Lung Cancer Risk Research Articles

Metabolomics signatures of air pollution mixtures and lung cancer risk: Large-Scale Metabolome-Wide Association Study in the Cancer Prevention Study Cohorts

Metabolomics signatures of air pollution mixtures and lung cancer risk: Large-Scale Metabolome-Wide Association Study in the Cancer Prevention Study Cohorts

Quantitative lung cancer risk assessment associated with hexavalent chromium: Results using pooled analysis of three cohorts

Quantitative lung cancer risk assessment associated with hexavalent chromium: Results using pooled analysis of three cohorts

Height and cancer risk in East Asians: Evidence from a prospective cohort study and Mendelian randomization analyses

BackgroundHeight is associated with increased cancer risk, but most studies focus on Western populations. We aimed to evaluate this relationship in East Asians. MethodObservational analyses were performed utilizing data from China Kadoorie Biobank (CKB) prospective cohort. Adjusted hazard ratios (HRs) and corresponding 95 % confidence intervals (CIs) were estimated using Cox proportional hazards models. Two-sample Mendelian randomization (MR) analyses explored causal effects between height and cancer using data from Korean Genome and Epidemiology Study (KoGES), Biobank Japan (BBJ), and CKB. ResultsOver a median 10.1-years follow-up, 22,731 incident cancers occurred. In observational analyses, after Bonferroni correction, each 10 cm increase in height was significantly associated with higher risk of overall cancer (HR 1.16, 95 % CI 1.14–1.19, P < 0.001), lung cancer (1.18, 95 % CI 1.12–1.24, P < 0.001), esophageal cancer (1.21, 95 % CI 1.12–1.30, P < 0.001), breast cancer (1.41, 95 % CI 1.31–1.53, P < 0.001), and cervix uteri cancer (1.29, 95 % CI 1.15–1.45, P < 0.001). Each 10 cm increase in height was suggestively associated with increased risk for lymphoma (1.18, 95 % CI 1.04–1.34, P = 0.010), colorectal cancer (1.09, 95 % CI 1.02–1.16, P = 0.010), and stomach cancer (1.07, 95 % CI 1.00–1.14, P = 0.044). In MR analyses, genetically predicted height (per 1 standard deviation increase, 8.07 cm) was suggestively associated with higher risk of lung cancer (odds ratio [OR] 1.17, 95 % confidence interval [CI] 1.02–1.35, P = 0.0244) and gastric cancer (OR 1.14, 95 % CI 1.02–1.29, P = 0.0233). ConclusionsTaller height was significantly related to a higher risk for overall cancer, lung cancer, esophageal cancer, breast cancer, and cervix uteri cancer. Our findings suggest that height may be a potential causal risk factor for lung and gastric cancers among East Asians.

Integration of QTL and comprehensive analysis in the circulating inflammatory cytokines for pan-cancer

BackgroundChemokines and cytokines are components of the tumor microenvironment and also influence tumorigenesis and its composition. However, whether they genetically proxy tumorigenesis is unclear. For causal inferences, eQTL and pQTL were used to determine the role of chemokines and cytokines in pan-cancer. The impact on the tumor immune microenvironment was also explored.MethodsThis study leveraged summary statistics from respective genome-wide association studies (GWAS) of 109 cytokines and chemokines in 18 types of solid tumors. Single nucleotide polymorphisms (SNPs) robustly associated with the cytokines and chemokines, located in or close to their coding gene (cis), were used as instrumental variables. A two-sample MR design was employed, followed by comprehensive sensitivity analyses to validate the robustness of results. The impact on immune infiltration was investigated using the TIMER and TISIDB websites. Survival analysis was conducted using the K-M plotter and TIMER 2.0 websites. The TISCH and GEO databases were used to carry out scRNA cell analysis.Analyzing relevant proteins using the STRING database and conducting enrichment pathways for GO analysis of the identified proteins.ResultsThe results of the inverse-variance weighted (IVW) method using cis-protein QTL (cis-pQTL) instruments showed the causal effects of TNF in reducing the risk of squamous cell lung cancer (LUSC) and HGF in reducing the risk of head and neck cancer (HNSC).The results were consistent with the eQTL. HGF was associated with better overall survival (OS) in HNSC, regardless of the types of cells enriched. However, high expression of the ligand MET for HGF leads to a decrease in overall survival in LUSC. TNF was related to poor OS in LUSC with no significant impact. However, in CD8 + T cell-enriched, eosinophil-enriched, macrophage-enriched, and NK cell-deficient types of LUSC, high expression of TNF leads to a poor prognosis, and there is statistical significance. The results showed a significant positive correlation between TNF and most immune cell infiltration, immunomodulator and chemokine in LUSC. HGF is positively correlated with the majority of immune cells except CD56 + cells, as well as some immune regulatory factors and chemotactic factors. According to single-cell sequencing results, HGF is mainly secreted by fibroblasts and myofibroblasts in HNSC, while in LUSC, it is primarily secreted by macrophages and CD8 + T cells secrete TNF. The GO/KEGG analysis suggests that proteins related to HGF are mainly involved in regulating peptidyl-tyrosine phosphorylation and positive regulation of the MAPK cascade. Proteins related to TNF are primarily associated with the regulation of I-kappaB kinase/NF-kappaB signaling and cytokine-mediated signaling pathway.ConclusionsHGF is primarily secreted by fibroblasts in HNSC and may have a protective effect on the occurrence and prognosis of HNSC. These effects are independent of immune cell influence, and this role may not necessarily be mediated through the HGF/MET pathway. On the other hand, TNF in LUSC is mainly secreted by immune cells like CD8 + T cell, and it may have a protective effect on the occurrence of LUSC. However, it’s impact on the prognosis of LUSC through the immune microenvironment may have a different effect.

The HUNT lung-SNP model: genetic variants plus clinical variables improve lung cancer risk assessment over clinical models

PurposeThe HUNT Lung Cancer Model (HUNT LCM) predicts individualized 6-year lung cancer (LC) risk among individuals who ever smoked cigarettes with high precision based on eight clinical variables. Can the performance be improved by adding genetic information?MethodsA polygenic model was developed in the prospective Norwegian HUNT2 study with clinical and genotype data of individuals who ever smoked cigarettes (n = 30749, median follow up 15.26 years) where 160 LC were diagnosed within six years. It included the variables of the original HUNT LCM plus 22 single nucleotide polymorphisms (SNPs) highly associated with LC. External validation was performed in the prospective Norwegian Tromsø Study (n = 2663).ResultsThe novel HUNT Lung-SNP model significantly improved risk ranking of individuals over the HUNT LCM in both HUNT2 (p < 0.001) and Tromsø (p < 0.05) cohorts. Furthermore, detection rate (number of participants selected to detect one LC case) was significantly better for the HUNT Lung-SNP vs. HUNT LCM in both cohorts (42 vs. 48, p = 0.003 and 11 vs. 14, p = 0.025, respectively) as well as versus the NLST, NELSON and 2021 USPSTF criteria. The area under the receiver operating characteristic curve (AUC) was higher for the HUNT Lung-SNP in both cohorts, but significant only in HUNT2 (AUC 0.875 vs. 0.844, p < 0.001). However, the integrated discrimination improvement index (IDI) indicates a significant improvement of LC risk stratification by the HUNT Lung-SNP in both cohorts (IDI 0.019, p < 0.001 (HUNT2) and 0.013, p < 0.001 (Tromsø)).ConclusionThe HUNT Lung-SNP model could have a clinical impact on LC screening and has the potential to replace the HUNT LCM as well as the NLST, NELSON and 2021 USPSTF criteria in a screening setting. However, the model should be further validated in other populations and evaluated in a prospective trial setting.

Integrating cardiovascular risk assessment into mobile low-dose CT lung screenings in rural Appalachia: A comprehensive analysis of the relationship between lung cancer risk, coronary artery calcium burden, and cardiovascular risk reduction strategies

ObjectiveMobile low-dose computed tomography (LDCT) lung screenings are part of an outreach program in rural Appalachia to detect early lung cancer. Coronary artery calcium (CAC) scoring on LDCT can identify calcium deposits in coronary arteries and can prompt consideration of risk modification for prevention of cardiovascular disease (CVD) events. It is not known if Lung CT Screening Reporting & Data System (Lung-RADS) scoring correlates with CAC scores. There is no clear guidance for patients undergoing LDCT screenings to receive follow-up regarding CAC or prevention of associated CVD risk. MethodsThis was a retrospective review of mobile LDCT LCS in adults with no known history of CVD. CT images were obtained at 100 kVp with a slice thickness of 3 mm. Agatston CAC scoring was performed retroactively. Lung-RADS scores were categorized as: Negative (1), Benign (2), Probably Benign (3), and Suspicious (4). CAC scoring was grouped as 0, 1–100, 101–399, and ≥400. Descriptive statistics and chi-square analyses were utilized. ResultsA total of 526 LDCT screenings were included. Over 54 % of patients had coronary calcification on LDCT LCS. 161 patients (30.6 %) had a CAC score of ≥100 and 75 patients (14.3 %) had a CAC score ≥400. Of patients with a CAC score ≥100, 7.5 % received referrals for follow-up after the LDCT screen and 9.3 % had additional cardiac testing. Of those with a CAC score ≥100 not already on a statin (45.3 %) and not already on aspirin (63.3 %), few were started within 3 months of LDCT for prevention (8.2 % and 5.9 % respectively). Among patients with a Lung-RADS score of 4, 17 % had a CAC score >400, whereas only 12 % with a Lung-RADS score of 1 fell into the same CAC category. Higher Lung-RADS scores correlated with fewer patients with CAC of 0. A significant correlation was observed between higher Lung-RADS scores and elevated CAC scores (p = 0.02). ConclusionIn patients with no CVD history, coronary artery calcification was frequently identified on mobile LDCT lung screenings in rural communities. Patients with higher probabilities of malignant lung nodules may also be at increased risk for significant coronary artery disease. Calcium scoring from LDCT screenings allowed for simultaneous assessment of lung cancer and CVD risk. Unfortunately, few referrals or CVD prevention medications were initiated. Awareness of CAC score utility, follow-up for identified coronary calcifications, and consideration of primary prevention medications when indicated, would be beneficial in patients undergoing LDCT lung screenings, especially in rural areas with limited healthcare access.

Association of Bronchial Asthma with Lung Cancer: A Systematic Review and Meta-analysis

The purpose of this study was to systematically examine the association between bronchial asthma and lung cancer. Research on the correlation between bronchial asthma and lung cancer was retrieved from the database. Literature was screened based on inclusion and exclusion criteria, and the number of patients in the included studies was extracted and analyzed. This study used Stata statistical software version 16.0 and Cochrane Review Manager version 5.4 for meta-analysis. In our study, 19 articles were selected. Without considering other influencing factors, the risk of lung cancer in asthma patients was relative risk (RR)=1.40 (95% CI: 1.17-1.67, I2=55.7%), and after correcting for risk factors such as smoking and age, it was found that the risk of small-cell lung cancer in asthma patients was RR=2.11 (95% CI: 1.45-3.24). Asthma may increase the risk of developing lung cancer, with an even higher likelihood for small cell lung cancer.

Advanced progress of the relationship between renin-angiotensin-aldosterone system inhibitors and cancers.

Hypertension and cancers are the most common causes of death in humans, as well as common co-diseases among elderly population. Studies have shown that hypertension is associated with carcinogenesis. The renin-angiotensin-aldosterone system (RAAS) is a crucial regulatory system of blood pressure, fluid, and electrolyte homeostasis, which plays an essential role in the pathogenesis of hypertension, whose mechanism is relatively clear. Studies have indicated that RAAS also widely exists in cancer tissues of different systems, which can affect the risk of cancers by stimulating cancer angiogenesis, participating in cancer-related oxidative stress, and regulating cancer-related immunity. Therefore, inhibiting RAAS activity seems beneficial to decreasing the risk of cancers. As one of the most commonly used antihypertensive drugs, RAAS inhibitors have been widely used in clinical practice. However, the conclusions of clinical studies on the relationship between RAAS inhibitors and cancers are not entirely consistent, which has been widely concerned by clinicians. The latest findings suggest that while RAAS inhibitors may reduce the risk of digestive cancers, respiratory cancers, urological cancers, gynecological cancers, and skin cancers, ACEIs may increase the risk of lung cancer, endometrial cancer, basal cell carcinoma, and squamous cell carcinoma. This article comprehensively reviews animal experiments, clinical studies, and meta-analyses on the relationship between RAAS inhibitors and cancers, to provide references for related studies in the future.

Metformin in Chemoprevention of Lung Cancer: A Retrospective Population-Based Cohort Study in Lithuania.

Background and Objectives: This study aimed to evaluate the potential chemopreventive effect of antidiabetic medications, specifically metformin and pioglitazone, on lung cancer in patients with type 2 diabetes mellitus (T2DM). Additionally, the potential dose-response relationship for metformin use was analyzed. Methods: We conducted a retrospective cohort study utilizing comprehensive national health insurance and cancer registry databases to gather a large cohort of T2DM patients. Cox proportional hazards regression models were used to assess the risk of lung cancer across different antidiabetic medication groups, adjusting for potential confounders such as age and gender. A dose-response analysis was conducted for metformin users. Results: Our results indicated that metformin users had a significantly lower lung cancer risk than the reference group (HR = 0.69, 95% CI [0.55-0.86], p = 0.001). The risk reduction increased with higher cumulative metformin doses: a metformin cumulative dose between 1,370,000 and 2,976,000 had an HR of 0.61 (95% CI [0.49-0.75], p < 0.001) vs. cumulative metformin dose >2,976,000 which had an HR of 0.35 (95% CI [0.21-0.59], p < 0.001). No significant association between pioglitazone use and the risk of lung cancer was found (HR = 1.00, 95% CI [0.25-4.02]). Conclusions: This study shows that metformin may have a dose-dependent chemopreventive effect against lung cancer in T2DM, while the impact of pioglitazone remains unclear and requires further investigation.

Unraveling the causality between gastroesophageal reflux disease and increased cancer risk: evidence from the UK Biobank and GWAS consortia

BackgroundGastroesophageal reflux disease (GERD) is a common condition characterized by the reflux of stomach contents into the esophagus. Despite its widespread prevalence worldwide, the causal link between GERD and various cancer risks has not been fully established, and past medical research has often underestimated or overlooked this relationship.MethodsThis study performed Mendelian randomization (MR) to investigate the causal relationship between GERD and 19 different cancers. We leveraged data from 129,080 GERD patients and 473,524 controls, along with cancer-related data, obtained from the UK Biobank and various Genome-Wide Association Studies (GWAS) consortia. Single nucleotide polymorphisms (SNPs) associated with GERD were used as instrumental variables, utilizing methods such as inverse variance weighting, weighted median, and MR-Egger to address potential pleiotropy and confounding factors.ResultsGERD was significantly associated with higher risks of nine types of cancer. Even after adjusting for all known risk factors—including smoking, alcohol consumption, major depression, and body mass index (BMI)—these associations remained significant, with higher risks for most cancers. For example, the adjusted risk for overall lung cancer was (OR, 1.23; 95% CI: 1.14–1.33), for lung adenocarcinoma was (OR, 1.18; 95% CI: 1.03–1.36), for lung squamous cell carcinoma was (OR, 1.35; 95% CI: 1.19–1.53), and for oral cavity and pharyngeal cancer was (OR, 1.73; 95% CI: 1.22–2.44). Especially noteworthy, the risk for esophageal cancer increased to (OR, 2.57; 95% CI: 1.23–5.37). Mediation analyses further highlighted GERD as a significant mediator in the relationships between BMI, smoking, major depression, and cancer risks.ConclusionsThis study identifies a significant causal relationship between GERD and increased cancer risk, highlighting its role in cancer development and underscoring the necessity of incorporating GERD management into cancer prevention strategies.

The clinical significance of endoplasmic reticulum stress related genes in non-small cell lung cancer and analysis of single nucleotide polymorphism for CAV1.

In recent years, protein homeostasis imbalance caused by endoplasmic reticulum stress has become a major hallmark of cancer. Studies have shown that endoplasmic reticulum stress is closely related to the occurrence, development, and drug resistance of non-small cell lung cancer, however, the role of various endoplasmic reticulum stress-related genes in non-small cell lung cancer is still unclear. In this study, we established an endoplasmic reticulum stress scores based on the Cancer Genome Atlas for non-small cell lung cancer to reflect patient features and predict prognosis. Survival analysis showed significant differences in overall survival among non-small cell lung cancer patients with different endoplasmic reticulum stress scores. In addition, endoplasmic reticulum stress scores was significantly correlated with the clinical features of non-small cell lung cancer patients, and can be served as an independent prognostic indicator. A nomogram based on endoplasmic reticulum stress scores indicated a certain clinical net benefit, while ssGSEA analysis demonstrated that there was a certain immunosuppressive microenvironment in high endoplasmic reticulum stress scores. Gene Set Enrichment Analysis showed that scores was associated with cancer pathways and metabolism. Finally, weighted gene co-expression network analysis displayed that CAV1 was closely related to the occurrence of non-small cell lung cancer. Therefore, in order to further analyze the role of this gene, Chinese non-smoking females were selected as the research subjects to investigate the relationship between CAV1 rs3779514 and susceptibility and prognosis of non-small cell lung cancer. The results showed that the mutation of rs3779514 significantly reduced the risk of non-small cell lung cancer in Chinese non-smoking females, but no prognostic effect was found. In summary, we proposed an endoplasmic reticulum stress scores, which was an independent prognostic factor and indicated immune characteristics in the microenvironment of non-small cell lung cancer. We also validated the relationship between single nucleotide polymorphism locus of core genes and susceptibility to non-small cell lung cancer.

Knowledge, attitude, and practice toward lung cancer risk among offspring of lung cancer patients: a cross-sectional study

Lung cancer is intricately associated with genetic susceptibility, leading to familial clustering among affected individuals. This cross-sectional study aimed to assess the knowledge, attitude, and practice (KAP) toward lung cancer risk among the offspring of lung cancer patients. This study was conducted at Guangdong Provincial People’s Hospital between April 2023 and August 2023. Participants’ demographic characteristics and KAP toward lung cancer risk were collected through questionnaires. A total of 481 valid questionnaires were enrolled, with 243 (50.52%) males, and 242 (50.31%) aged > 40 years old. The mean scores for knowledge, attitude, and practice were 8.54 ± 2.60 (range: 0–13), 25.93 ± 3.16 (range: 7–35), and 17.47 ± 4.30 (range: 5–25), respectively. Structural equation modeling indicated that knowledge exerted a negative direct effect on attitude (β = − 0.417, P = 0.006) but a positive direct effect on practice (β = 0.733, P = 0.025). Additionally, attitudes displayed a negative direct effect on practice (β = − 1.707, P = 0.002). In conclusion, offspring of lung cancer patients exhibited insufficient knowledge, positive attitude, and suboptimal practice toward lung cancer risk.

Blood Leukocyte DNA Methylation Markers of Periodontal Disease and Risk of Lung Cancer in a Case-Control Study Nested in the CLUE II Cohort.

Periodontal disease and DNA methylation markers have separately been associated with lung cancer risk. Examining methylation levels at genomic regions previously linked to periodontal disease may provide insights on the link between periodontal disease and lung cancer. In a nested case-control study drawn from the CLUE II cohort, we measured DNA methylation levels in 208 lung cancer cases and 208 controls. We examined the association between 37 DNA-methylated 5'-C-phosphate-G-3' (CpG) sites at three genomic regions, homeobox 4 (HOXA4), zinc finger protein (ZFP57), and a long noncoding RNA gene located in Chr10 (ENSG00000231601), and lung cancer risk. Statistically significant associations with lung cancer risk were observed for all 14 CpG sites from HOXA4 (OR ranging 1.41-1.62 for 1 SD increase in the DNA methylation level, especially within 15 years) and 1 CpG site on gene ENSG00000231601 (OR = 1.34 for 1 SD increase in the DNA methylation level). Although CpG sites on gene ZFP57 were not associated with lung cancer risk overall, statistically significant inverse associations were noted for six CpG sites when restricting follow-up to 15 years (OR = 0.73-0.77 for 1 SD increase in the DNA methylation level). Key methylation levels associated with periodontal disease are also associated with lung cancer risk. For both HOXA4 and ZFP57, the associations were stronger within 15 years of follow-up, which suggest that, if causal, the impact of methylation is acting late in the natural history of lung cancer. Identifying biological pathways that link periodontal disease and lung cancer could provide new opportunities for lung cancer detection and prevention.

Exploring the Disparity in Indoor/Outdoor Time and Radon Exposure as Possible Factors Contributing to the Unexpected Increase in Lung Cancer Risk among Non-Smoking Women.

According to a NIH study, Lung cancer among individuals who have never smoked is more prevalent in women and occurs at an earlier age than in smokers. The rise in lung cancer rates among female non-smokers might be linked to radon inhalation and should be further investigated. Our theory is based on the differences in radon exposure between males and females, which can be attributed to the variations in time spent indoors versus outdoors. Over the past few years, the smoking rates have shown a steady decline in the United States and other developed countries. This decrease in smoking prevalence has led to a new shift in the primary risk factors associated with lung cancer. Although tobacco smoke historically served as the primary cause of lung cancer, the reduction in smoking rates has allowed other risk factors, such as radon exposure, to come to the forefront. Given that women in certain countries, on average, might spend more time indoors compared to men, they are potentially exposed to higher levels of radon. This increased exposure could explain the rising rates of lung cancer among female non-smokers. The theory is still in its nascent stages and requires further research and validation. However, if proven correct, it could significantly alter our understanding of lung cancer risk factors and lead to new prevention. It is therefore crucial to expedite the review and publication of this theory, given its potential implications for public health.

From the International Association for the Study of Lung Cancer Early Detection and Screening Committee: Terminology Issues in Screening and Early Detection of Lung Cancer—International Association for the Study of Lung Cancer Early Detection and Screening Committee Expert Group Recommendations

IntroductionTo facilitate global implementation of lung cancer (LC) screening and early detection in a quality assured and consistent manner, common terminology is needed. Researchers and clinicians within different specialties may use the same terms but with different meanings or different terms for the same intended meanings. MethodsThe Diagnostics Working Group of the International Association for the Study of Lung Cancer Early Detection and Screening Committee has analyzed and discussed relevant terms used on a regular basis and suggests recommendations for consensus definitions of terminology applicable in this setting. We explored how to reach consensus to define relevant and unambiguous terminology for use by health care providers, researchers, patients, screening participants, and family. ResultsTerms and definitions for epidemiologic and health-economical purposes included the following: standardized incidence and mortality rates, LC-specific survival, long-term survival and cure rates, overdiagnosis, overtreatment, and undertreatment. Terms and definitions for defining screening findings included the following: positive, false-positive, negative, false-negative, and indeterminate findings and additional and incidental findings. Terms and definitions for describing parameters in screening programs included the following: opportunistic versus programmatic screening, screening rounds, interval or interim diagnoses, and invasive and minimally invasive procedures. Terms and definitions for shared decision-making included the following: LC screening—possible harms and risks and LC risk and modifiers prior and posterior to a measure. ConclusionsA common set of terminology with standard definitions is recommended for describing clinical LC screening programs, the discussion about effectiveness and outcomes, or the clinical setting. The use of the terms should be clearly defined and explained.

On the informative value of community-based indoor radon values in relation to lung cancer.

Radon is a radioactive gas and a major risk factor for lung cancer (LC). We investigated the dose-response relationship between radon and LC risk in the International Lung Cancer Consortium with 8927 cases and 5562 controls from Europe, North America, and Israel, conducted between 1992 and 2016. Spatial indoor radon exposure in the residential area (sIR) obtained from national surveys was linked to the participants' residential geolocation. Parametric linear and spline functions were fitted within a logistic regression framework. We observed a non-linear spatial-dose response relationship for sIR < 200 Bq/m3. The lowest risk was observed for areas of mean exposure of 58 Bq/m3 (95% CI: 56.1-59.2 Bq/m3). The relative risk of lung cancer increased to the same degree in areas averaging 25 Bq/m3 (OR = 1.31, 95% CI: 1.01-1.59) as in areas with a mean of 100 Bq/m3 (OR = 1.34, 95% CI: 1.20-1.45). The strongest association was observed for small cell lung cancer and the weakest for squamous cell carcinoma. A stronger association was also observed in men, but only at higher exposure levels. The non-linear association is primarily observed among the younger population (age < 69 years), but not in the older population, which can potentially represent different biological radiation responses. The sIR is useful as proxy of individual radon exposure in epidemiological studies on lung cancer. The usual assumption of a linear, no-threshold dose-response relationship, as can be made for individual radon exposures, may not be optimal for sIR values of less than 200 Bq/m3.

The updated relationship between the cleft‑lip and palate transmembrane protein‑1‑like rs401681 and lung cancer risk: A systematic review and meta‑analysis.

Currently, the role of cleft-lip and palate transmembrane protein-1-like (CLPTM1L) rs401681 in various tumor types, particularly lung cancer, has garnered significant attention. However, the findings across studies have shown discrepancies. The aim of the present meta-analysis was to provide a more nuanced understanding of the involvement of CLPTM1L rs401681 in lung cancer development. Several electronic databases were systematically searched, including PubMed, Cochrane Library, Embase, Medline, Wanfang, Google Scholar and Chinese National Knowledge Infrastructure. Odds ratios (ORs) and 95% confidence intervals (CIs) were synthesized using random-effects models. Heterogeneity of included studies was assessed using the I2 statistic and Q test. Sensitivity analysis was conducted to evaluate the stability of overall estimates. Moreover, Egger's test was utilized to detect potential publication bias. The collective ORs indicated a significant association between the CLPTM1L rs401681 polymorphism and susceptibility to lung cancer across various genetic comparisons. These encompass allele T vs. allele C (OR=0.93, 95% CI=0.88-0.99, P<0.001), TT + CT vs. CC (OR=0.91, 95% CI=0.87-0.96, P<0.001), TT vs. CC + CT (OR=0.88, 95% CI=0.80-0.96, P<0.001), TT vs. CC (OR=0.84, 95% CI=0.75-0.94, P<0.001) and CT vs. CC (OR=0.84, 95% CI=0.75-0.94, P<0.001). Examination through statistical Q test and I2 statistic revealed pronounced heterogeneity across four genetic comparisons (allele T vs. allele C, TT + CT vs. CC, TT vs. CC and CT vs. CC). Ethnical distinctions emerged as the primary, if not exclusive, sources of the significant heterogeneity. Upon stratification by ethnicity, a notable reduction in heterogeneity was discernible within the Caucasian demographic. However, heterogeneity persisted within the Asian population. Furthermore, lung cancer risks were statistically significantly decreased for individuals possessing allele T through all genetic comparisons within Caucasians; whereas among Asians, significant reduction was observed solely in the TT vs. CC comparison. The present meta-analysis uncovers a significant association between the CLPTM1L rs401681 polymorphism and altered susceptibility to lung cancer.

Carbohydrate quality indices and lung cancer risk: a case-control study from Iran.

Considering that carbohydrates play an important role in supplying the body with energy and exhibit diverse mechanisms that can either prevent or stimulate cancer, we hypothesize that the quality of carbohydrate intake may be associated with cancer risk, including lung cancer. This hospital-based case-control study was conducted on 135 newly diagnosed lung cancer patients, and 237 healthy age- and sex-matched hospitalized controls. We used a valid and reliable 148-item Food Frequency Questionnaire to collect the dietary intake of subjects. Multivariate logistic regression was used to estimate the association between carbohydrate quality indices and the odds of lung cancer. After adjustment for confounding variables, the high glycemic index appears to be an increased risk factor for lung cancer [odds ratio (OR) = 2.51, 95% confidence interval (CI): 1.28-4.91]. No statistically significant association was found between glycemic load and lung cancer (OR = 2.51, 95% CI: 0.98-6.43). In contrast, the carbohydrate quality index (OR = 0.23, 95% CI: 0.11-0.48) and low-carbohydrate diet score (OR = 0.17, 95% CI: 0.08-0.36), were associated with a decrease in the risk of lung cancer. In summary, our study showed that a high glycemic index is a risk factor for lung cancer, however carbohydrate quality index and low-carbohydrate diet score is a dietary approach to reduce the risk of lung cancer.

Data analysis of lung cancer incidence

Lung cancer has been widely considered as a global high incidence-disease, and its incidence is related to many factors, like smoking, genetics, and other diseases. This paper aims to model and analyse a database to further study the relationship between the incidence of lung cancer and other factors by utilizing a clinical database containing the patient information such as disease diagnoses, age, gender, and smoking. The model finds that patients with allergy and swallowing difficulty have significantly high incidence of lung cancer, while smoking does not show a highly positive association with lung cancer in the model which is widely confirmed should be highly related with lung cancer. The problem could be related to the sample in the database, since most of people in the dataset are getting respiratory diseases who are more likely to quit smoking. Finally, the paper discusses the associated causes of lung cancer and potential risks that other diseases may have based on the model result.

Brief Report: Understanding Program-Level Impact of COVID-19 in Lung Cancer Screening Programs in the United States

IntroductionLung cancer screening (LCS) reduces lung cancer mortality, yet uptake pre– and post–coronavirus disease 2019 (COVID-19) remains low. The impact of COVID-19 on LCS programs across the United States is unknown. Ours is the first multi-institutional study to identify barriers to LCS experienced during the pandemic. Our work will hopefully inform the development of targeted resources to facilitate increased uptake of LCS. MethodsA nationwide survey of Centers of Excellence (SCOE) in LCS was conducted by GO2 for Lung Cancer Foundation. In 2021, survey items included questions regarding program structure, screening rates, and systemic barriers to LCS delivery experienced amid COVID-19. ResultsA total of 99 programs representing 1112 screening sites responded. A median of 868 patients were screened during the year of 2020. Patient recruitment, patient education, and in-person service access were negatively affected by COVID-19, whereas the use of telemedicine was positively affected. Coordination of care and timely reporting of results were largely unaffected by the pandemic. ConclusionsOur findings provide a real-world snapshot of how COVID-19 affected LCS from a program perspective. These findings highlight ongoing challenges with educating and engaging those at high risk for lung cancer in LCS. Program resources should be directed toward increasing adherence to LCS among eligible patients.