinoma; after adjusting for all factors, 47% ([1.30–1.16]/[1.30–1]) and 4% ([7.02–6.75]/[7.02–1])) of the excess risk was explainable in adenocarcinoma and squamous cell carcinoma. The main causes of gender differences in lung cancer risk were lifestyle factors, baseline comorbidity, and family history.Conclusions:Significant gender differences in the risk of lung cancer were discovered in China non-smokers. Existing risk factors did not explain the excess lung cancer risk of all non-smoking men, and the internal causes for the excess risk still need to be explored; most known risk factors were more harmful to non-smoking women; further exploring the causes of the sex difference would help to improve the prevention and screening programs and protect the non-smoking males from lung cancers.

Circulating nucleosomes to identify non-smoker subjects at risk of lung cancer and triage them for low-dose CT scan.

e20558 Background: Lung cancer (LC) is the leading cause of cancer death worldwide and the most frequently occurring in men and the second most diagnosed cancer in woman after breast cancer. The primary risk factor leading to LC is tobacco smoke. Nevertheless, several studies in the US, UK and Asia reported an increasing rate of LC in non-smokers. 15-20% of LC patients worldwide are non-smokers with this percentage rising to 60% in non-smoking women in Asia. Current LC screening guidelines recommend a CT scan only for high-risk smokers. Despite there being no guidelines to recommend LC screening in non-smokers those with increased risk factors could be monitored. Therefore, a blood-test could offer a simple way to identify non-smokers at high-risk of LC and triage them to go for low-dose CT scan. Methods: We measured circulating levels of nucleosomes and CEA in 722 non-smoker subjects referred for CT scan at National Taiwan University Hospital. The patients were later confirmed to have either a LC (n = 509, including 401 patients at stage 0-1), non-malignant nodules (n = 142), or no-nodules (n = 71). Whole blood was collected in EDTA plasma tubes for analysis by six different Nu.Q chemiluminescent magnetic microparticle immunoassays (Belgian Volition SRL, Belgium) targeting H3.1-nucleosomes or different histone modifications (H3K9Me3-, H3K27Me3-, H3K36Me3-, H3K9Ac-, H3K14Ac-nucleosomes). CEA was analyzed on the Abbott ARCHITECT analyzer. We defined by logistic regression the best combination of biomarkers to identify LC cases in this non-smoking population in a rule-in approach. Results: At 95% specificity, none of the individual biomarkers exceed 24.8% of sensitivity for LC vs non-malignant nodules and no nodules. A combination of 2 nucleosome biomarkers: H3K9Me3- and H3K9Ac-nucleosomes with CEA in a logistic regression model showed improved sensitivity detecting 32.4% of LC in the non-smoker subjects at 95% specificity for LC vs non-malignant nodules and no nodules (area under the curve (AUC): 0.76, R2: 19.1%). In a non-smoking women sub-group by adding a third nucleosome biomarker: H3K36Me3-nucleosomes to the model we could detect 34.3% of the women who have lung cancer at 95% specificity (AUC: 0.75; R2: 20.2%). Conclusions: Our results indicate that a blood test combining circulating nucleosomes targeting different epigenetic modifications with CEA allow the detection of LC cases in a non-smokers population. This blood test could be part of the screening criteria for the non-smoking population at risk to develop LC and could help to triage them for low-dose CT scan.

Characteristics and clinical outcomes of patients with nonsmoking small cell lung cancer in Korea

BackgroundThe aim of this study was to investigate the characteristics and clinical outcomes of patients with nonsmoking small cell lung cancer (SCLC) using a nationwide registry in Korea.MethodsThe Korean Association for Lung Cancer developed a registry in cooperation with the Korean Central Cancer Registry (KCCR) and surveyed approximately 10% of recorded lung cancer cases.ResultsFrom 2014 to 2016, the KCCR registered 1,043 patients newly diagnosed with SCLC among a total of 8,110 lung cancer patients. In subgroup analysis, Kaplan meier survival analysis showed that the overall survival (OS) was significantly shorter in the nonsmoking subgroup than the ever-smoking subgroup of SCLC patients with extensive disease (6.99 vs. 9.68 months; P = 0.016). Among SCLC patients with limited disease, OS was also shorter in the nonsmoking subgroup, without statistical significance (19.4 vs. 23.5 months; P = 0.247). In a multivariate analysis using a Cox regression model, never smoking was not associated with shorter OS, but older age, extensive stage, poor performance status (Eastern Cooperative Oncology Group grade ≥ 2), male sex, no prophylactic cranial irradiation, and no active treatment (chemotherapy and/or radiotherapy) were associated with poor prognosis.ConclusionThis evaluation of an unbiased nationwide survey dataset revealed that a significant proportion of Korean SCLC patients were never-smokers. No history of smoking appeared to be a significant prognostic factor according to the univariate analysis but was confirmed to be statistically insignificant through a multivariate analysis of the total population. Reasons for a poor prognosis may include the possibility that a high rate of the elderly population is composed of nonsmokers who did not receive active treatment.

Identification of genes and pathways associated with sex in Non-smoking lung cancer population

IntroductionWomen represent a higher proportion than men among those with lung cancer in nonsmokers compared to smokers. The reason for this abnormally higher proportion is not yet clear, but sex differences suggest there may be a genetic component at play. Materials and MethodsThe gene expression determined by Illumina RNA Sequencing and the relevant clinical information of lung cancer patients was download from TCGA. The differentially expressed genes (DEGs) were screened between males and females in both nonsmoking and smoking populations. The top 50 validated DEGs are represented with heatmaps. Based on the DEGs, GO functional and KEGG pathway enrichment analyses were performed. PPI networks were constructed to further illustrate the direct and indirect associations among the DEGs. Survival analysis was performed to explore whether these genes can affect lung cancer patient prognosis. ResultsIn non-smoking patients, there were significantly more females than males (female 73.0% vs male 27.0%, P < 0.001). Such difference was not found in smoking patients (female 50.7% vs male 49.3%, P = 0.770). A total of 898 DEGs were identified in the non-smoking population, while a total of 992 DEGs were identified in the smoking population. Of these, only 122 genes were shared by both populations. Some pathways were enriched specifical in non-smoking population, such as cAMP signaling pathway and ovarian steroidogenesis. Several proteins related to estrogen function and MAPK/PI3K signaling, such as KRT16, ERBB4 and NTF4, showed differential effects on the lung adenocarcinoma progression in non-smoking males or females. ConclusionsSome genetic differences between male and female in non-smoking lung adenocarcinoma patients have been identified. Potentially, ER signaling and MAPK/PI3K signaling partially participated in this discrepancy.

Polymorphisms of COX/PEG2 pathway-related genes are associated with the risk of lung cancer: A case–control study in China

BackgroundThe COX/PGE2 pathway is widely involved in the development of tumors and the regulation of tumor immune cells such as T cells, NK cells and DCs. However, little information is available on the single nucleotide polymorphisms (SNPs) of COX/PGE2 pathway-related genes in patients with lung cancer. MethodsSeven SNPs of the PTGS2, PTGER2 and PTGIS genes were genotyped in a case–control cohort including 600 lung cancer cases and 600 controls using the MassARRAY platform. ResultsThe minor alleles of PTGS2-rs4648298, PTGS2-rs2745557, PTGER2-rs2075797 and PTGIS-rs6125671 were all risk alleles that led to a different degree of elevated lung cancer risk (p < 0.001). The rs4648298-TC/CC, rs2745557-GA/AA, rs2075797-CG/GG and rs6125671-TC/CC genotypes were markedly associated with an elevated risk of lung cancer (p < 0.0001). Moreover, genetic model results showed that PTGS2-rs4648298 was correlated with a 4.91-, 6.90- and 4.21-fold increased risk of lung cancer under dominant, recessive and log-additive models, respectively (p < 0.0001). Similarly, PTGS2-rs2745557, PTGER2-rs2075797 and PTGIS-rs6125671 were also related to an elevated risk of the disease under the three genetic models (p < 0.001). In addition, stratification analysis based on smoking status and pathological types showed that these four SNPs were associated with the risk of lung cancer in both smokers and nonsmokers and in all three pathological types, including adenocarcinoma, squamous cell carcinoma, and small cell lung cancer (p < 0.014). ConclusionThese results contribute to a better understanding of the pathogenesis of lung cancer and provide new clues for the early detection and personalized treatment of the disease.

Radon risk assessment and mitigation deadlines

Background: Radon is a radioactive natural gas that is the leading cause of death from lung cancer in non-smokers. It is responsible for the highest share of the yearly effective doses a person is exposed to, and, in many cases, it is the most important indoor pollutant. National regulations on radon typically use derived reference levels, except for occupationally exposed workers that are monitored using a graded approach (e.g. in Switzerland and EU). However, in some countries, radon concentrations in dwellings or workplaces are high and the effective doses are comparable, and even greater than those measured in occupational workplaces. The times spent in different places and the presence of children or disabled people (that usually spend more time indoor) bring a need for assessing the risks of indoor radon exposure using a graded approach for both dwellings and workplaces. It is essential to highlight that the Covid-19 pandemic made more people work from home, and this new situation may be permanent for some workers.&#x0D; Objective and Design: On this basis, the objectives of this work are to demonstrate the importance of adequate monitoring of natural radioactivity, simulate effective doses due to radon with the new effective dose coefficients (EDCs) proposed by International Commission on Radiological Protection (ICRP) (publication 137), show case studies that illustrate the need for effective dose calculation and propose a method to set radon mitigation deadlines for buildings with high radon activity concentrations. Moreover, this work will shed light in the question about the possible need for new radon reference levels after the new EDCs were proposed.&#x0D; Conclusions: One important outcome of this work is the application of the dose approach in a case study conducted in a dwelling, the measurements and calculations show high annual effective doses (up to 350 mSv/year).

Inhibition of ZAR1 Enhances Cancer Cell Proliferation on Non-smoking Lung Cancer Patients

Inhibition of ZAR1 Enhances Cancer Cell Proliferation on Non-smoking Lung Cancer Patients

Ionizing radiation-induced epigenetic modifications and transgenerational effects

Nowadays a number of nations are exploring differences in gene expression resulting from changes in DNA methylation and modification of chromatin structure in response to external stimuli, such as radiation. It has been also well known that Ionizing radiation affects variety processes in exposed cells, in particular, cause changes in gene expression, mitochondria metabolic activity, chromosomal instability, apoptotic cell death and other changes at the molecular level. The point of view of the transgenerational nature of genomic instability suggests the possible involvement of epigenetic mechanisms. Kazakhstan has the potential to be exposed to a variety of hazardous materials, including radon, a radioactive gas that naturally occurs as a result of the indirect decay of uranium. It is also important to indicate that the Republic of Kazakhstan is considered the leader in terms of large reserves of uranium ores. Radioactive contamination is considered to be an important point that affects both the surrounding environment and human health. According to the World Health Organization, chronic exposure to radon and its decay products is the number one cause of lung cancer in non-smokers. All of the above facts prove the long-term pollution of the atmosphere by radiation has consequences for the health of the nation. Taking into account the importance of radon as a risk factor for lung cancer, this review focuses on discussion of possible radiation-induced alterations.

Lung cancer symptom appraisal, help-seeking and diagnosis - rapid systematic review of differences between patients with and without a smoking history.

Lung cancer is the leading cause of cancer death in the world. A significant minority of lung cancer patients have never smoked (14% in the UK, and ranging from 10% to 25% worldwide). Current evidence suggests that never-smokers encounter delays during the diagnostic pathway, yet it is unclear how their experiences and reasons for delayed diagnoses differ from those of current and former smokers. This rapid review assessed literature about patient experiences in relation to symptom awareness and appraisal, help-seeking, and the lung cancer diagnostic pathway, comparing patients with and without a smoking history. MEDLINE, PsychINFO and Google Scholar were searched for studies (2010-2020) that investigated experiences of the pathway to diagnosis for patients with and without a smoking history. Findings are presented using a narrative synthesis. Analysis of seven quantitative and three qualitative studies revealed that some delays during symptom appraisal and diagnosis are unique to never-smokers. Due to the strong link between smoking and lung cancer, and low awareness of non-smoking related lung cancer risk factors and symptoms, never-smokers do not perceive themselves to be at risk. Never-smokers are also likely to evaluate their experiences in comparison with other non-smoking related cancers, where prognosis is likely better, potentially leading to lower satisfaction with healthcare. Never-smokers appear to have different experiences in relation to symptom appraisal and diagnosis. However, evidence in relation to help-seeking, and what is driving diagnostic delays for never-smoker patients specifically is lacking.

1349P Application of a classifier combining bronchial transcriptomics and chest CT features facilitates the diagnostic evaluation of lung cancer in smokers and non-smokers

Lung cancer screening by computed tomography (CT) reduces mortality but exhibited high false-positive rates. We established a diagnostic classifier combining chest CT features with bronchial transcriptomics.

Combined effects of lung disease history, environmental exposures, and family history of lung cancer to susceptibility of lung cancer in Chinese non-smokers

BackgroundAlthough cigarette smoking is a major risk factor for lung cancer, the incidence rate of lung cancer among non-smokers is notable. The etiology and potential mechanism of non-smoker lung cancer are worthy of further research. This study was designed to explore the collective effects of environmental factors and the relationship between environmental exposure index (EEI) and lung cancer among non-smokers by evaluating the joint effects among lung disease history, environmental factors, and family history of lung cancer without smoking confounders.MethodsA total of 767 never-smoked lung cancer cases and 767 sex- and age-matched controls were selected from the department of Thoracic Surgery and Respiratory Medicine of three hospitals in Fujian, China. We used two methods to develop the EEI according to 12 statistically significant environmental risk factors. Restricted cubic spline (RCS) was applied to analyze the non-linear relationship between EEI and lung cancer in non-smokers. Combined effects, additive interaction, and multiplicative interaction were assessed among lung disease history, EEI, and family history of lung cancer to estimate susceptibility to develop lung cancer.ResultsLung disease history, especially asthma, was significantly associated with an increased risk of lung cancer with an odds ratio (OR) for asthma history of 14.720 (95% CI: 1.877–115.449). Family history of lung cancer was related to susceptibility of lung cancer (OR = 3.347, 95% CI: 1.930–5.806). According to type of relatives and cancer, a parental or children’s history and a sibling’s history of lung cancer were significantly associated with an increased risk of lung cancer. The positive association between EEI and lung cancer was apparently stronger in those with lung disease history or family lung cancer history. Furthermore, there was a addictive interaction between EEI and lung disease history, and a possibly addictive interaction between EEI and family lung cancer history on development of lung cancer.ConclusionsThere were combined effects among lung disease history, environmental exposures, and family history of lung cancer toward susceptibility to lung cancer in Chinese non-smokers. Non-smokers who had a family history of lung cancer were at higher risk of lung cancer than non-smokers who had lung disease history. Non-smokers with family cancer history may obtain benefits from removal of environmental exposures and active treatment of lung disease.

Identification by MicroRNA Analysis of Environmental Risk Factors Bearing Pathogenic Relevance in Non-Smoker Lung Cancer.

MicroRNA and DNA adduct biomarkers may be used to identify the contribution of environmental pollution to some types of cancers. The aim of this study was to use integrated DNA adducts and microRNAs analyses to study retrospectively the contribution of exposures to environmental carcinogens to lung cancer in 64 non-smokers living in Sicily and Catania city near to the Etna volcano. MicroRNAs were extracted from cancer lung biopsies, and from the surrounding lung normal tissue. The expression of 2549 human microRNAs was analyzed by microarray. Benzo(a)Pyrene-DNA adducts levels were analyzed in the patients’ blood by HPLC−fluorescence detection. Correlations between tetrols and environmental exposures were calculated using Pearson coefficients and regression variable plots. Compared with the healthy tissue, 273 microRNAs were downregulated in lung cancer. Tetrols levels were inversely related both with the distance from Etna and years since smoking cessation, but they were not significantly correlated to environmental exposures. The analysis of the microRNA environmental signatures indicates the contribution of environmental factors to the analyzed lung cancers in the following decreasing rank: (a) car traffic, (b) passive smoke, (c) radon, and (d) volcano ashes. These results provide evidence that microRNA analysis can be used to retrospectively investigate the contribution of environmental factors in human lung cancer occurring in non-smokers.

CFD Simulation and Experimental Measurements of Radon Distribution in a Traditional Hammam

Radon natural is the main cause of lung cancer in non-smokers. Therefore, the study of the behavior of radon and its descendants in indoor air is of the highest importance, in order to limit the risk of radiation dose due to inhalation of radon by members of the public. This article focuses to study the effects of meteorological parameters on the concentration and distribution of radon in a traditional hammam by both numerical simulations and experiments. The results of the numerical simulations are qualitative and show that the concentration and distribution of radon decrease when the ventilation rate increase, as well as, when the temperature increases, however, it increases with the increase in relative humidity. The results obtained by the numerical simulations were in agreement with those obtained experimentally with a maximum deviation of 7%. Numerical simulations allow a better estimate of the distribution of radon in indoor air.

The role of gender in non-small cell lung cancer: a narrative review.

The role of gender in the development, treatment and prognosis of thoracic malignancies has been underappreciated and understudied. While most research has been grounded in tobacco-related malignancies, the incidence of non-smoking related lung cancer is on the rise and disproportionately affecting women. Recent research studies have unveiled critical differences between men and women with regard to risk factors, timeliness of diagnosis, incongruent screening practices, molecular and genetic mechanisms, as well as response to treatment and survival. These studies also highlight the increasingly recognized need for targeted therapies that account for variations in the response and complications as a function of gender. Similarly, screening recommendations continue to evolve as the role of gender is starting to be ellucidated. As women have been underrepresented in clinical trials until recently, the data regarding optimal care and outcomes is still lagging behind. Understanding the underlying similarities and differences between men and women is paramount to providing adequate care and prognostication to patients of either gender. This review provides an overview of the critical role that gender plays in the care of patients with non-small cell lung cancer and other thoracic malignancies, with an emphasis on the need for increased awareness and further research to continue elucidating these disparities.

50 - Case series of ctDNA EGFR testing for non-smoking lung cancer

50 - Case series of ctDNA EGFR testing for non-smoking lung cancer

Lung cancer screening: who pays? who receives?-the Chinese perspective.

The National Lung Screening Trial (NLST) revealed that low-dose computed tomography (LDCT) screening reduced lung cancer mortality by 20.0%. In China, LDCT is very cheap and easy to access. As a result, LDCT screening is not limited to “high-risk” population defined by the NLST trial. The results of LDCT screening in China are also quite different from that in Western countries. LDCT detected lung cancer in a significant proportion of young, female and non-smokers in China. There is also a higher proportion of adenocarcinoma (ADC), a lower proportion of squamous cell carcinoma, and a higher proportion of early-stage 0/I disease among LDCT-detected lung cancer in China. The issue of overdiagnosis and overtreatment is discussed. Finally, we call the global attention to clarify the etiology of lung cancer in young female non-smokers.