Clinical data is scarce in epidermal growth factor receptor (EGFR)-mutated lung squamous cell carcinoma (LUSC), and the resistance mechanisms to EGFR-tyrosine kinase inhibitor (TKI) is rarely studied. This study aimed to assess the efficacy of EGFR-TKI treatment in EGFR-mutated LUSC patients .

Data of a cohort of 99 LUSC patients who were treated with EGFR-TKI and were followed up to October 31, 2023.

The objective response rate (ORR) of EGFR-mutated LUSC patients was higher than that of EGFR wild-type patients (44.4% vs 4.4%, p < 0.001). The progression-free survival (PFS) of EGFR-mutated LUSC patients receiving EGFR-TKI treatment was significantly longer than that of EGFR wild-type patients (6.4 months vs. 1.3 months; p < 0.001). Resistance mechanisms to EGFR-TKI in EGFR-mutated LUSC patients included secondary T790M mutations, 19 deletion-insertion mutations, MET amplification, histological transformation, and loss of EGFR mutations. The tumor immune microenvironment (TIME) of EGFR-mutated LUSC showed a downregulation of CD4 (p = 0.047) and CD8 (p = 0.14), and an upregulation of PD-L1 (p = 0.0021) after EGFR-TKI treatment failure.

EGFR-mutated LUSC patients receiving EGFR-TKIs treatment had higher ORR and longer PFS than EGFR wild-type LUSC patients.

Cytochrome P450 CYP1B1 is a heme-thiolate monooxygenase traditionally recognized for its xenobiotic functions and extrahepatic expressions. Recent studies have suggested that CYP1B1 is also expressed in hepatic stellate cells, immune cells, endothelial cells, and fibroblasts within the tumor microenvironment, as well as tumor cells themselves. CYP1B1 is responsible for the metabolism of a wide range of substrates, including xenobiotics such as drugs, environmental chemicals, and endobiotics such as steroids, retinol, and fatty acids. Consequently, CYP1B1 and its associated exogenous and endogenous metabolites have been critically implicated in the pathogenesis of many diseases. Understanding the mode of action of CYP1B1 in different pathophysiological conditions and developing pharmacological inhibitors that allow for systemic or cell type-specific modulation of CYP1B1 may pave the way for novel therapeutic opportunities. This review highlights the significant role of CYP1B1 in maintaining physiological homeostasis and provides a comprehensive discussion of recent advancements in our understanding of CYP1B1's involvement in the pathogenesis of diseases such as fibrosis, cancer, glaucoma, and metabolic disorders. Finally, the review emphasizes the therapeutic potential of targeting CYP1B1 for drug development, particularly in the treatment and prevention of cancers and liver fibrosis. SIGNIFICANCE STATEMENT: CYP1B1 plays a critical role in various physiological processes. Dysregulation or genetic mutations of the gene encoding this enzyme can lead to health complications and may increase the risk of diseases such as cancer and liver fibrosis. In this review, we summarize recent preclinical and clinical evidence that underscores the potential of CYP1B1 as a therapeutic target.

Rheumatoid arthritis (RA) is the most common chronic autoimmune arthropathy. If the disease is aggressive or left untreated, it becomes debilitating, affects a patient's functionality, and reduces the quality of life. Disease-modifying anti-rheumatic drugs (DMARDs), both conventional, targeted, and biological, decrease the disease progression and are key components of effective treatment. Recently, there has been a continuous debate about the possible carcinogenicity of various DMARDs. Lung cancer is a leading cause of cancer death worldwide. The available data show an increased risk of lung cancer in RA patients, but the link between RA and cancer is poorly understood. Carcinogenesis in RA seems to be related to chronic inflammation, familial predisposition, risky behaviors (e.g., smoking), and iatrogenic complications. The main mechanisms of carcinogenic processes in patients with RA are the up-regulation of interleukin-6 (IL-6) cytokine production and wingless/integrated WNT signaling. Up-regulation of WNT5A is an important mechanism that links chronic inflammatory pathways to carcinogenesis observed in RA patients. Concomitant up-regulation of transcription factor STAT3 promotes cell proliferation and inhibits apoptosis. Conversely, suppressed inflammatory processes by DMARDs may decrease the risk of lung cancer. In this article, we discuss the molecular mechanisms of lung cancer in RA and the role of DMARDs in this process. Furthermore, we analyze the molecular effect of drug-induced cancer, which affects transcription factors and thus modulates carcinogenic processes. Finally, we describe risk factors and present preventive and therapeutic approaches.

Background/Objectives: Lung cancer is one of the leading causes of cancer-related mortality, with tobacco smoking being the primary risk factor. However, a significant percentage of lung cancer patients are non-smokers, suggesting the involvement of other risk factors, including alcohol consumption. The IARC classifies ethanol as a Group 1 carcinogen, but unlike other alcoholic beverages, wine contains polyphenols with potential health benefits. Some meta-analyses even suggest a protective effect, which led us to conduct our own meta-analysis to further investigate this possible correlation. Methods: We conducted a systematic review and stratified the risk across population subgroups based on smoking status and gender. We then performed a categorical "highest vs. lowest" meta-analysis, comparing heavy consumers with very occasional drinkers, using a random-effects model. Only studies examining the risk of developing lung cancer in wine drinkers were included, excluding those with different outcomes, non-primary, ineligible populations, or involving pregnant women. The literature search was conducted in three databases: PubMed, Scopus, and Web of Science. The risk of bias was assessed with the Newcastle-Ottawa quality rating scale for both case-control and cohort studies (NOS), while statistical analyses were performed using the ProMeta 3.0 software. Results: The overall analysis showed a non-statistically significant 11% reduction in lung cancer risk (OR = 0.89; 95% CI: 0.77-1.03). The analysis among smokers revealed a significant 22% reduction in lung cancer risk associated with wine consumption (OR = 0.78; 95% CI: 0.62-0.97). However, this effect was lost when the analysis was conducted separately based on the study design. Conclusions: No correlation emerged between wine consumption and lung cancer incidence, either in a protective sense or in terms of increased risk. However, further studies are needed to investigate this correlation more accurately, particularly among non-smokers.

Malignant brain and other central nervous system tumors (MBT) are the second leading cause of cancer death among males aged 39 years and younger, and the leading cause of cancer death among males and females younger than 20. There are few widely accepted predictors and a lack of United States Preventive Services Taskforce recommendations for MBT. This study examined how medical history could be used to assess the risk of MBT.

Using over 400,000 patients' medical histories, including nearly 1,800 with MBT, Logistic Least Absolute Shrinkage and Selection Operator (LASSO) regression was used to predict MBT. More than 25,000 diagnoses were grouped into 16 body systems, plus pairwise and triple combinations, as well as indicators for missing values. Data were split into 80/20 training and validation sets with fit and accuracy assessed using McFadden's R2 and the area under the receiver operating characteristic curve (AUC).

Diagnoses of the endocrine, nervous, and lymphatic systems consistently showed greater than three times more association with MBT. The best performing model at an AUC of 0.83 consisted of 14 body system diagnosis groups and pairwise interactions among groups, in addition to demographic, social determinant of health, death, and six missing diagnosis grouping indicators.

This study demonstrated how large data models can predict MBT in patients using EHR data. With the lack of preventive screening guidelines and known risk factors associated with MBT, predictive models provide a universal, non-invasive, and inexpensive method of identifying at-risk patients.

Though indoor air pollution (IAP) is associated with elevated lung cancer risk, an integrated measure is imperative to thoroughly investigate this association. The interplay between sex and IAP on lung cancer remains unclear. We conducted a population-based case-control study in Jiangsu Province, China, from 2003 to 2010, with 2871 lung cancer cases and 8019 controls. Exposures and covariates information were collected via in-person interviews using a standardized questionnaire. An integrated weighted risk score (WRS), accounting for the effect sizes of each source of IAP, was introduced. Unconditional logistic regression was employed to estimate adjusted odds ratios (aORs) and their 95% confidence intervals (CIs). Interactions between sex and IAP by tobacco smoking status were evaluated. Environmental tobacco smoking (ETS) (aOR = 1.54, 95% CI: 1.40, 1.69), poor ventilation (aOR = 1.18, 95% CI: 1.07, 1.30), and coal used for cooking (aOR = 1.27, 95% CI: 1.15, 1.41) were associated with lung cancer. Dose-response relationships between lung cancer and WRS were observed, with p for trend less than 0.001. aOR for individuals at the highest quartile of the WRS of IAP was 1.74 (95% CI: 1.52, 2.00) compared to the lowest quartile. The associations were more profound among never-smokers than ever-smokers. Females tended to be more vulnerable to IAP, and sex interacted with IAP beyond multiplicativity on the odds scale. IAP is associated with lung cancer, with a stronger impact among never-smokers. An interaction between IAP and sex was observed. These results underscore the importance of controlling IAP, especially ETS in order to reduce the risk of lung cancer.

Anti-PD-1 immunotherapy plus chemotherapy (combo) exhibits significantly prolonged survival for squamous cell lung cancer (LUSC). An exploration of predictive biomarkers is still needed.

High-throughput RNA sequencing (RNA-seq) of 349 LUSC samples from the randomized, multi-center, phase 3 trial ORIENT-12 (ClinicalTrials.gov: NCT03629925) was conducted for biomarker discovery, followed by flow cytometry and multiplex immunohistochemistry (mIHC) in additional clinical cohorts, and in vitro experiments were performed for verification.

A high abundance of activated CD8+ T and CD56bright natural killer (NK) cells benefited patients' outcomes (progression-free survival [PFS]; overall survival [OS]) with combo treatment. Tumor cornification level remarkably affected the infiltration of the two crucial immune cells. Thus, a novel scheme of LUSC immune infiltration and cornification characterization-based classification (LICC) was established for combo efficacy prediction. Patients who received combo treatment achieved significant PFS improvements in LICC1 (hazard ratio [HR] = 0.43, 95% confidence interval [CI]: 0.25-0.75, p = 0.0029) and LICC2 (HR = 0.32, 95% CI: 0.17-0.58, p = 0.0002) subtypes but not in the LICC3 subtype (HR = 0.86, 95% CI: 0.60-1.23, p = 0.4053). Via single-cell RNA-seq analysis, the tumor cornification signal was mainly mapped to SPRR3+ tumor cells, whose relationships with activated CD8+ T or CD56bright NK cells were verified using flow cytometry and mIHC. Our data suggest that SPRR3+ tumor cells might evade immune surveillance via the CD24-SIGLEC10 (M2 macrophage) axis to maintain a suppressive tumor microenvironment.

Tumor cornification greatly impacts immune infiltration, and the LICC scheme may guide clinical medication of anti-PD-1+chemo treatment in patients with LUSC.

The study was funded by the National Key R&D Program of China, the National Natural Science Foundation of China, Shanghia Multidisplinary Cooperation Building Project for Diagnosis and Treatment of Major Disease, and Innovent Biologics, Inc.

A 58-year-old male presented with large yellowish choroidal mass lesions with exudative subretinal fluid (SRF) in both eyes. A computed tomography (CT) scan of the thorax revealed a mass lesion in the apical segment of the right upper lobe. Fine needle aspiration cytology (FNAC) of right supraclavicular lymph nodes revealed metastatic mucinous adenocarcinoma. Positron emission tomography-computed tomography scan (PET-CT) showed multiple lymphatic, pulmonary, and skeletal metastases. After six cycles of chemotherapy (platinum doublet and systemic bevacizumab), clinical examination and multimodal imaging showed complete regression of the choroidal lesions. Ours is the first case report of bilateral choroidal metastases from primary pulmonary adenocarcinoma (possibly arising from hazardous occupational exposure in the sericulture industry) that showed complete regression in response to standalone systemic chemotherapy agents, platinum doublet and systemic bevacizumab.

Nicotine is a highly addictive agent in tobacco products. On June 21, 2022, the US Food and Drug Administration (FDA) announced a plan to propose a rule to establish a maximum nicotine level in cigarettes and other combusted tobacco products.

This study aimed to understand public perception and discussion of very low nicotine content (VLNC) on Twitter (rebranded as X in July 2023).

From December 12, 2021, to January 1, 2023, we collected Twitter data using relevant keywords such as "vln," "low nicotine," and "reduced nicotine." After a series of preprocessing steps (such as removing duplicates, retweets, and commercial tweets), we identified 3270 unique noncommercial tweets related to VLNC. We used an inductive method to assess the public perception and discussion of VLNC on Twitter. To establish a codebook, we randomly selected 300 tweets for hand-coding, including the attitudes (positive, neutral, and negative) toward VLNC (including its proposed rule) and major topics (13 topics). The Cohen κ statistic between the 2 human coders reached over 70%, indicating a substantial interrater agreement. The rest of the tweets were single-coded according to the codebook.

We observed a significant peak in the discussion of VLNC on Twitter within 4 days of the FDA's announcement of the proposed rule on June 21, 2022. The proportion of tweets with a negative attitude toward VLNC was significantly lower than those with a positive attitude, 24.5% (801/3270) versus 37.09% (1213/3270) with P<.001 from the 2-proportion z test. Among tweets with a positive attitude, the topic "Reduce cigarette consumption or help smoking cessation" was dominant (1097/1213, 90.44%). Among tweets with a negative attitude, the topic "VLNC leads to more smoking" was the most popular topic (227/801, 28.34%), followed by "Similar toxicity of VLNC as a regular cigarette" (223/801, 27.84%), and "VLNC is not a good method for quitting smoking" (211/801, 26.34%).

There is a more positive attitude toward VLNC than a negative attitude on Twitter, resulting from different opinions about VLNC. Discussions around VLNC mainly focused on whether VLNC could help people quit smoking.

Purpose. Lung cancer is the leading cause of cancer death, with most cases attributable to cigarette smoking. Many communities within the lesbian, gay, bisexual, transgender and queer/questioning (LGBTQ+) umbrella have high rates of smoking, but focused lung cancer prevention is limited. Our objective was to utilize a community-based participatory research (CBPR) approach to guide the development of a program focused on lung cancer prevention in LGBTQ+ elders. Methods. Through community partnerships, we recruited participants who self-identified as LGBTQ+ and were eligible for lung cancer screening (LCS) to participate in semi-structured qualitative discussions with complementary surveys. Qualitative guides were developed to collect data on determinants of smoking cessation and LCS and to elicit feedback on interventions to support lung cancer prevention through a tailored approach to patient navigation. Qualitative data were analyzed using rapid templated analysis to elucidate themes. Results. The 21 enrolled participants had diverse sexual and gender identities and 57% were of minoritized race/ethnicity. Most (81%) had experience with smoking cessation but few (10%) had undergone LCS. Overall themes suggest interest in personalized (to individuals), tailored (to the LGBTQ+ community) and integrated longitudinal programs to support lung cancer prevention. Themes suggest strong endorsement of focused messaging to LGBTQ+ persons and reducing stigma related to LGBTQ+ identity and smoking. Conclusions. Themes highlight the need for integrated tobacco and LCS programming which can provide longitudinal support, and ideally, center community settings and peer support. This formative work will be utilized to adapt a patient navigation program to assist screen-eligible LGBTQ+ elders.

Lung adenocarcinoma (LUAD) represents a significant global health burden, necessitating advanced prognostic tools for improved patient management. RNA modifications (m6A, m1A, m5C, m7G), and disulfidptosis, a novel cell death mechanism, have emerged as promising biomarkers and therapeutic targets in cancer.

We systematically compiled disulfidptosis-correlated genes and RNA modification-related genes from existing literature. A novel disulfidptosis-correlated m6A/m1A/m5C/m7G riskscore was computed using integrated machine-learning algorithms. Transcriptomic data from TCGA and GEO databases were downloaded analyzed. Single-cell RNA-sequencing data from the TISCH database was processed using the Seurat package. Genes' protein-protein interaction network was constructed using the String database. Functional phenotype analysis was performed using GSVA, ClusterProfiler, and IOBR packages. Consensus clustering divided patients into two distinct groups. Drug sensitivity predictions were obtained from the GDSC1 database and predicted using the Oncopredict package.

The disulfidptosis-correlated m6A/m1A/m5C/m7G risk score effectively stratified LUAD patients into prognostically distinct groups, demonstrating superior predictive accuracy compared to conventional clinical parameters. Patients in different risk groups exhibited significant molecular and clinical differences. Subsequent analyses identified two molecular subtypes associated with RNA modification and disulfidptosis, revealing differences in immune infiltration and prognosis. Functional enrichment analyses highlighted pathways involving RNA modification and disulfidptosis, underscoring their roles in LUAD pathogenesis. Single-cell analysis revealed distinct features between high- and low-risk status cells.

This study introduces a novel disulfidptosis-correlated m6A/m1A/m5C/m7G risk score as a robust prognostic tool for LUAD, integrating insights from RNA modifications and cell death mechanisms. The risk score enhances prognostic stratification and identifies potential targets for personalized therapeutic strategies in LUAD. This comprehensive approach emphasizes the critical roles of RNA modifications and disulfidptosis in LUAD biology, paving the way for future research and clinical applications aimed at improving patient outcomes.

Exposure to cigarette smoke significantly enhances susceptibility to bacterial infections by inducing physiological and structural alterations, including immune system dysregulation. This exposure also augments bacterial virulence including biofilm formation, leading to severe infectious diseases and antibiotic resistance. Notably, cigarette smoke exposure increases the incidence of pneumonia by up to 2.5-fold and tuberculosis by up to 4.1-fold. Nicotine, a primary constituent of cigarette smoke, has been extensively characterized for its immunomodulatory effects. However, despite the wealth of knowledge on nicotine's impact on the host immune response, there is a paucity of data regarding its direct effects on various pulmonary pathogens. In the present review, we discuss the main findings in this field.

Lung cancer is the most common cancer and a leading cause of cancer-related deaths globally. The aim of this study was to evaluate the incidence and mortality of lung cancer worldwide in 2022 and to project the number of new cases and deaths due to lung cancer in China and the United States in 2050.

In this study, data from the GLOBCAN 2022 database were used to analyze lung cancer incidence and mortality. The current status of lung cancer incidence and deaths was described by country/region, sex, age, and the human development index (HDI), and future lung cancer incidence and deaths in China and the United States were projected for 2050.

Globally, an estimated 2,480,675 new lung cancer cases and 1,817,469 lung cancer-related deaths occurred in 2022, with age-standardized incidence rates (ASIRs) and age-standardized mortality rates (ASMRs) of 23.6/100,000 and 16.8/100,000, respectively. In China, the ASIR and ASMR for male lung cancer patients were approximately 1.7 times and 2.7 times greater than those for female lung cancer patients, respectively. The ASIR and ASMR in high-HDI countries were approximately 8.5 times and 6.5 times those in low-HDI countries, respectively. It is estimated that in 2050, there will be approximately 1120 thousand new cases and 960 thousand deaths among Chinese men, 680 thousand new cases and 450 thousand deaths among Chinese women, approximately 170 thousand new cases and 110 thousand deaths among American men, and 160 thousand new cases and 90 thousand deaths among American women.

There are significant differences in the incidence and mortality of lung cancer among different regions and sexes. Therefore, sex factors need to be considered in the prevention, screening, and treatment strategies of lung cancer, and the implementation of tertiary prevention measures for lung cancer, especially primary and secondary prevention, needs to be actively promoted.

General medical practitioners are responsible for promoting and prescribing lifestyle modification and serve as role models for healthy behaviors. We aimed to assess self-reported knowledge, adherence, barriers and time spent on all recommended health behaviors among medical students.

A cross-sectional online survey of eight behavioral domains among undergraduate medical students in The University of British Columbia, Canada, was analysed using descriptive statistics and visual display.

Between March and April 2023, 137 medical students participated in the survey (74% female). Over 80% had knowledge of five health behavior recommendations, but lacked knowledge of specific dietary recommendations in particular. Over 60% reported meeting guideline-recommended levels for tobacco, weekly alcohol, daily alcohol (females only), and physical activity (males only). Large gaps existed between knowledge and adherence for physical activity, sleep, sedentariness, screen time, and dietary recommendations. Sex differences in knowledge and adherence to recommended health behaviors were identified. Time spent on wellness focused on sleep (47-49 h/week), diet (9.6 h/week), exercise (5.8 h/week), and hobbies (6.1 h/week). Forgetting recommendations (69% of females, 71% of males), and lack of time (72% of females, 52% of males) were principal barriers to knowledge and adherence.

Most medical students in Western Canada reported not meeting multiple recommended health behaviors. Time was the largest barrier to adherence and free time was spent on sleep. Medical education may require protected time and dedicated content for health behaviors to ensure future physicians can be role models of health promotion for patients.

Lung cancer continues to be the leading cause of death among cancer patients worldwide. This study aimed to estimate the clinical, economic, and social burdens of stage IV non-small cell lung cancer (NSCLC) in private and public healthcare centers in Mexico, utilizing real-world evidence.

The study population included patients >18 years of age diagnosed with stage IV NSCLC who received cancer treatment at the Centro Médico Nacional Siglo XXI (IMSS), the Centro Médico Nacional "20 de Noviembre" (ISSSTE), the Mexican Institute of Respiratory Diseases (INER), and the Medical Center ABC (American British Cowdray) from 1 January 2019 to 31 December 2020. The analysis included evaluation of epidemiological data, treatment regimens, and clinical outcomes, and emphasized pharmacological and non-pharmacological treatments, including detailed follow-up investigations, as part of comprehensive clinical management. Additionally, the study assessed the social burden through variables such as working-age absenteeism and presenteeism and caregiver productivity loss, as well as economic burden, considering both clinical and social components, with costs adjusted to 2022 Mexican pesos (MXN) values.

A total of 188 patients with metastatic NSCLC were studied. The main type of NSCLC tumor found in the sample was adenocarcinoma (81%). Treatment regimens included pharmacological treatments (78%), non-pharmacological treatments (25%), and palliative care (24%). Complications were present in 73% of the cohort, while 60% presented adverse events. Clinical management costs of up to MXN1,001,579 per patient in the public sector and MXN2,140,604 in the private sector were reported. It was estimated that working-age patients lose 84-335 days yearly due to absenteeism and presenteeism, while caregivers report a productivity loss equivalent to 13-30 days due to the management of NSCLC patients. These indirect costs of NSCLC contribute to the social burden. A working-age patient with stage IV disease is associated with an average indirect cost of MXN49,731-178,287 in public institutions, while in private institutions, the cost elevates to MXN438,103.

This study highlights the substantial clinical, economic, and social burdens of stage IV NSCLC in Mexico, revealing significant disparities between public and private healthcare sectors. It underscores the urgent need for standardized practices and equitable care across all systems.

Mitochondria serve as central hubs for regulating numerous cellular processes that include metabolism, apoptosis, cell cycle progression, proliferation, differentiation, epigenetics, immune signaling, and aging. The voltage-dependent anion channel 1 (VDAC1) functions as a crucial mitochondrial gatekeeper, controlling the flow of ions, such as Ca2+, nucleotides, and metabolites across the outer mitochondrial membrane, and is also integral to mitochondria-mediated apoptosis. VDAC1 functions in regulating ATP production, Ca2+ homeostasis, and apoptosis, which are essential for maintaining mitochondrial function and overall cellular health. Most cancer cells undergo metabolic reprogramming, often referred to as the "Warburg effect", supplying tumors with energy and precursors for the biosynthesis of nucleic acids, phospholipids, fatty acids, cholesterol, and porphyrins. Given its multifunctional nature and overexpression in many cancers, VDAC1 presents an attractive target for therapeutic intervention. Our research has demonstrated that silencing VDAC1 expression using specific siRNA in various tumor types leads to a metabolic rewiring of the malignant cancer phenotype. This results in a reversal of oncogenic properties that include reduced tumor growth, invasiveness, stemness, epithelial-mesenchymal transition. Additionally, VDAC1 depletion alters the tumor microenvironment by reducing angiogenesis and modifying the expression of extracellular matrix- and structure-related genes, such as collagens and glycoproteins. Furthermore, VDAC1 depletion affects several epigenetic-related enzymes and substrates, including the acetylation-related enzymes SIRT1, SIRT6, and HDAC2, which in turn modify the acetylation and methylation profiles of histone 3 and histone 4. These epigenetic changes can explain the altered expression levels of approximately 4000 genes that are associated with reversing cancer cells oncogenic properties. Given VDAC1's critical role in regulating metabolic and energy processes, targeting it offers a promising strategy for anti-cancer therapy. We also highlight the role of VDAC1 expression in various disease pathologies, including cardiovascular, neurodegenerative, and viral and bacterial infections, as explored through siRNA targeting VDAC1. Thus, this review underscores the potential of targeting VDAC1 as a strategy for addressing high-energy-demand cancers. By thoroughly understanding VDAC1's diverse roles in metabolism, energy regulation, mitochondrial functions, and other cellular processes, silencing VDAC1 emerges as a novel and strategic approach to combat cancer.

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.

Due to the high mortality rate, more effective non-invasive diagnostic methods are still needed for lung cancer, the most common cause of cancer-related death worldwide. In this study, the integration of Raman and Fourier-transform infrared spectroscopy with advanced data-fusion techniques is investigated to improve the detection of lung cancer from human blood plasma samples. A high statistical significance was found for important protein-related oscillations, which are crucial for differentiating between lung cancer patients and healthy controls. The use of low-level data fusion and feature selection significantly improved model accuracy and emphasizes the importance of structural protein changes in cancer detection. Although other biomolecules such as carbohydrates and nucleic acids also contributed, proteins proved to be the decisive markers found using this technique. This research highlights the power of these combined spectroscopic methods to develop a non-invasive diagnostic tool for discriminating lung cancer from healthy state, with the potential to extend such studies to a variety of other diseases.

Lung cancer, a leading global cause of cancer-related mortality, necessitates enhanced prognostic markers for improved treatment outcomes. We have previously shown a tumor suppressive role of cytosolic arginine sensor for mTORC1 subunit 1 (CASTOR1), which is targeted for degradation upon phosphorylation at S14 (pCASTOR1) in multiple types of cancer. This study focuses on the predictive value of pCASTOR1 in lung adenocarcinoma (LUAD) patients with KRAS mutations.

Employing a newly developed pCASTOR1 specific antibody, we found that tumor cells exhibited significantly elevated pCASTOR1 scores compared to non-tumor cells (P < 0.05). Higher pCASTOR1 scores predicted poorer overall survival (OS) (HR = 3.3, P = 0.0008) and relapse-free survival (RFS) (HR = 3.0, P = 0.0035) in male patients with KRAS mutations. pCASTOR1 remained an independent predictor for OS (HR = 4.1, P = 0.0047) and RFS (HR = 3.5, P = 0.0342) after controlling for other factors. Notably, in early-stage LUAD, elevated pCASTOR1 scores were associated with significantly worse OS (HR = 3.3, P = 0.0176) and RFS (HR = 3.1, P = 0.0277) in male patients with KRAS mutations, akin to late-stage patients.

Elevated pCASTOR1 scores serve as biomarkers predicting poorer OS and RFS in male LUAD patients with KRAS mutations, offering potential clinical utility in optimizing treatment strategies for this subgroup.

The purpose of this study was to assess performance in the Brazilian Lung Cancer Registry Database by using the parsimonious EuroLung risk models for morbidity and mortality.

The EuroLung1 and EuroLung2 models were tested and evaluated through calibration (calibration plot, Brier score, and the Hosmer-Lemeshow test) and discrimination (ROC AUCs), in a national multicenter registry of 1,031 patients undergoing anatomic lung resection.

The evaluation of performance in Brazilian health care facilities utilizing risk-adjustment models, specifically EuroLung1 and EuroLung2, revealed substantial miscalibration, as evidenced by calibration plots and Hosmer-Lemeshow tests in both models. In terms of calibration, EuroLung1 exhibited a calibration plot with overlapping points, characterized by a slope of 1.11 and a Brier score of 0.15; the Hosmer-Lemeshow test yielded a statistically significant p-value of 0.015; and the corresponding ROC AUC was 0.678 (95% CI: 0.636-0.721). The EuroLung2 model displayed better calibration, featuring fewer overlapping points in the calibration plot, with a slope of 1.22, with acceptable discrimination, as indicated by a ROC AUC of 0.756 (95% CI: 0.670-0.842). Both models failed to accurately predict morbidity and mortality outcomes in this specific health care context.

Discrepancies between the EuroLung model predictions and outcomes in Brazil underscore the need for model refinement and for a probe into inefficiencies in the Brazilian health care system.

Alterations in cellular metabolism are vital for cancer cell growth and motility. Here, we focused on metabolic reprogramming and changes in tumor hallmarks in lung cancer by silencing the expression of the mitochondrial gatekeeper VDAC1. To better mimic the clinical situation of lung cancer, we induced lung cancer in A/J mice using the carcinogen urethane and examined the effectiveness of si-m/hVDAC1-B encapsulated in PLGA-PEI nanoparticles. si-m/hVDAC1-B, given intravenously, induced metabolism reprogramming and inhibited tumor growth as monitored using MRI. Mice treated with non-targeted (NT) PLGA-PEI-si-NT showed many large size tumors in the lungs, while in PLGA-PEI-si-m/hVDAC-B-treated mice, lung tumor number and area were markedly decreased. Immunofluorescence staining showed decreased expression of VDAC1 and metabolism-related proteins and altered expression of cancer stem cell markers. Morphological analysis showed two types of tumors differing in their morphology; cell size and organization within the tumor. Based on specific markers, the two tumor types were identified as small cell (SCLC) and non-small cell (NSCLC) lung cancer. These two types of tumors were found only in control tumors, suggesting that PLGA-PEI-si-m/hVDAC1-B also targeted SCLC. Indeed, using a xenograft mouse model of human-derived SCLC H69 cells, si-m/hVDAC1-B inhibited tumor growth and reduced the expression of VDAC1 and energy- and metabolism-related enzymes, and of cancer stem cells in the established xenograft. Additionally, intravenous treatment of urethane-induced lung cancer mice with the VDAC1-based peptide, Retro-Tf-D-LP4, showed inhibition of tumor growth, and decreased expression levels of metabolism- and cancer stem cells-related proteins. Thus, silencing VDAC1 targeting both NSCLC and SCLC points to si-VDAC1 as a possible therapeutic tool to treat these lung cancer types. This is important as target NSCLC tumors undergo transformation to SCLC.

Accumulating data have revealed the pivotal function of tripartite motif protein 38 (TRIM38) in tumors. In view of this, this investigation aims to explore the function and potential mechanism of TRIM38 in non-small cell lung cancer (NSCLC). A xenotypic tumor model was established in vivo by subcutaneously injecting NSCLC cells (2 × 106 cells) in tail vein of each mouse. Relative expression of TRIM38 mRNA was detected via quantitative real-time polymerase chain reaction (qRT-PCR). For exploring the role of TRIM38 in vivo and in vitro, mice or NSCLC cells were divided into two groups: the vector group and the TRIM38 overexpression group. Also, protein expression levels of TRIM38, Vimentin, E-cadherin, and N-cadherin were determined using western blotting and immunohistochemistry staining. Tumor nodules of mouse lung tissues were assessed via performing H&E staining. Moreover, proliferation of NSCLC cells was evaluated through colony formation and CCK-8 assays. Further, migration and invasion of NSCLC cells were assessed through wound healing and transwell assays. Protein levels of pathway-related proteins including p-p65, p65, IκB, p-IκB, p-AMPK, AMPK, and NLRP3 were examined through western blotting analysis. Tumor lung tissues of mice and NSCLC cells showed low protein and mRNA expression of TRIM38. Functionally, up-regulation of TRIM38 reduced the number of tumor nodules and suppressed epithelial-to-mesenchymal transition (EMT) in lung tissues of mice. Furthermore, up-regulation of TRIM38 in NSCLC cells inhibited migration, invasion, EMT, and proliferation. With respect to the mechanism, in vivo experiments, the inhibitory effects of TRIM38 overexpression on tumor nodules, and EMT were reversed by AMPK inhibitor. In vitro experiments, TRIM38 overexpression caused down-regulation of p-IκB and p-p65 as well as up-regulation of p-AMPK. The inhibitory effects of TRIM38 overexpression on migration, proliferation, invasion, and EMT of NSCLC cells were reversed by overexpression of NLRP3. Concurrently, AMPK inhibitor enhanced the TRIM38-overexpressed NSCLC cell's abilities in migration, clone formation, invasion, and proliferation. TRIM38 regulated the AMPK/NF-κB/NLRP3 pathway to suppress the NSCLC's progression and development.

Over 200,000 individuals are diagnosed with lung cancer in the United States every year, with a growing proportion of cases, especially lung adenocarcinoma, occurring in individuals who have never smoked. Women over the age of 50 comprise the largest affected demographic. To understand the genomic drivers of lung adenocarcinoma and therapeutic response in this population, we performed whole genome and/or whole exome sequencing on 73 matched lung tumor/normal pairs from postmenopausal women who participated in the Women's Health Initiative. Somatic copy number alterations showed little variation by smoking status, suggesting that aneuploidy may be a general characteristic of lung cancer regardless of smoke exposure. Similarly, clock-like and APOBEC mutation signatures were prevalent but did not differ in tumors from smokers and never-smokers. However, mutations in both EGFR and KRAS showed unique allelic differences determined by smoking status that are known to alter tumor response to targeted therapy. Mutations in the MYC-network member MGA were more prevalent in tumors from smokers. Fusion events in ALK, RET, and ROS1 were absent, likely due to age-related differences in fusion prevalence. Our work underscores the profound effect of smoking status, age, and sex on the tumor mutational landscape and identifies areas of unmet medical need.

Lung carcinoma, including both non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC), remains a significant global health challenge due to its high morbidity and mortality rates. The objsective of this review is to meticulously examine the current advancements and strategies in the delivery of CRISPR-Cas9 gene-editing technology for the treatment of lung carcinoma. This technology heralds a new era in molecular biology, offering unprecedented precision in genomic modifications. However, its therapeutic potential is contingent upon the development of effective delivery mechanisms that ensure the efficient and specific transport of gene-editing tools to tumor cells. We explore a variety of delivery approaches, such as viral vectors, lipid-based nanoparticles, and physical methods, highlighting their respective advantages, limitations, and recent breakthroughs. This review also delves into the translational and clinical significance of these strategies, discussing preclinical and clinical studies that investigate the feasibility, efficacy, and safety of CRISPR-Cas9 delivery for lung carcinoma. By scrutinizing the landscape of ongoing clinical trials and offering translational perspectives, we aim to elucidate the current state and future directions of this rapidly evolving field. The review is structured to first introduce the problem and significance of lung carcinoma, followed by an overview of CRISPR-Cas9 technology, a detailed examination of delivery strategies, and an analysis of clinical applications and regulatory considerations. Our discussion concludes with future perspectives and challenges, such as optimizing delivery strategies, enhancing specificity, mitigating immunogenicity concerns, and addressing regulatory issues. This comprehensive overview seeks to provide insights into the potential of CRISPR-Cas9 as a revolutionary approach for targeted therapies and personalized medicine in lung carcinoma, emphasizing the importance of delivery strategy development in realizing the full potential of this groundbreaking technology.

NSCLC is a leading cause of cancer-related mortality worldwide. Specific genetic alterations, such as MET exon 14 (METex14) skipping, have been identified in NSCLC, allowing targeted therapy. Tepotinib, a highly selective MET inhibitor, has displayed promise in patients with advanced NSCLC. Nevertheless, challenges arise when identifying treatment strategies for patients with discordant results regarding METex14 skipping detection between diagnostic tests.

We investigated patients with NSCLC and discordant results for METex14 skipping between the Oncomine Dx Target Test (ODxTT) and ArcherMET. Clinical response, adverse events, and the duration of tepotinib treatment were assessed, and statistical analysis was performed.

Among the 19 patients deemed METex14 skipping positive by ODxTT, only 10 had concordant results with ArcherMET. The number of METex14 skipping reads detected by ODxTT was significantly lower in discordant cases. Of the 19 patients, 14 received tepotinib, and comparable response and disease control rates were observed in both concordant and discordant cases. The duration of treatment did not significantly differ between the two groups.

Our findings suggest that tepotinib has comparable therapeutic effects in patients with METex14 skipping-positive NSCLC irrespective of the concordance of results between ODxTT and ArcherMET. Tepotinib is a possible treatment option for patients with METex14 skipping, even in patients with discordant test results.

Companion diagnostic (CDx) tests play important roles in identifying oncogenic driver genes and tailoring effective molecularly targeted therapies for lung cancer patients. In Japan, the Oncomine Dx target test (ODxTT) and the AmoyDx pan lung cancer PCR panel (AmoyDx) are prominent CDx tests and only one of these tests is covered by the domestic insurance system. However, these CDx tests cover different target regions and apply different technologies (ODxTT is amplicon-based next-generation sequencing and AmoyDx is multiplex PCR-based assay), which may lead to missing of actionable mutations affecting patient prognosis. Here, we performed a direct comparison analysis of 1059 genetic alterations of eight driver genes from 131 samples and evaluated the concordance between two CDx tests for detecting actionable variants and fusions. When excluding the eight uncovered variants (ODxTT: two variants, AmoyDx: six variants), the overall percent agreement was 97.6% (1026/1051) with 89.0% of overall positive percent agreement (89/100) and 98.5% of overall negative percent agreement (937/951). Of the 25 discordant genetic alterations, two were undetected despite being covered in the AmoyDx (one EGFR variant and one ROS1 fusion). Furthermore, there were potential false positives in the ODxTT (nine MET exon 14 skippings) and in the AmoyDx (five variants, six ROS1 and three RET fusions). These potential false positives in the AmoyDx likely due to non-specific amplification, which was validated by the unique molecular barcoding sequencing. The ODxTT missed two uncovered EGFR rare variants, which was visually confirmed in the raw sequencing data. Our study provides insights into real-world performance of CDx tests for lung cancer and ensures reliability to advance precision medicine.

Identifying novel biomarkers for early detection of lung cancer is crucial. Non-invasively available saliva is an ideal biofluid for biomarker exploration; however, the rationale underlying biomarker detection from organs distal to the oral cavity in saliva requires clarification. Therefore, we analyzed metabolomic profiles of cancer tissues compared with those of adjacent non-cancerous tissues, as well as plasma and saliva samples collected from patients with lung cancer (n = 109 pairs). Additionally, we analyzed plasma and saliva samples collected from control participants (n = 83 and 71, respectively). Capillary electrophoresis-mass spectrometry and liquid chromatography-mass spectrometry were performed to comprehensively quantify hydrophilic metabolites. Paired tissues were compared, revealing 53 significantly different metabolites. Plasma and saliva showed 44 and 40 significantly different metabolites, respectively, between patients and controls. Of these, 12 metabolites exhibited significant differences in all three comparisons and primarily belonged to the polyamine and amino acid pathways; N1-acetylspermidine exhibited the highest discrimination ability. A combination of 12 salivary metabolites was evaluated using a machine learning method to differentiate patients with lung cancer from controls. Salivary data were randomly split into training and validation datasets. Areas under the receiver operating characteristic curve were 0.744 for cross-validation using training data and 0.792 for validation data. This model exhibited a higher discrimination ability for N1-acetylspermidine than that for other metabolites. The probability of lung cancer calculated using this model was independent of most patient characteristics. These results suggest that consistently different salivary biomarkers in both plasma and lung tissues might facilitate non-invasive lung cancer screening.

Lung cancer (LC) and chronic obstructive pulmonary disease (COPD) are among the leading causes of mortality worldwide. Cigarette smoking is among the main aetiologic factors for both ailments. These diseases share common pathogenetic mechanisms including inflammation, oxidative stress, and tissue remodelling. Current therapeutic approaches are limited by low efficacy and adverse effects. Consequentially, LC has a 5-year survival of < 20%, while COPD is incurable, underlining the necessity for innovative treatment strategies. Two promising emerging classes of therapy against these diseases include plant-derived molecules (phytoceuticals) and nucleic acid-based therapies. The clinical application of both is limited by issues including poor solubility, poor permeability, and, in the case of nucleic acids, susceptibility to enzymatic degradation, large size, and electrostatic charge density. Nanoparticle-based advanced drug delivery systems are currently being explored as flexible systems allowing to overcome these limitations. In this review, an updated summary of the most recent studies using nanoparticle-based advanced drug delivery systems to improve the delivery of nucleic acids and phytoceuticals for the treatment of LC and COPD is provided. This review highlights the enormous relevance of these delivery systems as tools that are set to facilitate the clinical application of novel categories of therapeutics with poor pharmacokinetic properties.

EGFR-tyrosine kinase inhibitors (TKI) are the first-line therapies for EGFR mutation-positive lung cancer. EGFR-TKIs have favorable therapeutic effects. However, a large proportion of patients with EGFR mutation-positive lung cancer subsequently relapse. Some cancer cells survive the initial treatment with EGFR-TKIs, and this initial survival may be associated with subsequent recurrence. Therefore, we aimed to overcome the initial survival against EGFR-TKIs. We hypothesized that yes-associated protein 1 (YAP1) is involved in the initial survival against EGFR-TKIs, and we confirmed the combined effect of EGFR-TKIs and a YAP1-TEAD pathway inhibitor. The KTOR27 (EGFR kinase domain duplication) lung cancer cell lines established from a patient with EGFR mutation-positive lung cancer and commercially available PC-9 and HCC827 (EGFR exon 19 deletions) lung cancer cell lines were used. These cells were used to evaluate the in vitro and in vivo effects of VT104, a TEAD inhibitor. In addition, YAP1 involvement was investigated in pathologic specimens. YAP1 was activated by short-term EGFR-TKI treatment in EGFR mutation-positive lung cancer cells. In addition, inhibiting YAP1 function using siRNA increased the sensitivity to EGFR-TKIs. Combination therapy with VT104 and EGFR-TKIs showed better tumor-suppressive effects than EGFR-TKIs alone, in vitro and in vivo. Moreover, the combined effect of VT104 and EGFR-TKIs was observed regardless of the localization status of YAP1 before EGFR-TKI exposure. These results suggest that combination therapy with the TEAD inhibitor and EGFR-TKIs may improve the prognosis of patients with EGFR mutation-positive lung cancer.

To examine and interpret trends in UK cancer incidence and mortality for all cancers combined and for the most common cancer sites in adults aged 35-69 years.

Retrospective secondary data analysis.

Cancer registration data, cancer mortality and national population data from the Office for National Statistics, Public Health Wales, Public Health Scotland, Northern Ireland Cancer Registry, NHS England, and the General Register Office for Northern Ireland.

23 cancer sites were included in the analysis in the UK.

Men and women aged 35-69 years diagnosed with or who died from cancer between 1993 to 2018.

Change in cancer incidence and mortality age standardised rates over time.

The number of cancer cases in this age range rose by 57% for men (from 55 014 cases registered in 1993 to 86 297 in 2018) and by 48% for women (60 187 to 88 970) with age standardised rates showing average annual increases of 0.8% in both sexes. The increase in incidence was predominantly driven by increases in prostate (male) and breast (female) cancers. Without these two sites, all cancer trends in age standardised incidence rates were relatively stable. Trends for a small number of less common cancers showed concerning increases in incidence rates, for example, in melanoma skin, liver, oral, and kidney cancers. The number of cancer deaths decreased over the 25 year period, by 20% in men (from 32 878 to 26 322) and 17% in women (28 516 to 23 719); age standardised mortality rates reduced for all cancers combined by 37% in men (-2.0% per year) and 33% in women (-1.6% per year). The largest decreases in mortality were noted for stomach, mesothelioma, and bladder cancers in men and stomach and cervical cancers and non-Hodgkin lymphoma in women. Most incidence and mortality changes were statistically significant even when the size of change was relatively small.

Cancer mortality had a substantial reduction during the past 25 years in both men and women aged 35-69 years. This decline is likely a reflection of the successes in cancer prevention (eg, smoking prevention policies and cessation programmes), earlier detection (eg, screening programmes) and improved diagnostic tests, and more effective treatment. By contrast, increased prevalence of non-smoking risk factors are the likely cause of the observed increased incidence for a small number of specific cancers. This analysis also provides a benchmark for the following decade, which will include the impact of covid-19 on cancer incidence and outcomes.

Tumor-to-tumor metastasis (TTM) is a rare phenomenon documented in patients with multiple primary cancers. This condition is defined as a metastasis between two true primary tumors. The most frequently reported recipient tumor is renal cell carcinoma (RCC), and the lung carcinomas are the most common metastatic tumor donors. Therefore, this paper attempts to address the current gap in knowledge about this rare phenomenon. The first part of this review outlines the recently proposed models and mechanisms involved in the TTM process. The second part then summarizes and analyzes previous case reports in the literature. We also present our experience with the case of lung cancer that metastasized into RCC. Given the sporadic incidence of TTM, no specific management guidelines exist. Therefore, considering TTM in patients with multiple primary tumors is important as it could potentially modify the oncological management offered.

Lung cancer is currently the most fatal form of cancer worldwide, ranking as the fourth most prevalent type in Saudi Arabia, particularly among males. This trend is expected to increase with growing population, lifestyle changes, and aging population. Understanding the awareness of the Saudi population regarding the risk factors and symptoms of lung cancer is necessary to attenuate the predicted increase in cases.

A cross-sectional, population-based survey was performed using a previously validated questionnaire (Lung CAM). Multiple linear regression analysis was used to assess variables associated with deficiency in knowledge and awareness of risk factors and symptoms of lung cancer.

Majority of the 15,099 respondents were male (65%), aged between 18 and 30 years (53%), 50% of which were educated up to a bachelor's degree level. Overall awareness of lung cancer signs and symptoms was 53%, with painful cough and coughing up blood being the best-known symptoms. Conversely, persistent shoulder pain (44%) and clubbing fingers (47%) were the least known lung cancer symptoms. Also, 60% of the respondents showed low confidence in identifying the signs and symptoms of lung cancer. The overall awareness of the risk factors for lung cancer development was 74%, with first-hand (74%) and second-hand (68%) smoking being the most known risk factors. However, only ≤ 62% know the other non-smoking risk factors. Awareness of the risk factors and symptoms of lung cancer depended on age, gender, education, marital and employment status (p < 0.001).

Public awareness of the risk factors and symptoms of lung cancer in Saudi Arabia is inadequate and heavily dependent on education and socio-economic status. Awareness can be improved through campaigns to raise awareness about other lesser-known lung cancer risk factors and symptoms.

Metastasis is one of the major causes of death in patients with cancer, and cell invasion plays a fundamental part in this process. Because of the absence of efficacious treatments, caring for these patients is challenging. Recently, we optimized the structure of the naturally occurring lasso peptide sungsanpin. We identified two peptides, octapeptide S3 and cyclic peptide S4, which inhibited invasion into A549 cells effectively. We undertook an alanine scan of S3 to explore the structure-activity relationship. The linear octapeptide S3-4 and cyclic peptide S4-1 exhibited improved inhibition of invasion into A549 cells. We modified S3-4 to obtain S3-4K, which displayed much higher inhibitory activity against invasion into A549 cells than S3-4. Of all peptides tested, S4-1 upregulated significantly mRNA of tissue inhibitor matrix metalloproteinase TIMP-1 and TIMP-2.

Cancer is one of the leading causes of increasing global mortality with uprising health concerns and threats. Unfortunately, conventional chemotherapy has substantial side effects, limiting its relevance and prompting a quest for safe and efficient alternatives. For thousands of years, plants have provided a rich reservoir for curing a variety of ailments, including cancer. According to the World Health Organization, medicinal plants would be the best source of medications. However, only 25% of drugs in the present pharmacopoeia are derived from plants. Hence, further research into different plants is required to better understand their efficacy. Twenty extracts of widely distributed Middle Eastern plants were screened for the cytotoxic effect against lung cancer cell lines (A549). Eleven plants showed IC50 below 25 μg/mL, consequently, the bioactive extracts were further fractionated by graded precipitation using absolute ethanol. All fraction A (FA; crude polysaccharides precipitate) showed potent IC50, 0.2-5.5 μg/mL except the FA of Brassica juncea, Silybum marianum, and Phaseolus vulgaris, whereas FB fractions (filtrate) of Anastatica hierochuntica, Plantago ovate, Tussilago farfara, and Cucurbita moschata had lower efficacy than other fractions with IC50 values in the range of 0.1-7.7 μg/mL. The fractions of FA Taraxacum officinale and FB Ziziphus spina possess the most potent cytotoxic activity with IC50, 0.2 and 0.1 μg/mL, respectively. Moreover, cell cycle analysis of both fractions revealed an arrest at G1/S-phase and activation of apoptosis rather than necrosis as the mode of cell death. Therefore, T. officinale and Z. spina fractions may pave the way to manage lung carcinoma as an alternative and complementary food regimen.

Lung cancer is a leading cause of cancer-related deaths worldwide. Epidermal growth factor receptor (EGFR) driver mutations are crucial for treatment decisions for patients with non-small cell lung cancer (NSCLC). This study aimed to assess the differences in EGFR mutation detection between two companion diagnostic (CDx) tests-the Oncomine Dx Target Test (ODxTT) and the AmoyDx Pan Lung Cancer PCR Panel-and their impact on treatment applicability. To this end, we used an in-house targeted sequencing dataset of 282 samples from 127 EGFR-mutated NSCLC patients to simulate the concordance between the EGFR variants targeted by the ODxTT and AmoyDx panel, the oncogenicity of the variants, and their therapeutic potential. Of the 216 EGFR mutations identified by the in-house panel, 51% were detectable by both CDx tests, 3% were specific to ODxTT, and 46% were not targeted by either test. Most non-targeted mutations did not have oncogenicity and were located outside exons 18-21. Notably, 95% of the mutations detectable by both tests had potential oncogenicity. Furthermore, among the 96 patients harboring actionable EGFR mutations, 97% had mutations detectable by both CDx tests and 1% by ODxTT, while 2% had mutations not covered by either test. These findings suggest that while both CDx tests are effective in detecting almost all actionable EGFR mutations, ODxTT provides slightly broader coverage. These results emphasize the importance of selecting appropriate CDx tests to inform treatment decisions for EGFR-positive NSCLC patients.

Lung cancer is the one of the most prevalent cancer in the world. It kills more people from cancer than any other cause and is especially common in underdeveloped nations. With 1.2 million instances, it is also the most prevalent cancer in men worldwide, making about 16.7% of the total cancer burden. Surgery is the main form of curative treatment for early-stage lung cancer. However, the majority of patients had incurable advanced non-small cell lung cancer (NSCLC) recurrence after curative purpose surgery, which is indicative of the aggressiveness of the illness and the dismal outlook. The gold standard of treatment for NSCLC patients includes drug targeting of specific mutated genes drive in development of lung cancer. Furthermore, patients with advanced NSCLC and those with early-stage illness needing adjuvant therapy should use cisplatin as it is the more active platinum drug. So, this review encompasses the non-small cell lung cancer microenvironment, treatment approaches, and use of cisplatin as a first-line regimen for NSCLC, its mechanism of action, cisplatin resistance in NSCLC and also the prevention strategies to revert the drug resistance.

Little is known about the relationship between sleep quality and lung cancer incidence. Thus, this study was conducted to investigate the potential connection between sleep quality and lung cancer incidence.

We performed and selected a nested case-control study that included 150 lung cancer cases and 150 matched controls based on the Lianyungang cohort. Univariate and multivariate logistic regression was utilized to investigate the connection between potential risk factors and lung cancer incidence risk.

In this study, the average age of participants was 66.5 ± 9.1 years, with 58.7% being male, and 52.7% reportedly experiencing sleep quality problems. The results of multivariate logistic regression showed that poor sleep quality was connected to an increased lung cancer incidence risk (P = 0.033, odds ratio = 1.83, 95% confidence interval = [1.05-3.19]) compared with those with good sleep quality. The stratified analyses showed a significantly positive connection between poor sleep quality (vs. good sleep quality) and cancer risk in smokers (vs. non-smoker, P for interaction = 0.085). The combined effect analysis indicated that smokers with poor sleep quality suffered from a 2.79-fold increase in cancer incidence rates when compared with non-smokers with good sleep quality.

Poor sleep quality was positively connected to an increased lung cancer incidence risk. In addition, among those individuals with poor sleep quality, smoking increased the lung cancer incidence risk.