Reduce Lung Cancer Incidence Research Articles

Lung Cancer Screening Health Belief Model: Psychometric Properties of the Arabic Version and Factors Influencing Screening and Prevention Among Jordanians.

Several screening models have recently been applied to study awareness and help people make informed decisions regarding cancer screening. This study aimed to explore the knowledge, attitudes, and lung cancer screening health beliefs (LCSHBs) among Jordanians. Moreover, we intended to translate the LCSHBs scale into the Arabic language and test its validity and reliability. An online survey (Google Forms) was completed by 916 participants in Jordan via snowball sampling technique from February 10, 2024, to March 2, 2024, assessing lung cancer screening knowledge, lung cancer preventive attitudes, screening-related health beliefs, and stages of screening adoption. Linear regression analysis, correlations, and non-parametric statistics were utilized for statistical inference. Participants had high mean percentage scores of 86.56% and 85.75% for knowledge and preventive attitudes towards lung cancer screening, respectively. The Arabic version of the LCSHBs model was found to be a valid and reliable tool, as indicated by principal component analysis extraction and Cronbach's alpha values. Lung cancer screening knowledge was positively associated with perceived benefits and negatively associated with perceived barriers to screening. Knowledge, perceived barriers, perceived risk of lung cancer, self-efficacy (SE) to screen, and lung cancer preventive attitudes were significantly associated with the perceived benefits of lung cancer screening (p<0.05). We also found that the higher the SE, the higher the physical activity and the lower the perceived barriers. The Arabic version of the LCSHBs model is valid and reliable for assessing health beliefs toward lung cancer screening. We recommend enhancing targeted interventions, educational outreach, and improving health insurance access to reduce lung cancer incidence in Jordan and promote screening behaviors.

Lung cancer screening: Real screening site data, Vojvodina, Serbia

Abstract Background Lung cancer (LC) is the top cause of cancer-related deaths globally and in Serbia, often diagnosed in advanced stage of disease with when 5-year survival is 10% to 20%. LC screening with low-dose CT (LDCT) can decrease LC mortality and overall mortality. The first pilot LC screening program in Serbia started in the Institute for Pulmonary Diseases of Vojvodina in September 2020. The main objective of this study was to analyze LC patient characteristics according to their screening status. Methods This retrospective study utilized LC hospital registry data from September 2020 to December 2023, including gender, age at diagnosis, settlement area, smoking habits, cancer histological type, TNM classification, disease stage (1-4), and data on participation in LC screening. Group differences were assessed using chi-square and Student’s t-tests, with analyses conducted in SPSS v24.0. Results During observed period from a total of 4649 LC cases 2948 (63.4%) were males, and 73 (1.6%) were included in LC screening. Average age of all LC patients was 66 years, without differences between groups (p = 0.778). Significant differences between groups by gender were find (p = 0.042). Non-screened LC patients were significantly common males compared to females (63.6% vs 36.4%), while among screened difference by gender were lower (52.1% vs 47.9%, respectively). Screened compared to non-screened LC patients have significantly lower percentage of SCLC (9.6% vs 19.1%), and higher percentage of NSCLC (90.4% vs 80.9%), (p = 0.040). According to LC stage, screened compared to non-screened patients were significantly common diagnosed in stage I of disease (45.8% vs 7.8%), and significantly less common in higher LC stages; stage IIIB (11.1% vs 22.5%), and in stage IV (22.2% vs 45.7%), (p &amp;lt; 0.001). Conclusions LC screening with LDCT is proven secondary preventive measure with significant influence on decreasing LC mortality by increasing number of LC patients in early stages of disease. Key messages • Lung cancer screening with low-dose CT significantly increases early-stage diagnoses, improving survival chances. • Population strategies to prevent smoking and screening programs for high-risk groups are needed to reduce lung cancer incidence and mortality rates in Serbia.

Time to treatment initiation: An assessment of trends in delays in patients with lung cancer across Missouri.

11186 Background: Lung cancer is a major health challenge globally. Missouri's incidence rate of 68.1% exceeds the national rate of 54.0% indicating a significant disease burden. It is the 2nd most common malignancy in men and women in the state. Timely treatment can significantly improve while delays can worsen outcomes. The Institute of Medicine strongly recommends efforts promoting timely care in lung cancer. The RAND Cooperation suggests treatment should begin within 6 weeks after diagnosis. These priorities align with the Healthy People 2030 Initiative which aims to reduce lung cancer incidence and mortality through enhanced screening and early treatment. The U.S. National Committee on Health Care identified a goal of 60% of lung cancer patients receiving treatment within 30-days of diagnosis. Our primary objective was to assess delays in treatment initiation post-diagnosis and to investigate Missouri’s adherence to treatment delay guidelines in lung cancer patients. Methods: Study population included adults (age&gt;18) with a diagnosis of Lung Cancer, identified using ICD-10 codes C50.0-C50.9. Records were retrieved from the Missouri Cancer Registry and Research Center database for the years 2012-2022. Data for 2022 had a completion rate of 90%, all others had at least 95% completeness. We used the RAND guidelines 42-day treatment delay rule and the Missouri Cancer Action Plan's (MCAP) 30 day treatment delay metric as our benchmarks. Treatment delay was determined by subtracting the Date of Initial Diagnosis from the Date of First Course Treatment. Records with missing or incomplete dates were excluded. Data processing and analyses were performed using Python 3.11. Results: Of the 68,293 adult lung cancer patients in the database, 7,882 were excluded due to missing or incomplete data. Among the eligible 60,411 patients, 89.5% were Caucasian, median age was 69 (range 18-105), gender distribution was nearly equal with males accounting for 51.3% of the total. Average time from diagnosis to treatment was 36.8 days, with a median of 27 days. About 31.2% of patients had a gap over 42 days from diagnosis to first treatment. This delay has risen from 26.3% in 2012 to 42.6% in 2022, marking a 16.3% increase. In terms of adherence to the MCAP’s 30 day treatment delay metric, 45.6% of patients experienced more than a 30-day gap between diagnosis and treatment. The trend shows an increase in delays, from 40.4% in 2012 to 58.1% in 2022, reflecting a 17.7% rise. Conclusions: Despite the declining incidence rate of lung cancer in Missouri over the years, our analysis revealed a surprising increase in treatment initiation delays over the years. The average time from diagnosis to treatment and the percentage of patients experiencing delays exceed the RAND guideline and the MCAP's treatment delay metric and with a rising trend from 2012 to 2022. Further analysis into factors causing delay in treatment initiation is needed and being planned.

Effect of forest cover on lung cancer incidence: a case study in Southwest China.

Forests are closely linked to human health, particularly about lung cancer incidence. However, there is currently limited research on how forest coverage and different types of forests influence lung cancer rates. This study aims to address this gap by examining how the coverage of various forest types impacts lung cancer incidence in Southwest China, thereby providing theoretical support for health-oriented forest structure planning. We focused on 438 counties in Southwest China, employing spatial autocorrelation analysis (Moran's I) and spatial regression models [including Spatial Lag Model (SLM), Spatial Error Model (SEM), and Spatial Durbin Model (SDM)] to explore the effects of forest coverage and internal forest structure on lung cancer incidence. We used ArcGIS to visualize lung cancer incidence and forest coverage rates across the study area. The study found a significant negative correlation between forest coverage and lung cancer incidence. Specifically, for every 1% increase in forest coverage, lung cancer incidence decreased by 0.017 levels. Evergreen forests and mixed forests showed a significant negative impact on lung cancer rates, with evergreen forests having a particularly strong effect; a 1% increase in evergreen forest coverage was associated with a 0.027 level decrease in lung cancer incidence. In contrast, deciduous forests had no significant impact. Additionally, the study revealed a marked spatial heterogeneity in lung cancer incidence and forest coverage across Southwest China: higher lung cancer rates were observed in the eastern regions, while forest coverage was predominantly concentrated in the western and southern regions. This study demonstrates that increasing forest coverage, particularly of evergreen and mixed forests, can help reduce lung cancer incidence. This effect may be related to the ability of forests to absorb harmful gasses and particulate matter from the air. Furthermore, the spatial heterogeneity in lung cancer incidence suggests that regional economic development levels and urbanization processes may also play significant roles in the spatial distribution of lung cancer rates. The findings provide empirical support for the development of targeted forest conservation and development policies aimed at optimizing regional forest structures to reduce the risk of lung cancer.

Deciphering the impact of urban built environment density on respiratory health using a quasi-cohort analysis of 5495 non-smoking lung cancer cases

IntroductionLung cancer is a major health concern and is influenced by air pollution, which can be affected by the density of urban built environment. The spatiotemporal impact of urban density on lung cancer incidence remains unclear, especially at the sub-city level. We aimed to determine cumulative effect of community-level density attributes of the built environment on lung cancer incidence in high-density urban areas. MethodsWe selected 78 communities in the central city of Shanghai, China as the study site; communities included in the analysis had an averaged population density of 313 residents per hectare. Using data from the city cancer surveillance system, an age-period-cohort analysis of lung cancer incidence was performed over a five-year period (2009–2013), with a total of 5495 non-smoking/non-secondhand smoking exposure lung cancer cases. Community-level density measures included the density of road network, facilities, buildings, green spaces, and land use mixture. ResultsIn multivariate models, built environment density and the exposure time duration had an interactive effect on lung cancer incidence. Lung cancer incidence of birth cohorts was associated with road density and building coverage across communities, with a relative risk of 1·142 (95 % CI: 1·056–1·234, P = 0·001) and 1·090 (95 % CI: 1·053–1·128, P < 0·001) at the baseline year (2009), respectively. The relative risk increased exponentially with the exposure time duration. As for the change in lung cancer incidence over the five-year period, lung cancer incidence of birth cohorts tended to increase faster in communities with a higher road density and building coverage. ConclusionUrban planning policies that improve road network design and building layout could be important strategies to reduce lung cancer incidence in high-density urban areas.

Association of quality of life with performance status, circadian rhythm, and activity level of lung cancer patients using wearable devices as ambulatory monitoring

Lung cancer survivorship has two critical attributes: survival time or quantity and quality of life (QoL).[1][1] After decades of efforts focusing on reducing lung cancer incidence and mortality, we are now challenged by the lack of understanding of the health conditions and QoL among people who

Garlic oil blocks tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis by inducing phase II drug-metabolizing enzymes

Lung cancer caused one-quarter of all cancer deaths that was more than other cancers. Chemoprevention is a potential strategy to reducing lung cancer incidence and death, and the effective chemopreventive agents are needed. We investigated the efficacy and mechanism of garlic oil (GO), the garlic product, in the chemoprevention of tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung cancer in A/J mice and MRC-5 cell models in the present study. As a result, it was demonstrated that GO significantly inhibited the NNK-induced lung cancer in vivo and protected MRC-5 cells from NNK-induced cell damage. GO could induce the expressions of the phase II drug-metabolizing enzymes, including NAD(P)H: quinone oxidoreductase 1 (NQO-1), glutathione S-transferase alpha 1 (GSTA1), and antioxidative enzymes heme oxygenase-1 (HO-1). These results supported the potential of GO as a novel candidate agent for the chemoprevention of tobacco carcinogens induced lung cancer.

Primary care and pulmonary physicians' knowledge and practice concerning screening for lung cancer in Lebanon, a middle-income country.

ABSTRACTBackgroundScreening for lung cancer with low‐dose computed tomography (LDCT) was shown to reduce lung cancer incidence and overall mortality, and it has been recently included in international guidelines. Despite the rising burden of lung cancer in low and middle‐income countries (LMICs) such as Lebanon, little is known about what primary care physicians or pulmonologists know and think about LDCT as a screening procedure for lung cancer, and if they recommend it.ObjectivesEvaluate the knowledge about LDCT and implementation of international guidelines for lung cancer screening among Lebanese primary care physicians (PCPs) and pulmonary specialists.MethodologyPCPs and PUs based in Lebanon were surveyed concerning knowledge and practices related to lung cancer screening by self‐administered paper questionnaires.Results73.8% of PCPs and 60.7% of pulmonary specialists recognized LDCT as an effective tool for lung cancer screening, with 63.6% of PCPs and 71% of pulmonary specialists having used it for screening. However, only 23.4% of PCPs and 14.5% of pulmonary specialists recognized the eligibility criteria for screening. Chest X‐ray was recognized as ineffective by only 55.8% of PCPs and 40.7% of pulmonary specialists; indeed, 30.2% of PCPs and 46% of pulmonary specialists continue using it for screening. The majority have initiated a discussion about the risks and benefits of lung cancer screening.ConclusionPCPs and pulmonary specialists are initiating discussions and ordering LDCT for lung cancer screening. However, a significant proportion of both specialties are still using a non‐recommended screening tool (chest x‐ray); only few PCPs and pulmonary specialists recognized the population at risk for which screening is recommended. Targeted provider education is needed to close the knowledge gap and promote proper implementation of guidelines for lung cancer screening.

Novel function of PERP-428 variants impacts lung cancer risk through the differential regulation of PTEN/MDM2/p53-mediated antioxidant activity

Lung cancer is the leading cause of cancer-related deaths worldwide. Identifying genetic risk factors and understanding their mechanisms will help reduce lung cancer incidence. The p53 apoptosis effect is related to PMP-22 (PERP), a tetraspan membrane protein, and an apoptotic effector protein downstream of p53. Although historically considered a tumor suppressor, PERP is highly expressed in lung cancers. Stable knockdown of PERP expression induces CL1-5 and A549 lung cancer cell death, but transient knockdown has no effect. Interestingly, relative to the PERP-428GG genotype, PERP-428CC was associated with the highest lung cancer risk (OR = 5.38; 95% CI = 2.12–13.65, p < 0.001), followed by the PERP-428CG genotype (OR = 2.34; 95% CI = 1.55–3.55, p < 0.001). Ectopic expression of PERP-428G, but not PERP-428C, protects lung cancer cells against ROS-induced DNA damage. Mechanistically, PERP-428 SNPs differentially regulate p53 protein stability. p53 negatively regulates the expression of the antioxidant enzymes catalase (CAT) and glutathione reductase (GR), thereby modulating redox status. p53 protein stability is higher in PERP-428C-expressing cells than in PERP-428G-expressing cells because MDM2 expression is decreased and p53 Ser20 phosphorylation is enhanced in PERP-428C-expressing cells. The MDM2 mRNA level is decreased in PERP-428C-expressing cells via PTEN-mediated downregulation of the MDM2 constitutive p1 promoter. This study reveals that in individuals with PERP-428CC, CAT/GR expression is decreased via the PTEN/MDM2/p53 pathway. These individuals have an increased lung cancer risk. Preventive antioxidants and avoidance of ROS stressors are recommended to prevent lung cancer or other ROS-related chronic diseases.

Abstract PO033: Regulation of immune checkpoint proteins in NSCLC adenocarcinoma

Abstract Lung cancer is the leading cause of cancer-related deaths in both men and women. Approximately 85% of lung cancers are non-small cell lung cancer (NSCLC), with adenocarcinoma (adenoCa) being the main subtype. Well-defined mutational signatures of various lung cancer subtypes have been exploited for targeted therapies, but cancer cells often acquire resistance to these treatments, which could be mediated by the inflammatory tumor microenvironment (TME). Inflammation within the TME is known to promote cancer progression and therapy resistance. The inflammatory cytokine, interleukin-1 beta (IL-1β) is elevated in the TME of several cancers and correlates with poor outcomes. In NSCLC patients, serum IL-1β is elevated relative to normal subjects; within the same patient, IL-1β is elevated in the tumor relative to adjacent non-tumor tissue. Significantly, the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) showed that blockade of IL-1 signaling could drastically reduce lung cancer incidence and mortality. Interestingly, we observed that NSCLC adenoCa cell lines H1838, H2228, H2347, HCC4150 and HCC827 have significantly higher basal expression of the Type 1 IL-1 receptor (IL-1R1), relative to immortalized normal Human Bronchial Epithelial Cell (HBEC-3KT) and Human Small Airway Epithelial Cell (HSAEC-1KT) lines, suggesting that adenoCa cells are primed to respond to IL-1 signaling. Cancer cells can promote immunosuppression through the expression of immune checkpoint proteins (ICPs). Previously, we identified several ICPs, including programmed death-ligand 1 (PD-L1), tryptophan 2,3-dioxygenase 2 (TDO2), indoleamine 2, 3-dioxygenase 1 (IDO1) and growth differentiation factor 15 (GDF15), that were developmentally upregulated by transcription factor nuclear factor erythroid 2-related factor 2 (NRF2/NFE2L2) in human fetal lung epithelial cells during differentiation in culture. Importantly, genomic studies have revealed that &amp;gt;20% of lung adenoCa harbor mutations in NRF2 or its inhibitor KEAP1, which cause NRF2 activation. Lung adenoCa with signatures of increased NRF2 activation manifest reduced immune cell infiltration, suggesting that increased expression of NRF2 might create a more permissive immune cell environment, resulting in evasion and tolerance to the host immune system. Given that IL-1β induces ROS which can activate NRF2, we hypothesized that IL-1β present in the TME may enhance expression of NRF2 and ICPs in NSCLC adenoCa. We found that increased expression of ICPs in adenoCa cell lines H1838, H2228, H2347, HCC4150 and HCC827 compared to HBEC-3KT and HSAEC-1KT cells was correlated with significantly increased expression of NRF2. When these adenoCa cell lines were treated with IL-1β, we observed a marked induction in NRF2 and ICP mRNA and protein levels. Taken together our studies indicate that NSCLC adenoCa cells are primed to respond to IL-1 signaling which induces NRF2 and ICPs to promote tumor cell survival through immunosuppression. Citation Format: Afshan Fathima Nawas, Ritu Mishra, Carole R. Mendelson. Regulation of immune checkpoint proteins in NSCLC adenocarcinoma [abstract]. In: Proceedings of the AACR Virtual Special Conference on the Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; 2021 Jan 11-12. Philadelphia (PA): AACR; Cancer Res 2021;81(5 Suppl):Abstract nr PO033.

Inhibition of IL1β by Canakinumab May Be Effective against Diverse Molecular Subtypes of Lung Cancer: An Exploratory Analysis of the CANTOS Trial

In the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS), inhibition of the IL1β inflammatory pathway by canakinumab has been shown to significantly reduce lung cancer incidence and mortality. Here we performed molecular characterization of CANTOS patients who developed lung cancer during the study, including circulating tumor DNA (ctDNA) and soluble inflammatory biomarker analysis. Catalogue of Somatic Mutations in Cancer (COSMIC) database ctDNA mutations were detected in 65% (46/71) of the CANTOS patients with lung cancer, with 51% (36/71) having detectable ctDNA at the time point closest to lung cancer diagnosis and 43% (29/67) having detectable ctDNA at trial randomization. Mutations commonly found in lung cancer were observed with no evidence of enrichment in any mutation following canakinumab treatment. Median time to lung cancer diagnosis in patients with (n = 29) versus without (n = 38) detectable COSMIC ctDNA mutations at baseline was 407 days versus 837 days (P = 0.011). For serum inflammatory biomarker analysis, circulating levels of C-reactive protein (CRP), IL6, IL18, IL1 receptor antagonist, TNFα, leptin, adiponectin, fibrinogen, and plasminogen activator inhibitor-1 were determined. Patients with the highest level of baseline CRP or IL6, both downstream of IL1β signaling, trended toward a shorter time to lung cancer diagnosis. Other inflammation markers outside of the IL1β pathway at baseline did not trend with time to lung cancer diagnosis. These results provide further evidence for the importance of IL1β-mediated protumor inflammation in lung cancer and suggest canakinumab's effect may be mediated in part by delaying disease progression of diverse molecular subtypes of lung cancer. SIGNIFICANCE: These findings suggest that targeting the IL1β inflammatory pathway might be critical in reducing tumor-promoting inflammation and lung cancer incidence.

Diabetes, Metformin, and Lung Cancer: Retrospective Study of the Korean NHIS-HEALS Database

BackgroundMetformin is the first option in managing type 2 diabetes mellitus (DM) and has pleotropic effects. We studied the incidence of lung cancer in patients who received metformin therapy. Patients and MethodsThis study was retrospectively designed and based on the Korean National Health Insurance Service–National Health Screening Cohort to determine whether metformin reduces lung cancer risk in the diabetic population. At baseline, all participants were 40 to 69 years old and were categorized into 3 groups: metformin nonrecipients with DM, metformin recipients with DM, and the nondiabetic group. ResultsA total of 336,168 individuals were included in the final analysis (314,291 nondiabetic individuals, 8806 metformin recipients, and 13,071 metformin nonrecipients). The study median follow-up period was 12.86 years. The estimated cumulative lung cancer incidence of metformin nonrecipients, metformin recipients, and the nondiabetic group was 1.80%, 1.97%, and 1.24% in men and 1.87%, 0.61%, and 0.41% in women, respectively (P < .05). Compared to metformin nonrecipients, the hazard ratios (95% confidence intervals) for lung cancer incidence of metformin recipients and the nondiabetic group were 1.287 (0.979-1.691) and 0.835 (0.684-1.019) in men and 0.664 (0.374-1.177) and 0.553 (0.359-0.890) in women, respectively. The hazard ratios (95% confidence intervals) were statistically significant in male ever smokers (0.784 [0.627-0.979]) and female nonsmokers (0.498 [0.320-0.774]) after stratification according to smoking status. ConclusionMetformin therapy did not reduce lung cancer incidence in the diabetic population. However, individuals without DM were at a lower risk of lung cancer, especially in male ever smokers and female nonsmokers.

Drugs for preventing lung cancer in healthy people.

This is the second update of this Cochrane Review. Some studies have suggested a protective effect of antioxidant nutrients and higher dietary levels of fruits and vegetables on lung cancer. To determine whether vitamins and minerals and other potential agents, alone or in combination, reduce lung cancer incidence and lung cancer mortality in healthy populations. We searched CENTRAL, MEDLINE and Embase from 1974 to May 2019 and screened references included in published studies and reviews. We included randomised controlled trials (RCTs) comparing vitamins or mineral supplements with placebo, administered to healthy people with the aim of preventing lung cancer. Four review authors independently selected the trials to be included in the review, assessed their methodological quality and extracted data. For dichotomous outcomes we calculated risk ratios (RRs) and 95% confidence intervals (CIs) and pooled results using the random-effects model. We assessed the risk of bias using Cochrane's 'Risk of bias' assessment tool and certainty of evidence using the GRADE approach. In this update, we identified three new trials for a total of 12 studies. Six analysed vitamin A, three vitamin C, three combined vitamin D3 + calcium, four vitamin E combined with other products, one selenium supplements and nine studied combinations of two or more products. Four studies included only men and five only women. Vitamin A results in little to no difference in lung cancer incidence (RR 1.09, 95% CI 1.00 to 1.19; 5 RCTs, 212314 participants; high-certainty evidence) and lung cancer mortality (RR 1.06, 95% CI 0.81 to 1.38; 3 RCTs, 190118 participants; high-certainty evidence). But in smokers or asbestos workers vitamin A increases the risk of lung cancer incidence (RR 1.10, 95% CI 1.01 to 1.20; 3 RCTs, 43995 participants; high-certainty evidence), lung cancer mortality (RR 1.18, 95% CI 1.01 to 1.38; 2 RCTs, 29426 participants; high-certainty evidence) and all-cause mortality (RR 1.09, 95% CI 1.05 to 1.13; 2 RCTs, 32883 participants; high-certainty evidence). Vitamin A increases the risk of minor side effects, such as yellowing of the skin and minor gastrointestinal symptoms (high-certainty evidence). Vitamin C likely results in little to no difference in lung cancer incidence (RR 1.29, 95% CI 0.67 to 2.49; 2 RCTs, 14953 participants; moderate-certainty evidence). In women, vitamin C increases the risk of lung cancer incidence (RR 1.84, 95% CI 1.14 to 2.95; 1 RCT, 7627 participants; high-certainty evidence). In men, vitamin C results in little to no difference in mortality for lung cancer (RR 0.81, 95% CI 0.53 to 1.23; 1 RCT, 7326 participants; high-certainty evidence). Vitamin D + calcium may result in little to no difference in lung cancer incidence in postmenopausal women (RR 0.90, 95% CI 0.39 to 2.08; 3 RCTs, 37601 women; low-certainty evidence). Vitamin E results in little to no difference in lung cancer incidence (RR 1.01, 95% CI 0.90 to 1.14; 3 RCTs, 36841 participants; high-certainty evidence) or to lung cancer mortality (RR 0.96, 95% CI 0.77 to 1.18; 2 RCTs, 29214 participants; high-certainty evidence), but increases the risk of haemorrhagic strokes (hazard ratio (HR), 1.74, 95% CI 1.04 to 2.91; 1 RCT, 14641 participants; high-certainty evidence). Calcium results in little to no difference in lung cancer incidence in postmenopausal women (RR 0.65, 95% CI 0.13 to 3.18; 1 RCT, 733 participants) or in risk of renal calculi (RR 1.94, 95% CI 0.20 to 18.57; 1 RCT, 733 participants; low-certainty evidence). Selenium in men results in little to no difference in lung cancer incidence (RR 1.11, 95% CI 0.80 to 1.54; 1 RCT, 17448 participants; high-certainty evidence) and lung cancer mortality (RR 1.09, 95% CI 0.72 to 1.66; 1 RCT, 17448 participants; high-certainty evidence) and increases the risk for grade 1 to 2 dermatitis (RR 1.16, 95% CI 1.04 to 1.31; 1 RCT, 17448 participants; high-certainty evidence) and for alopecia (RR 1.28, 95% CI 1.07 to 1.53; 1 RCT, 17448 participants; high-certainty evidence). The combination of vitamins A, C, E + selenium + zinc results in little to no difference in lung cancer incidence (RR 0.64, 95% CI 0.28 to 1.48; 1 RCT, 12741 participants; high-certainty evidence). Well-designed RCTs have shown no beneficial effect of supplements for the prevention of lung cancer and lung cancer mortality in healthy people. Vitamin A supplements increase lung cancer incidence and mortality in smokers or persons exposed to asbestos. Vitamin C increases lung cancer incidence in women. Vitamin E increases the risk of haemorrhagic strokes.

LDCT LUNG SCREENING SAVES LIVES BUT AT A LOW YIELD: ANALYSIS OF LDCT LUNG SCREENING POPULATION AT SEYH 2015-2018

SESSION TITLE: Tuesday Abstract Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM PURPOSE: To better understand the benefits and disadvantages of LDCT lung screening by analyzing patients who underwent LDCT lung screening at St Elizabeth hospital (SEH) from 2015 to 2018. METHODS: A retrospective study based on questionnaires and screening results that were collected from participants. RESULTS: There were a total of 1,340 person-year participants. There was high all abnormality detection rate (85%). The top three abnormalities were non-calcified nodule or mass > 4 mm (17%), other potentially significant abnormalities above diaphragm (15%) and cardiovascular abnormalities (15%). Based on the quality assurance tool Lung-RADS score, majority of the nodules (78%, 1046/1340) were assigned score of 1 to 3 (negative or benign findings). Among nodules suspicious for malignancy requesting additional diagnostic testing, 5.37% (Lung-RAD 4A, 72 patients) and 1.27% (4B, 17 patients). Among those patients with RADS 4A or 4B, 19 were diagnosed with lung cancer (3 small cell, 4 squamous cell, 12 adenocarcinoma). Based on AJCC tumor staging, lung screening detected mostly stage I (58%) while cancer registry detected mostly stage 4 (44%) cancer. Race, gender, symptoms and risk factor exposure were compared between lung cancer patients and the screening population. There were no significant differences between the two populations. Interestingly, about 60% in both groups reported exposure to second hand smoke, significantly higher than national nonsmoker second hand exposure rate of 25%. The distribution of PPY showed a bimodal distribution in both screening and lung cancer populations. About 68% (13 out of 19) of lung cancer patients had 100 PPY smoking history. However, smoking cessation was not favored by the screening population with only 6.7% (56 out of 830) of current smokers enrolled in a smoking cessation program. It was also striking that 47% (366 out of 774) of current smokers who were not enrolled in a smoking cessation program did not want further information on smoking cessation. CONCLUSIONS: LDCT lung screening detects lung cancer in early stages. However, based on current screening criteria, lung cancer detection rate was very low. A risk stratification model for selecting lung cancer screening candidates is needed. In addition, to reduce lung cancer incidence, smoking cessation remains the most effective method. Better strategies and more aggressive efforts are needed to promote smoking cessation especially in the high-risk groups. CLINICAL IMPLICATIONS: A risk stratification model for selecting lung cancer screening candidates is needed.Better strategies and more aggressive efforts are needed to promote smoking cessation especially in the high-risk groups. DISCLOSURES: No relevant relationships by Timothy Barreiro, source=Web Response No relevant relationships by David Gemmel, source=Web Response No relevant relationships by Yan Jiang, source=Web Response

The CANOPY program: Canakinumab in patients (pts) with non-small cell lung cancer (NSCLC).

TPS9124 Background: Inflammatory pathways can be pro-tumorigenic or anti-tumorigenic. The cytokine interleukin-1β (IL-1β) can promote the infiltration of immunosuppressive cells into the tumor microenvironment leading to a pro-tumorigenic microenvironment that promotes carcinogenesis, tumor invasiveness, and immunosuppression. Canakinumab is a human monoclonal antibody that binds and neutralizes IL-1β. Previous clinical data (CANTOS study) has shown that canakinumab could significantly reduce lung cancer incidence and mortality. This data along with the preclinical results that IL-1β does support tumorigenic inflammation provide the rationale to investigate the therapeutic role of canakinumab in lung cancer. Methods: Three Phase 3 trials have been designed in parallel to evaluate canakinumab in NSCLC (Table). Clinical trial information: NCT03447769, NCT03631199, NCT03626545. [Table: see text]

Epidemiology of lung cancer in China.

The incidence and mortality rates of lung cancer, the leading cause of cancer death in China, have significantly increased in recent years, and present geographic and gender differences as a result of diversity in lifestyles and socioeconomic development. A series of attribute risk analyses have shown that factors such as smoking, air pollution, and occupational factors are all related to lung cancer. Behavioral intervention, such as smoking cessation and screening, could effectively reduce lung cancer incidence and mortality.

Smoke-free laws for reducing lung cancer incidence in Kentucky: warrants further implementation and investigation

According to the latest update of cancer statistics in the United States, lung cancer has been the leading cause of cancer death for more than 25 years (1). Its incidence in both males and females is the second highest among all cancer types, with a total of 234,030 estimated new cases in 2018. The 5-year survival rate is low (only 18%), almost the worst of all cancers. Much attention should be paid to the fact that Kentucky is still the state with both the highest lung cancer incidence and the highest mortality during the past 10 years (1,2).

Regional Socio-Demographic Determinants of Lung Cancer Incidence in the United States

SESSION TITLE: Quality Improvement 2 SESSION TYPE: Original Investigation Poster PRESENTED ON: Wednesday, November 1, 2017 at 01:30 PM - 02:30 PM PURPOSE: Lung cancer is the leading cause of cancer death in the United States (U.S). Several studies done at the individual level, have assessed the correlation between lung cancer incidence and some socio-demographic factors; but little has been done at the population level and has included body max index (BMI), smoking rate, median income, insurance coverage rate. We wanted to investigate the correlation between the following reported socio-demographic factors (BMI, smoking rate, median income, insurance coverage rate) and lung cancer incidence at the population level. Because cancer incidence can vary by socio-demographic characteristics, we planned to use regional variations in these socio-demographic factors to examine correlation patterns with U.S lung cancer incidence geographical variations between 1999-2012. METHODS: From 1999 to 2012, data for median income and for insurance coverage rate per state were obtained from the United States census bureau (Current Population Survey), data for body mass index per state were obtained from the Robert Wood Johnson Foundation, data for smoking rate per state were obtained from the Institute for Health Metrics and Evaluation, data for lung cancer incidence were obtained from the Centers for Disease Control and Prevention (United States Cancer Statistics) to construct the dataset. All 50 states were grouped into 7 regional subdivisions (West, Southern Rockies, Northern Rockies, South Central, North Central, Southeast and Northeast). A regression analysis was performed using IBM SPSS for data analysis. RESULTS: Our study revealed that yearly lung cancer incidence decreased in most regions with the exception of states in the Southern Rockies and the Northeast (Unstandardized Correlation Coefficient (UCC) 3.78 and 1.39 respectively). Additionally, lung cancer incidence increased as BMI increased in most regions with the exception of states in the Southern Rockies (UCC 2.05). Generally, lung cancer incidence decreased as income increased with the exception of the Southern Rockies (UCC 0.002), and lung cancer incidence increased as smoking rates increased in most of the regions (UCC varying from 1.37 to 6.57). Likewise, lung cancer incidence increased as the percentage of insured increased in some of the regions (UCC from 0.69 to 2.00). CONCLUSIONS: Regional differences exist in the correlation coefficient between lung cancer incidence and the selected socio-demographic factors, suggestive of their various level of influence in lung cancer incidence. CLINICAL IMPLICATIONS: Our results suggest that the most efficient way to decrease lung cancer incidence will be to concomitantly decrease smoking rate, decrease average BMI, increase median income and insurance coverage. As healthcare professionals, we tend to focus on the individual level as we care for our patient. Our study shows that we need to be looking at the population level as well and advocate for policies that address some socio-demographic determinants by working in a more concerted effort wih governmental, state and local public health entities to inact strategies to reduce lung cancer incidence even further. DISCLOSURE: The following authors have nothing to disclose: Hermann Simo, Zaid Ammari, Abhinav Tiwari, Sheza Darr, William Barnett, Mohammad Khan, Arjan Flora No Product/Research Disclosure Information

Calcium plus vitamin D supplementation and lung cancer incidence among postmenopausal women in the Women’s Health Initiative

BackgroundMagnesium and calcium are antagonistic in many physiologic processes. However, few studies have investigated the associations of supplemental calcium with lung cancer risk taking this antagonism into account. We evaluated the effect of calcium and vitamin D supplementation on lung cancer incidence and explored whether the ratio of baseline calcium to magnesium (Ca:Mg) intake modifies the association in the Women’s Health Initiative (WHI) calcium plus vitamin D supplementation (CaD) trial. MethodsThe intervention phase of the WHI CaD was a double-blinded, randomized, placebo-controlled trial in 36,382 postmenopausal women aged 50–79 years, recruited at 40U.S. centers. Post-intervention follow-up continued among 29,862 (86%) of the surviving participants. Risk of lung cancer in association with CaD supplementation was evaluated using proportional hazard regression models. ResultsAfter 11 years’ cumulative follow-up, there were 207 lung cancers (incidence 0.11% per year) in the supplement arm and 241 (0.12%) in the placebo arm (hazard ratio (HR) for the intervention, 0.91; 95% confidence interval (CI), 0.71–1.17). Subgroup analyses suggested that the HR for lung cancer varied by baseline Ca:Mg intake ratio among women who were current smokers at enrollment (p=0.04 for interaction). ConclusionsOver the entire follow-up period, calcium and vitamin D supplementation did not reduce lung cancer incidence among postmenopausal women. In exploratory analyses, an interaction was found for the baseline Ca:Mg intake ratio on lung cancer among current smokers at the trial entry. This findings need to be further studied for the role of calcium with magnesium in lung carcinogenesis in current smokers.

Multiregion whole exome seuquencing of pre- and early neoplastic lung lesions.

e20042 Background: The widespread use of CT for lung cancer screening and other reasons has resulted in a dramatic increase in the number of indeterminate ground glass opacities (GGOs). While many of GGOs can be resected with minimal morbidity, the cost has been called into question. Furthermore, multifocality is a relatively common, which makes decisions on extent of surgical resection and potential benefit less clear. Chemoprevention is a theoretically appealing approach to reduce lung cancer incidence and mortality. However, randomized trials have been disappointing to date. This may be due to the constellation of many factors including lack of reliable biomarkers to identify high-risk patients, lack of appropriate molecular targets and appropriate drugs because of our rudimentary knowledge on early carcinogenesis of lung cancers. It has been postulated that atypical adenomatous hyperplasia (AAH) represents preneoplastic lesion that can progress to adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and further to frankly invasive adenocarcinoma (ADC). However, the biology of these lesions is poorly understood and the definition and management of these lesions remain controversial. Methods: Study on early carcinogenesis is hampered by the small size of lesions and challenge of obtaining longitudinal samples at different stages of disease progression. Multiregion sequencing can depict genomic events relative to molecular time with early events ubiquitously present in all regions and late mutations confined to spatially separated regions of lesions. Using this approach, our recent work has reported that 20/21 canonical cancer gene mutations were early genetic events. Results: With intent to delineate the pivotal molecular events driving early carcinogenesis of lung cancer, we have collected 154 resected GGOs with including AAH (N = 40), AIS (N = 39), MIA (N = 55) and ADC (N = 20) based on the IASLC/ATS/ERS classification from 89 patients including 38 patients presenting with multifocal GGOs and 18 patients carry more than one type of pathology. Two to five spatially separated regions from each of the 154 lesions are subjected to whole exome sequencing. Conclusions: The data will be ready to present at the meeting.