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The 60% of patients at highest risk for lung cancer in the National Lung Screening Trial accounted for 88% of the lung-cancer deaths prevented by low-dose CT screening. The use of risk assessment can improve the yield from low-dose CT screening for lung cancer. Lung cancer is the most common cause of cancer-related death in the United States, accounting for 28% and 26% of all cancer deaths among men and women, respectively. 1 Recent results from the National Lung Screening Trial (NLST), which showed a 20% reduction in lung-cancer mortality with low-dose computed tomography (CT) screening, as compared with chest radiography, highlighted the opportunity to reduce the burden of death from lung cancer. 2 With 94 million current and former smokers in the United States, 3 deciding which smokers to target for low-dose CT screening remains an important public health challenge, given the potential costs and harms . . .

The National Lung Screening Trial investigators report that persons undergoing three annual screening examinations with low-dose computed tomography had a 20% reduction in lung-cancer mortality as compared with those screened with annual chest radiography. Lung cancer is an aggressive and heterogeneous disease. 1 , 2 Advances in surgical, radiotherapeutic, and chemotherapeutic approaches have been made, but the long-term survival rate remains low. 3 After the Surgeon General's 1964 report on smoking and health, mortality from lung cancer among men peaked and then fell; among women, the peak occurred later and a slight decline has occurred more recently. 4 Even though the rate of heavy smoking continues to decline in the United States, 5 94 million current or former smokers remain at elevated risk for the disease, 6 and lung cancer remains the leading cause of death from cancer in this . . .

Abstract Background Changes in smoking habits and predictors of smoking cessation were examined in the randomized ITALUNG lung cancer screening trial. Methods In three centers, eligible smokers or ex-smokers (55–69 years, ≥20 pack-years in the last 10 years) were randomized to receive annual invitation for low-dose computed tomography for 4 years or usual care. At invitation, subjects received written information for a free smoking cessation program. Quitting outcome was assessed at year 4. Results Among participants who completed baseline assessments and year 4 screening, higher quitting (20.8% vs. 16.7%, p = .029) and lower relapse (6.41% vs. 7.56%, p = .50) rates were observed in the active screening group as compared to the usual-care control group. Corresponding figures in the intention-to-treat analysis were as follows: 16.04% versus 14.64% (p = .059) and 4.88% versus 6.43% (p = .26). Quitting smoking was significantly associated to male gender, lower pack-years, and having pulmonary nodules at baseline. Center-specific analyses showed a threefold statistically significant higher probability to quit associated with participating in the smoking cessation program. A subsample of smokers of the scan group from one center showed higher quitting rates over 12-month follow-up as compared to matched controls from the general population who underwent the same smoking cessation program. Conclusions Consistently with previous reports, in the ITALUNG trial, screened subjects showed significantly higher quit rates than controls, and higher quit rates were associated with both the presence of pulmonary nodules and participating in a smoking cessation program. Maximal effect on quitting outcome was observed with the participation in the smoking cessation program. Implications Participating in lung cancer screening promotes smoking cessation. An effective “teachable moment” may be achieved when the smoking cessation intervention is structured as integral part of the screening clinical visits and conducted by a dedicated team of health care professionals. Standardized guidelines for smoking cessation interventions in lung cancer screening are needed.

The Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study demonstrated that β-carotene supplementation increases lung cancer incidence in smokers. Further, cigarettes with higher tar and nicotine content are associated with a higher risk of lung cancer. However, no studies have examined whether the increased risk associated with β-carotene supplementation in smokers varies by the tar or nicotine content of cigarettes. The ATBC Study was a randomized, double-blind intervention trial conducted in southwest Finland. A total of 29 133 male smokers, aged 50-69 years, were enrolled and randomly assigned to one of four groups (α-tocopherol, β-carotene, both, or placebo). Cox proportional hazards models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of lung cancer risk by β-carotene trial assignment stratified by a priori categories of cigarette tar and nicotine content. The β-carotene supplementation group had significantly higher risk of developing lung cancer in all categories of tar content (yes vs. no β-carotene supplementation-ultralight cigarettes [≤7 mg tar]: HR = 1.31, 95% CI = 0.91 to 1.89; nonfiltered cigarettes [≥21 mg tar]: HR = 1.22, 95% CI = 0.91 to 1.64; p for interaction = .91). Similarly, there was no interaction with nicotine content (yes vs. no β-carotene supplementation-ventilated cigarettes [≤0.8 µg nicotine]: HR = 1.23, 95% CI = 0.98 to 1.54; nonfiltered cigarettes [≥1.3 µg nicotine]: HR = 1.22, 95% CI = 0.91 to 1.64; p for interaction = .83). These findings support the conclusion that supplementation with β-carotene increases the risk of lung cancer in smokers regardless of the tar or nicotine content of cigarettes smoked. Our data suggest that all smokers should continue to avoid β-carotene supplementation. Previous studies demonstrated that β-carotene supplementation increases risk of lung cancer in smokers. This study moves the field forward by examining the potential for modification of risk of lung cancer with different levels of tar and nicotine in cigarettes smoked, as interaction with carcinogens in these components of cigarette smoke is hypothesized to be the mechanism by which β-carotene increases risk. Our study provides evidence that the increased risk of lung cancer in smokers who take β-carotene supplements is not dependent upon the tar or nicotine level of cigarettes smoked and suggests that all smokers should continue to avoid β-carotene supplementation.

The microbiota is increasingly recognized as a critical player in cancer onset and progression and response to cancer chemotherapy treatment. In recent years, several preclinical and clinical studies have evidenced the involvement of microbiota in lung cancer, one of the world’s deadliest cancers. However, the mechanisms by which the microbiota can impact this type of cancer and patient survival and response to treatments remain poorly investigated. In this review, the peculiarities of the gut and lung microbial ecosystems have been highlighted, and recent findings illustrating the possible mechanisms underlying the microbiota–lung cancer interaction and the host immune response have been discussed. In addition, the mucosal immune system has been identified as a crucial communication frame to ease interactive dynamics between the immune system and the microbiota. Finally, the use of specific next-generation intestinal probiotic strains in counteracting airway diseases has been evaluated. We believe that restoring homeostasis and the balance of bacterial microflora should become part of the routine of integrated cancer interventions, using probiotics, prebiotics, and postbiotics, and promoting a healthy diet and lifestyle.

Human lung adenocarcinoma, the most prevalent form of lung cancer, is characterized by many molecular abnormalities. K-ras mutations are associated with the initiation of lung adenocarcinomas, but K-ras- independent mechanisms may also initiate lung tumors. Here, we find that the runt-related transcription factor Runx3 is essential for normal murine lung development and is a tumor suppressor that prevents lung adenocarcinoma. Runx3 −/− mice, which die soon after birth, exhibit alveolar hyperplasia. Importantly, Runx3 −/− bronchioli exhibit impaired differentiation, as evidenced by the accumulation of epithelial cells containing specific markers for both alveolar (that is SP-B) and bronchiolar (that is CC10) lineages. Runx3 −/− epithelial cells also express Bmi1, which supports self-renewal of stem cells. Lung adenomas spontaneously develop in aging Runx3 +/− mice (∼18 months after birth) and invariably exhibit reduced levels of Runx3. As K-ras mutations are very rare in these adenomas, Runx3 +/− mice provide an animal model for lung tumorigenesis that recapitulates the preneoplastic stage of human lung adenocarcinoma development, which is independent of K-Ras mutation. We conclude that Runx3 is essential for lung epithelial cell differentiation, and that downregulation of Runx3 is causally linked to the preneoplastic stage of lung adenocarcinoma.

PurposeMedicare requires tobacco dependence counseling and shared decision-making (SDM) for lung cancer screening (LCS) reimbursement. We hypothesized that initiating SDM during inpatient tobacco treatment visits would increase LCS among patients with barriers to proactively seeking outpatient preventive care. MethodsWe collected baseline assessments and performed two pilot randomized trials at our safety-net hospital. Pilot 1 tested feasibility, acceptability, and preliminary efficacy of a nurse practitioner initiating SDM for LCS during hospitalization (Inpatient SDM). We collected qualitative data on barriers encountered during Pilot 1. Pilot 2 added a community health worker (CHW) to address barriers to LCS completion (Inpatient SDM + CHW-navigation). For both studies, preliminary efficacy was an intention-to-treat analysis of LCS completion at 3 months between intervention and comparator (furnishing of LCS decision aid only) groups. ResultsBaseline assessments showed that patients preferred in-person LCS discussions versus self-reviewing materials; overall 20% had difficulty understanding written information. In Pilot 1, 4% (2/52) in Inpatient SDM versus 2% (1/48, comparator) completed LCS (p = 0.6), despite 89% (89/100) desiring LCS. Primary care providers noted that competing priorities and patient factors (e.g., social barriers to keeping appointments) prevented the intervention from working as intended. In Pilot 2, 50% (5/10) in Inpatient SDM + CHW-navigation versus 9% (1/11, comparator) completed LCS (p < 0.05). Many patients were ineligible due to recent diagnostic chest CT (Pilot 1: 255/659; Pilot 2: 239/527).ConclusionsInpatient SDM + CHW-navigation shows promise to improve LCS rates among underserved patients who smoke, but feasibility is limited by recent diagnostic chest CT among inpatients. Implementing CHW-navigation in other clinical settings may facilitate LCS for underserved patients.Trail registrationClinicalTrials.gov Identifier: NCT03276806 (8 September 2017); NCT03793894 (4 January 2019).

Background Lung cancer is the leading cause of cancer death for both men and women in the United States. The National Lung Screening Trial (NLST) demonstrated that low-dose computed tomography (LDCT) screening can reduce lung cancer mortality among high-risk individuals, but uptake of lung screening remains low. Social media platforms have the potential to reach a large number of people, including those who are at high risk for lung cancer but who may not be aware of or have access to lung screening. Methods This paper discusses the protocol for a randomized controlled trial (RCT) that leverages FBTA to reach screening-eligible individuals in the community at large and intervene with a public-facing, tailored health communication intervention ( LungTalk ) to increase awareness of, and knowledge about, lung screening. Discussion This study will provide important information to inform the ability to refine implementation processes for national population efforts to scale a public-facing health communication focused intervention using social media to increase screening uptake of appropriate, high-risk individuals. Trial registration The trial is registered at clinicaltrials.gov (#NCT05824273).

The Mediterranean diet (MD) has been inversely associated with lung cancer (LC) risk. Hereby we show the preliminary results of our prospective randomised controlled trial in inflammatory and nutritional status of LC patients after 3-month implementation of MD. In total, 30 patients with small-cell or non-small-cell LC (stages III–IV) were enrolled. They were randomly assigned either to Control group, receiving general nutritional guidelines, or the MD group, in which a personalised MD plan was provided. Medical and dietary history, anthropometrics, blood biomarkers, and circulating antioxidant vitamins were assessed. The main outcome was a significantly higher advanced lung cancer inflammation index (ALI) in patients of the control arm than those following MD (p = 0.003). In the MD group, platelets were significantly reduced at the study endpoint (p = 0.044). BMI and body fat mass remained unchanged in both arms, but serum glucose was significantly higher in control compared to MD group (p = 0.017). In conclusion, we showed for the first time that implementing a personalised MD for 3 months is promising to regulate prognostic biomarkers in advanced LC. The final results of our on-going trial will shed a light on the inflammatory, antioxidant and nutritional status of LC patients following MD.

Lung screening is an opportunity for smoking cessation and relapse prevention, but smoking behaviors may differ across screening results. Changes in smoking were evaluated among 18 840 current and former smokers aged 55-74 scheduled to receive three annual lung screenings. Participants were randomized to low-dose computed tomography or single-view chest radiography in the American College of Radiology/National Lung Screening Trial. Outcome measures included point and sustained (6-month) abstinence and motivation to quit among smokers; and relapse among smokers who quit during follow-up, recent quitters (quit < 6 months), and long-term former smokers (quit ≥ 6 months). During five years of follow-up, annual point prevalence quit rates ranged from 11.6%-13.4%; 48% of current smokers reported a quit attempt and 7% of long-term former smokers relapsed. Any false positive screening result was associated with subsequent increased point (multivariable hazard ratio HR = 1.23, 95% CI = 1.13, 1.35) and sustained (HR = 1.28, 95% CI = 1.15, 1.43) abstinence among smokers. Recent quitters with ≥1 false positive screen were less likely to relapse (HR = 0.72, 95% CI = 0.54, 0.96). Screening result was not associated with relapse among long-term former smokers or among baseline smokers who quit during follow-up. A false positive screen was associated with increased smoking cessation and less relapse among recent quitters. Consistently negative screens were not associated with greater relapse among long-term former smokers. Given the Affordable Care Act requires most health plans to cover smoking cessation and lung screening, the impact and cost-effectiveness of lung screening could be further enhanced with the addition of smoking cessation interventions.