Prevalence Of Lung Cancer Research Articles

Selinexor as a Therapeutic Target: Advances in Non-small Cell and Small Cell Lung Cancer Treatment Strategies.

Selinexor treats lung cancer, particularly non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). This review summarizes the prevalence and types of lung cancer and emphasizes the challenges associated with current treatments like resistance and limited effectiveness. Selinexor is a selective inhibitor of nuclear export (SINE) that has emerged as a potential therapy that targets the nuclear export of tumor suppressor proteins. The mechanisms of selinexor, its potential in combination therapies, and challenges like side effects and drug resistance are explained in this review. Key findings highlight the effectiveness of selinexor in preclinical studies, particularly against KRAS-mutant NSCLC and in combination with chemotherapy for SCLC. The review concludes with a discussion of future directions and underscores the potential of selinexor to improve the treatment strategies for lung cancer.

The burden of lung cancer attributable to ambient PM2.5 exposure: a systematic literature review

Abstract Background Lung cancer is recognized as one of the most common causes of cancer morbidity and mortality worldwide and is the second cause of death with highest years of life lost in highly developed regions. Ambient exposure to particulate matter (PM2.5) is the leading global environmental risk factor. Long-term exposure to PM2.5 is associated with several health outcomes, including lung cancer, ischemic heart disease, and chronic obstructive pulmonary disease. Aim To review and estimate the impact attributable to PM2.5 exposure due to lung cancer. Methods A systematic review and a meta-analysis were conducted to determine whether long-term exposure to PM2.5 increases the risk of lung cancer and to derive exposure-response relationships between PM2.5 and lung cancer. The literature search was performed in databases (i.e., Pubmed/Scopus) and studies published from January 1, 2010 onwards were considered. Studies describing the association between long-term exposure to the pollutant under research and the incidence, prevalence, and mortality of lung cancer, considering a relative measure of association were included, with no restriction in geographical area. Results In the literature review, 2215 articles were considered for the first step of data synthesis, all articles were screened, considering the screening of titles (first step), abstracts (second step) and full-text (third step) considering the inclusion criteria. In a second step the data was extracted from the included articles (n = 129) and considering the variables related to the characteristics of the study and the study population, exposure, and outcome measurement, and details of risk of bias assessment. Conclusions These findings provide data to synthesize effect size estimates using a Meta-Regression - Bayesian, Ensemble, Regularized, Trimmed (MR-BRT) model, important to provide evidence data on the impact of air pollution on human health, which is crucial for decision-making. Key messages • Long-term exposure to PM2.5 increases lung cancer risk so the estimating of the impact of the exposure is an urgent need to provide evidence-based data for air quality improvement. • Meta-analysis aims to establish a relation between PM2.5 exposure and the burden of lung cancer.

Association of chronic obstructive pulmonary disease with risk of lung cancer in individuals aged 40 years and older: A cross-sectional study based on NHANES 2013-2018.

It remains unclear whether chronic obstructive pulmonary disease (COPD) is an independent risk factor for lung cancer after excluding confounding factors such as smoking, age, sex, body mass index (BMI), comorbidities, etc. Data from 11,440 participants (≥ 40 years old) in the National Health and Nutrition Examination Survey (NHANES) 2013-2018 were analyzed. Weighted multivariable logistic regression models were used to assess the association between COPD and lung cancer risk. Subgroup analyses were based on age, sex, BMI, and smoking. This study included 660 patients with COPD and 10,780 participants without COPD. The prevalence of lung cancer was significantly higher in patients with COPD compared to participants without COPD (3.39% vs 0.14%). After adjusting for confounding factors, COPD was associated with a significantly increased risk of lung cancer (OR, 12.24, 95% CI, 4.99-30.06, p < 0.001). This association remained significant in all subgroups, particularly in individuals aged > 65 years (OR, 20.05, 95% CI, 6.85-58.72, p < 0.001), smokers (OR, 19.38, 95% CI, 2.02-185.66, p = 0.010), males (OR, 17.39, 95% CI, 5.28-57.31, p < 0.001), individuals who quit smoking within 10 years (OR, 12.86, 95% CI, 2.59, 63.99, p = 0.002), and individuals with a BMI > 25 kg/m2 (OR, 14.56, 95% CI, 3.88-54.69, p < 0.001). COPD is an independent risk factor for lung cancer, especially in certain subgroups. The combination of COPD and smoking greatly amplifies the lung cancer risk. These findings highlight the importance of early lung cancer screening in patients with COPD.

Interstitial lung abnormality in COPD is inversely associated with the comorbidity of lung cancer

BackgroundInterstitial lung abnormality (ILA) has been recognized as a pertinent factor in the development and prognosis of various pulmonary conditions. However, its correlation with co-morbidities remains understudied. The current study endeavors to elucidate the association between ILA and both clinical features and co-morbidities in patients with chronic obstructive pulmonary disease (COPD).MethodsA retrospective cohort comprising 1131 hospitalized patients diagnosed with COPD was examined in this observational study. Patients were dichotomously classified based on the presence or absence of ILA, and subsequent analyses scrutinized disparities in demographic, clinical, and laboratory profiles, alongside co-morbid conditions, between the two subgroups.ResultsOf the 1131 COPD patients, 165 (14.6%) exhibited ILA. No statistically significant differences were discerned between COPD patients with and without ILA concerning demographic, clinical, or laboratory parameters, except for levels of circulating fibrinogen and procalcitonin. Nevertheless, a notable discrepancy emerged in the prevalence of multiple co-morbidities. Relative to COPD patients devoid of ILA, those presenting with ILA manifested a diminished prevalence of lung cancer (OR = 0.50, 95% CI: 0.30–0.83, p = 0.006), particularly of the lung adenocarcinoma (OR = 0.32, 95% CI: 0.15–0.71, p = 0.005). Additionally, the presence of ILA in COPD was positively associated with heart failure (OR = 1.75, 95% CI: 1.04-3.00, p = 0.040) and cancers other than lung cancer (OR = 2.27, 95% CI: 1.16–4.39, p = 0.012).ConclusionThese findings demonstrate that the presence of ILA is associated with co-morbidities of COPD, particularly lung cancer.

SPP1 induces idiopathic pulmonary fibrosis and NSCLC progression via the PI3K/Akt/mTOR pathway

BackgroundThe prevalence of non-small cell lung cancer (NSCLC) is notably elevated in individuals diagnosed with idiopathic pulmonary fibrosis (IPF). Secreted phosphoprotein 1 (SPP1), known for its involvement in diverse physiological processes, including oncogenesis and organ fibrosis, has an ambiguous role at the intersection of IPF and NSCLC. Our study sought to elucidate the function of SPP1 within the pathogenesis of IPF and its subsequent impact on NSCLC progression.MethodsFour GEO datasets was analyzed for common differential genes and TCGA database was used to analyze the prognosis. The immune infiltration was analyzed by TIMER database. SPP1 expression was examined in human lung tissues, the IPF fibroblasts and the BLM-induced mouse lung fibrosis model. Combined with SPP1 gene gain- and loss-of-function, qRT-PCR, Western blot, EdU and CCK-8 experiments were performed to evaluate the effects and mechanisms of SPP1 in IPF progression. Effect of SPP1 on NSCLC was detected by co-cultured IPF fibroblasts and NSCLC cells.ResultsThrough bioinformatics analysis, we observed a significant overexpression of SPP1 in both IPF and NSCLC patient datasets, correlating with enhanced immune infiltration of cancer-associated fibroblasts in NSCLC. Elevated levels of SPP1 were detected in lung tissue samples from IPF patients and bleomycin-induced mouse models, with partial colocalization observed with α-smooth muscle actin. Knockdown of SPP1 inhibits TGF-β1-induced differentiation of fibroblasts to myofibroblasts and the proliferation of IPF fibroblasts. Conversely, SPP1 overexpression promoted IPF fibroblast proliferation via PI3K/Akt/mTOR pathway. Furthermore, IPF fibroblasts promoted NSCLC cell proliferation and activated the PI3K/Akt/mTOR pathway; these effects were attenuated by SPP1 knockdown in IPF fibroblasts.ConclusionsOur findings suggest that SPP1 functions as a molecule promoting both fibrosis and tumorigenesis, positioning it as a prospective therapeutic target for managing the co-occurrence of IPF and NSCLC.

Evaluation of lung cancer probability models and guideline-recommendations in high prevalence of cancer settings

BackgroundGuideline-recommended management of patients with pulmonary nodules includes assessing the pretest probability of cancer. The performance of four models (the Mayo, Brock, VA, and PKU models) has been validated in several populations, but not in a high-prevalence setting. Research QuestionTo evaluate the performance of lung cancer probability models within the context of a population with a high prevalence of lung cancer at a tertiary care center. Study Design and MethodsClinical and radiologic data were retrospectively reviewed for 1518 patients with 6-30 mm nodules referred to a pulmonologist or thoracic surgeon at [REDACTED INSTITUION] and [REDACTED INSTITUTION] from 2002 to 2021 for evaluation and treatment of pulmonary nodules. Probability of cancer for each patient was calculated according to four validated models. Model performance was assessed based on ROC, calibration, sensitivity, and specificity. ResultsOf the total cohort (n=1518), 1098 (72.3%) patients had a malignant nodule. The Mayo model discriminated between patients with benign and malignant nodules with the highest AUC (0.74). The Brock and VA models performed similarly in cohort discrimination (0.71 and 0.70, respectively), but the VA model was better calibrated (Brier score = 0.24). The PKU model discriminated between patients’ benign and malignant nodules with the lowest AUC (0.66) but the best calibration (Brier score = 0.19). InterpretationThe classification accuracy of the models did not differ greatly, but the calibration, and resulting sensitivity and specificity at guideline-recommended thresholds, was greatly dependent upon the prevalence of cancer in the population in which the model was trained. The prevalence of cancer in the clinical setting should be considered when use of a clinical prediction models for IPN management.

Incidence, prevalence, and survival of lung cancer in the United Kingdom from 2000-2021: a population-based cohort study.

Lung cancer is the leading cause of cancer-associated mortality worldwide. In the United Kingdom (UK), there has been a major reduction in smoking, the leading risk factor for lung cancer. Therefore, an up-to-date assessment of the trends of lung cancer is required in the UK. This study aims to describe lung cancer burden and trends in terms of incidence, prevalence, and survival from 2000-2021, using two UK primary care databases. We performed a population-based cohort study using the UK primary care Clinical Practice Research Datalink (CPRD) GOLD database, compared with CPRD Aurum. Participants aged 18+ years, with 1-year of prior data availability, were included. We estimated lung cancer incidence rates (IRs), period prevalence (PP), and survival at 1, 5 and 10 years after diagnosis using the Kaplan-Meier (KM) method. Overall, 11,388,117 participants, with 45,563 lung cancer cases were studied. The IR of lung cancer was 52.0 [95% confidence interval (CI): 51.5 to 52.5] per 100,000 person-years, with incidence increasing from 2000 to 2021. Females aged over 50 years of age showed increases in incidence over the study period, ranging from increases of 8 to 123 per 100,000 person-years, with the greatest increase in females aged 80-89 years. Alternatively, for males, only cohorts aged over 80 years showed increases in incidence over the study period. The highest IR was observed in people aged 80-89 years. PP in 2021 was 0.18%, with the largest rise seen in participants aged over 60 years. Median survival post-diagnosis increased from 6.6 months in those diagnosed between 2000-2004 to 10.0 months between 2015-2019. Both short and long-term survival was higher in younger cohorts, with 82.7% 1-year survival in those aged 18-29 years, versus 24.2% in the age 90+ years cohort. Throughout the study period, survival was longer in females, with a larger increase in survival over time than in males. The incidence and prevalence of lung cancer diagnoses in the UK have increased, especially in female and older populations, with a small increase in median survival. This study will enable future comparisons of overall disease burden, so the overall impact may be seen.

The impact of coffee consumption on human health

Coffee consumption is a key aspect of modern lifestyle. Caffeine, the major component of coffee, has an impact on various human tissues and organs after being absorbed in the gastrointestinal tract. Its beneficial effects on reducing both the incidence of many diseases, including cancer, and overall mortality has been described. According to most cohort studies, coffee has a positive impact on cardiovascular diseases as it lowers the risk of cardiovascular diseases and does not increase blood pressure. Meta-analyses suggest a protective effect of caffeine contained in coffee on neurological disorders such as migraines, dementia, and slowing the progression of Alzheimer’s disease and Parkinson’s disease. However, research on malignant tumour development in humans is inconsistent. On the one hand, caffeine contained in coffee has been shown to significantly reduce the risk of breast cancer, endometrial cancer and prostate cancer. On the other hand, most meta-analyses have shown an association between coffee intake and an increased prevalence of lung cancer. In some cases, it can even lead to significant rise in morbidity. The positive impact of chlorogenic acid (a polyphenol in coffee) administered with doxorubicin has been described in in vitro and in vivo lung cancer studies.

Liposomal encapsulated curcumin attenuates lung cancer proliferation, migration, and induces apoptosis

Lung cancer is one of the most diagnosed types of cancer worldwide, accounting to one fifth of cancer-related deaths. The high prevalence of lung cancer (LC) is due to various factors such as environmental pollution or lifestyle factors such as cigarette smoking. Non-small cell lung cancer (NSCLC) is the most diagnosed type of lung cancer. Despite the availability of several lines of treatment for NSCLC, including surgery, chemotherapy, radiotherapy, immunotherapy, and combinations of these, this disease still has very low survival rate, highlighting the urgent need to develop novel therapeutics. Phytoceuticals, or plant-derived bioactives are a promising source of biologically active compounds. Among these, curcumin is particularly relevant due to its wide range of anticancer, antioxidant, and anti-inflammatory activity. However, its poor solubility causes low bioavailability, severely limiting its clinical application. Encapsulation of curcumin in nanoparticle-based delivery systems such as liposomes holds promise to overcome this limitation. In the present study, we demonstrate promising in vitro anticancer affect or curcumin-loaded liposomes (PlexoZome®) on A549 human lung adenocarcinoma cells. The study reveals how liposomal curcumin functionally supresses the proliferation, migration, and colony formation of these cells whilst also drastically reducing the expression of multiple cancer marker proteins. This work provides foundational data for the development of a curcumin-based nano formulation to be used as therapy for NSCLC.

Linkage error and ethnicity information source affect estimates of ethnic disparities in non-communicable disease rates

Objective and ApproachThis study examined the impact of two sources of bias on differences in ethnic disparities in non-communicable disease rates in New Zealand (NZ). Data were sourced from Stats NZ’s Integrated Data Infrastructure (IDI), a collection of deidentified whole-population administrative (eg, health, justice, housing) and survey datasets (eg, NZ Census) linked at the individual level using probabilistic linkage procedures. Linking several datasets reduces the size of the population available for study because not all individuals can be linked. In addition, there are several sources of ethnicity information that may disagree with each other. We will illustrate the impact of population loss due to linkage and ethnicity data source on Māori-European gaps in lung cancer and cardiovascular disease. ResultsOur results showed that the choice of ethnicity information source and the population used had an impact on the size of ethnic disparities in lung cancer and cardiovascular disease. For lung cancer the age standardised rate ratio for Māori:European ranged from 2.88 to 3.21, and for CVD 1.70 to 1.87. Population loss and ethnicity data source each had independent effects on the size of ethnic differences. ConclusionsDifferent combinations of population and ethnicity information source produced different estimates of ethnic gaps in lung cancer and CVD prevalence. Population and source of ethnicity data both had independent effects on the size of ethnic differences. ImplicationsComparisons of ethnic differences in disease prevalence between studies, or over time, may be misleading if they do not use the same population and ethnicity data source.

Diseases, drugs and dust

From 1 January to 20 June 2024, there were 186,900 reported flu cases resulting in 14 deaths in various regions of Thailand and on 21 August 2024 Thailand confirmed the first case of a new lethal variant of mpox. Thailand's Ministry of Public Health has announced plans to reclassify cannabis and hemp as illegal narcotics starting 1 January 2025. Vaping bans were emphasized on 31 May, the World No Tobacco Day. The organized Lung Cancer Screening program was started in the Northern Thailand where the prevalence of lung cancer and the level of PM 2.5 were high.

Gender-specific outcomes of low-dose computed tomography screening for lung cancer detection: A retrospective study in Chinese never-smoker population.

Low-dose computed tomography (LDCT) has emerged as a pivotal tool for detecting lung cancer among ever-smokers. This study aims to evaluate the gender-specific outcomes of LDCT screening within the Chinese never-smoking population. We conducted a single-center, retrospective cohort study, which analyzed LDCT screening outcomes for 42,018 asymptomatic participants. Specifically, we focused on assessing gender-specific differences in the prevalence of pulmonary nodules, and the incidence of lung cancer diagnosis among never-smokers. Among the 42,018 eligible participants, 41.50% were females and 58.50% were males. Most participants were non-smokers (77.57%), with a significantly higher proportion of non-smokers among females than males (99.33% vs. 62.14%). Pulmonary nodules were identified in 2.66% of participants, with a higher prevalence in females (2.99%) than males (2.43%) (p < 0.001). Non-smoking females had a higher incidence of positive nodules than non-smoking males (2.98% vs. 2.38%, p < 0.001). Invasive biopsies were performed in 334 individuals with nodules, confirming lung cancer in 258 cases. The majority of these cancer cases were non-smokers (212), with non-smoking females showing a higher incidence (0.85%) compared to males (0.43%) (p < 0.001). There was no significant difference in the false-positive rates between non-smoking females (0.14%) and males (0.13%). Multivariate analysis showed that never-smoking women were more likely to undergo biopsies (OR 1.65, p = 0.0016) and had a higher, though not statistically significant, probability of lung cancer diagnosis (OR 1.84, p = 0.06). This study elucidates sex-based differences within the Chinese population, revealing a higher prevalence of pulmonary nodules and lung cancers among non-smoking females. These findings offer valuable reference for both clinical practice and future research initiatives.

Trends in lung cancer incidence in Iraq during the period 2005-2019

Lung cancer, a prominent global malignancy and a significant contributor to cancer-related deaths, was examined in Iraq from 2005 to 2019 using data from the cancer registry. Age-standardized incidence rates (ASIR), categorized by sex and age at diagnosis, were analyzed to identify trends, utilizing annual percent change (APC) and average annual percent change (AAPC). During the 2005-2019 period, ASIR was 18.339/100,000 for males and 5.861/100,000 for females. Lung cancer ASIR experienced a notable 48.027% increase, starting at 9.426/100,000 in 2005 and reaching 13.953/100,000 in the most recent year. The rates demonstrated significant growth, with AAPC values of +2.857% for both sexes, +2.495% for males, and +4.474% for females. The highest incidences of lung cancer were among the elderly (70+ years) in both sexes, particularly pronounced in females (8.961%) and males (5.601%). In contrast, the lowest rates were found in individuals aged 0 to 49 years, showing negative APC values: -1.359% (males) and -0.843% (females). The study underscores the escalating prevalence of lung cancer in Iraq, particularly impacting older females. Urgent and targeted efforts are necessary to mitigate the rising incidence rates.

Emerging Epidemic: Non-Smoker Lung Cancer in India\'s Urban Centres

Abstract: Recent research has revealed a concerning trend in the incidence of lung cancer among non-smokers in India, particularly within urban centers. Contrary to the traditional association of lung cancer with smoking, a significant proportion of cases in India are now emerging in individuals with no history of tobacco use. This phenomenon is primarily attributed to severe air pollution, which has become a critical public health issue in many Indian cities. Rapid industrialization and urbanization have led to increased exposure to airborne pollutants, including fine particulate matter (PM2.5), nitrogen dioxide (NO2), and other carcinogens, which are now recognized as significant risk factors for lung cancer. Genetic predispositions further exacerbate this risk, with studies indicating that certain populations are more susceptible to developing lung cancer due to genetic mutations influenced by environmental exposures. These mutations and biomarkers, such as EGFR and ALK gene rearrangements, have been increasingly identified in Indian non-smoker lung cancer patients, providing critical insights into the disease's etiology and potential targeted therapies. India currently ranks fourth globally in lung cancer prevalence, with urban areas experiencing the highest growth rates. Projections suggest that the incidence of lung cancer will continue to rise, potentially reaching alarming levels by 2025. This emerging epidemic highlights the urgent need for comprehensive public health strategies to address air pollution and its associated health risks. Efforts must be directed towards reducing pollution levels through stringent regulatory measures, promoting cleaner technologies, and enhancing public awareness about the health impacts of air pollution. Additionally, implementing widespread screening programs and advancing research on genetic and environmental interactions can aid in early detection and personalized treatment approaches for affected individuals. In conclusion, the rising incidence of lung cancer among non-smokers in urban India signifies a shifting landscape in the disease's epidemiology. Addressing this public health challenge requires an integrated approach that combines environmental, genetic, and healthcare interventions to mitigate the growing burden of lung cancer in non-smoking populations.

Assessing the diagnostic utility of serum tumor markers for lung cancer detection in patients with interstitial pneumonia.

The prevalence of lung cancer among individuals afflicted with interstitial pneumonia (IP) stands at approximately 20%. The early detection of lung cancer via chest computed tomography (CT) surveillance proves challenging in IP patients. Our investigation sought to identify a potential biomarker capable of providing early indications of the presence of lung tumors in such patients. We examined the attributes of serum tumor markers, imaging characteristics, and histological findings in individuals diagnosed with IP, both with and without concurrent lung cancer. 106 patients diagnosed with IP were included in the study, comprising 36 individuals with concurrent lung cancer and 70 patients solely diagnosed with IP. Serum concentrations of CEA and CA12-5 were notably elevated in IP patients with lung cancer, compared to those with IP alone. Logistic regression analyses revealed that, in comparison to IP patients within the first quartile of CEA levels, the relative risk of developing lung cancer associated with IP escalated by 4.0-fold, 3.1-fold, 11.0-fold, and 13.3-fold in the second, third, fourth, and fifth quartiles, respectively. Upon controlling for gender and age, statistical significance in risk was observed solely for the fourth and fifth quartiles. Receiver operating characteristic (ROC) curve analysis conducted in patients diagnosed with ILD-CA identified a CEA cutoff point of 6.9ng/mL, demonstrating sensitivities of 61.1% and specificities of 78.5%. The area under the curve was calculated as 0.7(95% CI: 0.63-0.81). The serum levels of CEA were notably elevated in IP patients with concurrent lung cancer in contrast to those who were just suffering from IP. The heightened serum CEA levels correlate with an escalated risk of cancer occurrence among IP patients, suggesting that serum CEA levels could potentially serve as an indicative marker for the presence of cancer in IP patients.

Reprint of: Smoking and pulmonary health in women: A narrative review and behavioral health perspective

ObjectiveCigarette smoking prevalence has declined slower among women than men, and smoking-related pulmonary disease (PD) has risen among women. Given these trends, there is a critical need to understand and mitigate PD risk among women who smoke. The purpose of this narrative review and commentary is to highlight important evidence from the literature on smoking and PD among women. MethodsThis review focuses broadly on examining cigarette smoking and PD among women within six topic areas: (1) demographic characteristics and prevalence of smoking, (2) smoking behavior, (3) lung cancer, (4) obstructive PD, (5) diagnostic and treatment disparities, and (6) gaps in the literature and potential directions for future research and treatment. ResultsGrowing evidence indicates that compared to men, women are at increased risk for developing smoking-related PD and poorer PD outcomes. Gender disparities in smoking-related PD may be largely accounted for by genetic differences and sex hormones contributing to PD pathogenesis and presentation, smoking behavior, nicotine dependence, and pathogen/carcinogen clearance. Moreover, gender disparities in smoking-related PD may be exacerbated by important social determinants (e.g., women with less formal education and those from minoritized groups may be at especially high risk for poor PD outcomes due to higher rates of smoking). ConclusionRising rates of smoking-related PD among women risk widening diagnostic and treatment disparities. Ongoing research is needed to explore potentially complex relationships between sex, gender, and smoking-related PD processes and outcomes, and to improve smoking-cessation and PD treatment for women.

Screening and identification of miRNAs negatively regulating FAM83A/Wnt/β-catenin signaling pathway in non-small cell lung cancer

The prevalence of non-small cell lung cancer (NSCLC) accounts for 85% of all lung cancers, with the Wnt/β-catenin signaling pathway exhibiting robust activation in this particular subtype. The expression of FAM83A (family with sequence similarity 83, member A) has been found to be significantly upregulated in lung cancer, leading to the stabilization of β-catenin and activation of the Wnt signaling pathway. In this study, we conducted a screening of down-regulated miRNAs in lung cancer with FAM83A as the target. Ultimately, we identified miR-1 as a negative regulator of FAM83A and confirmed that FAM83A is a direct target gene of miR-1 through dual luciferase reporter assays. The overexpression of miR-1 significantly attenuated the expression level of FAM83A and suppressed the Wnt signaling pathway, leading to a reduction in the expression levels of downstream target genes AXIN2, CyclinD1, and C-MYC. Additionally, it decreased the nuclear translocation of β-catenin. In addition, overexpression of miR-1 accelerated the degradation of β-catenin by inhibiting FAM83A, promoted the assembly of β-catenin degradation complex, and inhibited the proliferation, migration and invasion of NSCLC cells. In summary, miR-1 may be a potential candidate miRNA for the treatment of NSCLC.

PP01.102 Lung Cancer Screening at an Appalachian VA Medical Center found over 2x the Prevalence of Lung Cancers compared to the National Lung Screening Trial

PP01.102 Lung Cancer Screening at an Appalachian VA Medical Center found over 2x the Prevalence of Lung Cancers compared to the National Lung Screening Trial

The Relationship between Lung Cancer Prevalence and Air Quality and Other Factors

The Relationship between Lung Cancer Prevalence and Air Quality and Other Factors

Impact of annual trend volume of low-dose computed tomography for lung cancer screening on overdiagnosis, overmanagement, and gender disparities

BackgroundWith the increasing prevalence of nonsmoking-related lung cancer in Asia, Asian countries have increasingly adopted low-dose computed tomography (LDCT) for lung cancer screening, particularly in private screening programs. This study examined how annual LDCT volume affects lung cancer stage distribution, overdiagnosis, and gender disparities using a hospital-based lung cancer database.MethodsThis study analyzed the annual utilized LDCT volume, clinical characteristics of lung cancer, stage shift distribution, and potential overdiagnosis. At the individual level, this study also investigated the relationship between stage 0 lung cancer (potential strict definition regarding overdiagnosis) and the clinical characteristics of lung cancer.ResultsThis study reviewed the annual trend of 4971 confirmed lung cancer cases from 2008 to 2021 and conducted a link analysis with an LDCT imaging examination database over these years. As the volume of lung cancer screenings has increased over the years, the number and proportion of stage 0 lung cancers have increased proportionally.Our study revealed that the incidence of stage 0 lung cancer increased with increasing LDCT scan volume, particularly during the peak growth period from 2017 to 2020. Conversely, stage 4 lung cancer cases remained consistent across different time intervals. Furthermore, the increase in the lung cancer screening volume had a more pronounced effect on the increase in stage 0 lung cancer cases among females than it had among males. The estimated potential for overdiagnosis brought about by the screening process, compared to non-participating individuals, ranged from an odds ratio of 7.617 to one of 17.114. Both strict and lenient definitions of overdiagnosis (evaluating cases of stage 0 lung cancer and stages 0 to 1 lung cancer) were employed.ConclusionsThese results provide population-level evidence of potential lung cancer overdiagnosis in the Taiwanese population due to the growing use of LDCT screening, particularly concerning the strict definition of stage 0 lung cancer. The impact was greater in the female population than in the male population, especially among females younger than 40 years.To improve lung cancer screening in Asian populations, creating risk-based prediction models for smokers and nonsmokers, along with gender-specific strategies, is vital for ensuring survival benefits and minimizing overdiagnosis.