Prognosis Of Lung Cancer Patients Research Articles

ADAMTS4 exacerbates lung cancer progression via regulating c-Myc protein stability and activating MAPK signaling pathway

BackgroundLung cancer is one of the most frequent cancers and the leading cause of cancer-related deaths worldwide with poor prognosis. A disintegrin and metalloproteinase with thrombospondin motifs 4 (ADAMTS4) is crucial in the regulation of the extracellular matrix (ECM), impacting its formation, homeostasis and remodeling, and has been linked to cancer progression. However, the specific involvement of ADAMTS4 in the development of lung cancer remains unclear.MethodsADAMTS4 expression was identified in human lung cancer samples by immunohistochemical (IHC) staining and the correlation of ADAMTS4 with clinical outcome was determined. The functional impact of ADAMTS4 on malignant phenotypes of lung cancer cells was explored both in vitro and in vivo. The mechanisms underlying ADAMTS4-mediated lung cancer progression were explored by ubiquitination-related assays.ResultsOur study revealed a significant upregulation of ADAMTS4 at the protein level in lung cancer tissues compared to para-carcinoma normal tissues. High ADAMTS4 expression inversely correlated with the prognosis of lung cancer patients. Knockdown of ADAMTS4 inhibited the proliferation and migration of lung cancer cells, as well as the tubule formation of HUVECs, while ADAMTS4 overexpression exerted opposite effects. Mechanistically, we found that ADAMTS4 stabilized c-Myc by inhibiting its ubiquitination, thereby promoting the in vitro and in vivo growth of lung cancer cells and inducing HUVECs tubule formation in lung cancer. In addition, our results suggested that ADAMTS4 overexpression activated MAPK signaling pathway.ConclusionsWe highlighted the promoting role of ADAMTS4 in lung cancer progression and proposed ADAMTS4 as a promising therapeutic target for lung cancer patients.

The relationship between sarcopenia and metabolic parameters of 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) and the prognostic value of sarcopenia in early-stage non-small cell lung cancer.

Patients with lung cancer face a heightened risk of developing sarcopenia. Despite this known risk, the impact of sarcopenia on the long-term prognosis of lung cancer patients, specifically concerning progression-free survival (PFS) and overall survival (OS), remains unclear. The primary objective of our study was to examine the correlation between metabolic parameters derived from 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) and sarcopenia, as well as the prognostic value of sarcopenia in patients with surgically resected early-stage non-small cell lung cancer (NSCLC). In this retrospective cross-sectional study, we analyzed 187 NSCLC patients who underwent 18F-FDG PET/CT at the First Affiliated Hospital of Soochow University between March 2019 and October 2023. Patients were divided into two groups based on the presence (n=46) or absence (n=141) of sarcopenia. The correlation between sarcopenia, metabolic parameters, and patient characteristics was evaluated using chi-square and Mann-Whitney U tests. Survival analyses, including PFS and OS, were conducted using Kaplan-Meier analysis and Cox proportional hazards regression. Based on sarcopenia, metabolic parameters and patient characteristics, patients were classified into high-risk (n=28), intermediate-risk (n=121), and low-risk (n=38) groups. Our analysis identified gender, body mass index (BMI), psoas Hounsfield unit (HU), and maximum standardized uptake value of the psoas major muscle (SUVmax-Muscle) as independent predictors of sarcopenia (P<0.05 for all). A nomogram model, utilizing these parameters, was constructed to predict sarcopenia. Survival analysis further demonstrated that total lesion glycolysis [hazard ratio (HR) =2.499; 95% confidence interval (CI): 2.014-3.267; P=0.016], sarcopenia (HR =3.323; 95% CI: 1.748-6.316; P<0.001), and programmed death ligand-1 (PD-L1) expression (HR =0.093; 95% CI: 0.012-0.698; P=0.021) emerged as independent predictors of OS in early-stage NSCLC. Notably, patients categorized as high-risk, characterized by elevated total lesion glycolysis, presence of sarcopenia, and PD-L1 positivity, exhibited a significantly poorer prognosis compared to the intermediate-risk (P<0.05) and low-risk groups (P<0.05). Our findings indicated an inverse relationship between SUVmax-Muscle or psoas HU with the incidence of sarcopenia in NSCLC patients. Additionally, total lesion glycolysis, sarcopenia, and PD-L1 expression were identified as independent prognostic factors for OS in early-stage NSCLC. The risk stratification model, incorporating total lesion glycolysis, sarcopenia, and PD-L1 expression, assumed a pivotal role in guiding personalized therapy decisions and post-treatment monitoring.

Non-Coding RNA as a Biomarker in Lung Cancer.

Lung cancer remains one of the most prevalent and deadly cancers globally, with high mortality rates largely due to late-stage diagnosis, aggressive progression, and frequent recurrence. Despite advancements in diagnostic techniques and therapeutic interventions, the overall prognosis for lung cancer patients continues to be dismal. Emerging research has identified non-coding RNAs (ncRNAs), including microRNAs, long non-coding RNAs, and circular RNAs, as critical regulators of gene expression, significantly influencing cancer biology. These ncRNAs play pivotal roles in various aspects of lung cancer pathogenesis, including tumor initiation, progression, metastasis, and resistance to therapy. We provide a comprehensive analysis of the current understanding of ncRNAs in lung cancer, emphasizing their potential as biomarkers for early diagnosis, prognostication, and the prediction of the therapeutic response. We explore the biological functions of ncRNAs, their involvement in key oncogenic pathways, and the molecular mechanisms by which they modulate gene expression and cellular processes in lung cancer. Furthermore, this review highlights recent advances in ncRNA-based diagnostic tools and therapeutic strategies, such as miRNA mimics and inhibitors, lncRNA-targeted therapies, and circRNA-modulating approaches, offering promising avenues for personalized medicine. Finally, we discuss the challenges and future directions in ncRNA research, including the need for large-scale validation studies and the development of efficient delivery systems for ncRNA-based therapies. This review underscores the potential of ncRNAs to revolutionize lung cancer management by providing novel diagnostic and therapeutic options that could improve patient outcomes.

High RNF7 expression enhances PD-1 resistance of non-small cell lung cancer cells by promoting CXCL1 expression and myeloid-derived suppressor cell recruitment via activating NF-κB signaling

To investigate the mechanism of RNF7 for regulating myeloid-derived suppressor cells (MDSCs) in nonsmall cell lung cancer (NSCLC). TIMER2.0 database and immunohistochemistry were used to analyze RNF7 expression level and its correlation with immune cell infiltration in non-small cell lung cancer. The impact of RNF7 expression levels on prognosis of lung cancer patients was analyzed using Kaplan-Meier survival analysis. CMT-167 cells with RNF7 overexpression or knockdown were inoculated subcutaneously in C57BL/6 mice, and the mice in RNF7 knockdown group were treated with anti-PD-1 or IgG isotype control 7 days after the inoculation. The tumor tissues were harvested after 30 days for tumor volume measurement, detection of S100A8+A9 and Gr-1 expressions with immunohistochemistry, and analysis of MDSC infiltration. Gene set enrichment analysis (GSEA) was performed to identify the potential pathways regulated by RNF7 in NSCLC. Western blotting and luciferase assays were used to assess the impact of RNF7 on the NF-κB signaling pathway. ELISA and RT-qPCR were used to measure chemokine (C-X-C motif) ligand 1 (CXCL1) expression. RNF7 expression was significantly upregulated in NSCLC, and high RNF7 expression levels were associated with poor prognosis of the patients (P < 0.001). TIMER2.0 analysis revealed a positive correlation between RNF7 expression and MDSC infiltration (P < 0.001). GSEA suggested that RNF7 was enriched in the NF-κB signaling pathway. In NSCLC cells, RNF7 knockdown significantly inhibited NF-κB activation and reduced CXCL1 expression. In the tumor-bearing mice, RNF7 overexpression significantly increased MDSC infiltration in the tumor tissue, and RNF7 knockdown obviously reduced MDSC infiltration and enhanced the efficacy of anti-PD-1 therapy. High expression of RNF7 in NSCLC cells promotes CXCL1 expression by activating the NF-κB signaling pathway, thus leading to the chemotactic recruitment of MDSCs, which contributes to tumor resistance to antiPD-1 therapy.

Single G-quadruplex-based fluorescence method for the uracil-DNA glycosylase inhibitor screening

Uracil-DNA glycosylase (UDG) plays a pivotal role in the base repair system. Through bioinformatics, we found that the expression of the UDG enzyme in many cancer cells is increased, and its high expression is not conducive to the prognosis of lung cancer patients. The development of analytical techniques for the quantification of UDG activity and the identification of UDG inhibitors is of paramount importance. We found that when the T base in the G4 loop region mutated to uracil, the G4 structure was not disrupted and still retained the characteristics of a G4 structure (emitting strong fluorescence after binding with ThT (Thioflavin T). Inspired by this phenomenon, we developed a detection method for UDG and its inhibitors utilizing a single DNA strand engineered to form a G-quadruplex structure, containing uracil residues within the loop region, designated as G4-dU. The inclusion of uracil-DNA glycosylase (UDG) in the assay environment induces the removal of uracil, resulting in the formation of apurinic sites (AP) within the G4-dU sequence. Subsequent thermal denaturation leads to strand cleavage at AP sites, precluding the reformation of the G-quadruplex configuration and abrogating fluorescence emission. The detection process in this study can be completed in only 30 min to 1 h, offers a straightforward, expedient, and efficacious modality for assessing UDG activity and UDG inhibitor potency, thereby facilitating the discovery of novel therapeutic agents for cancer treatment.

The Role of ADCY1 in Regulating the Sensitivity of Platinum-Based Chemotherapy in NSCLC.

Lung cancer has the highest fatality rate among malignant tumors in the world. Finding new biomarkers of drug resistance is of great importance in the prognosis of lung cancer patients. We found that the polymorphisms of Adenylate Cyclase 1 (ADCY1) are significantly associated with platinum-based chemotherapy resistance in lung cancer patients in our previous research. In this study, we wanted to identify the mechanism of ADCY1 affecting platinum resistance. We used an MTT assay to find if the expression of ADCY1 is associated with the sensitivity of cisplatin in A549, H1299, and A549-DDP cells. Then, we performed CCK-8 tests to detect the absorbance of these cells stimulated by ADCY1, which can discover the cell proliferation that is affected by ADCY1. We investigated cell apoptosis and cell cycles regulated by ADCY1 through the flow cytometry assay. RNA sequencing was used to find the downstream genes affected by ADCY1 which may be associated with drug resistance in lung cancer patients. ADCY1 has higher expression in lung cancer cells than in normal cells. ADCY1 can affect cisplatin resistance in lung cancer cells by regulating cell proliferation, cell apoptosis, and the cell cycle. It may control cell apoptosis by regulating the classical apoptosis biomarkers Bax and Bcl2. Our study showed that ADCY1 may be a new biomarker in the prognosis of lung cancer patients. Much work remains to be carried out to clarify the mechanism in this important emerging field.

Chinese expert consensus on diagnosis and treatment of pulmonary nodules(2024)

Lung cancer is the leading cause of the incidence and mortality of malignant tumors in China. The 5-year survival rate released for China in 2018 was 19.7%. The 5-year survival rate for stage Ⅰ patients is 77%-92%. Early diagnosis and treatment of lung cancer are key to improving the 5-year overall survival rate and prognosis of lung cancer patients. Therefore, experts from the Academic Group of Lung Cancer in Chinese Thoracic Society and Chinese Alliance Against Lung Cancer Expert Group formulated the Chinese Expert Consensus on the Diagnosis and Treatment of Lung Nodules in 2015 to standardize the diagnosis and treatment of lung nodules. In 2018, this consensus was updated to formulate the Chinese Expert Consensus on Diagnosis and Treatment of Lung Nodules (2018 edition), and widely applied in multiple branch centers of Chinese Alliance Against Lung Cancer, proposing the Intelligent Treatment of Million Early Lung Cancer Project. Based on applied experience of the expert consensus in recent years, with reference to the latest evidence has been updated, Chinese Expert Consensus on Diagnosis and Treatment of Lung Nodules (2024 edition) was formulated. The updated content of this consensus mainly includes the following aspects: (1) Define the screening age of high-risk lung cancer populations in China based on the national conditions; (2) Propose definition of "difficult-to-determine pulmonary nodules" to avoid delaying the diagnosis and treatment; (3) Evaluate pulmonary nodules assisted by artificial intelligence (AI) imaging-assisted diagnostic system and propose human-machine MDT to avoid the limitations of AI; (4) Evaluate pulmonary nodules by routine and individualized evaluations for different populations, and make recommendations based on evidence-based management guidelines for different types and sizes of pulmonary nodules. In the updated consensus, 18 consensus points were recommended as a reference for clinical management of pulmonary nodules to improve the 5-year overall survival rate and the prognosis of lung cancer in China.

A non-enhanced CT-based deep learning diagnostic system for COVID-19 infection at high risk among lung cancer patients.

Pneumonia and lung cancer have a mutually reinforcing relationship. Lung cancer patients are prone to contracting COVID-19, with poorer prognoses. Additionally, COVID-19 infection can impact anticancer treatments for lung cancer patients. Developing an early diagnostic system for COVID-19 pneumonia can help improve the prognosis of lung cancer patients with COVID-19 infection. This study proposes a neural network for COVID-19 diagnosis based on non-enhanced CT scans, consisting of two 3D convolutional neural networks (CNN) connected in series to form two diagnostic modules. The first diagnostic module classifies COVID-19 pneumonia patients from other pneumonia patients, while the second diagnostic module distinguishes severe COVID-19 patients from ordinary COVID-19 patients. We also analyzed the correlation between the deep learning features of the two diagnostic modules and various laboratory parameters, including KL-6. The first diagnostic module achieved an accuracy of 0.9669 on the training set and 0.8884 on the test set, while the second diagnostic module achieved an accuracy of 0.9722 on the training set and 0.9184 on the test set. Strong correlation was observed between the deep learning parameters of the second diagnostic module and KL-6. Our neural network can differentiate between COVID-19 pneumonia and other pneumonias on CT images, while also distinguishing between ordinary COVID-19 patients and those with white lung. Patients with white lung in COVID-19 have greater alveolar damage compared to ordinary COVID-19 patients, and our deep learning features can serve as an imaging biomarker.

Homologous recombination deficiency status predicts response to immunotherapy-based treatment in non-small cell lung cancer patients.

Homologous recombination deficiency (HRD) is a biomarker that predicts response to ovarian cancer treatment with poly (ADP-ribose) polymerase (PARP) inhibitors or breast cancer treatment with first-line platinum-based chemotherapy. However, there are few studies on the prognosis of lung cancer patients treated with immune checkpoint inhibitor (ICI) therapy using HRD as a biomarker. We studied the relationship between HRD status and the effectiveness of first-line ICI-based therapy in EGFR/ALK wild-type metastatic non-small cell lung cancer patients (NSCLC) patients. This study included 22 treatment naïve NSCLC patients. The HRD score ranged from -26.37 to 92.34, with an average of 24.57. Based on analysis of the progression-free survival (PFS) data from the included NSCLC patients, threshold traversal was carried out. HRD (+) was defined as an HRD score of 31 or higher. Kaplan-Meier PFS survival analysis showed prolonged median PFS (mPFS) in NSCLC patients with HRD (+) versus HRD (-) (N/A vs. 7.0 ms, log-rank p = 0.029; HR 0.20, 95% CI: 0.04-0.96, likelihood-ratio p = 0.03). In patients with PD-L1 TPS ≥50% and HRD score ≥31 (co-status high), the mPFS was temporarily not reached during the follow-up period. In patients with PD-L1 TPS <1% and HRD score <31, the mPFS was 3 ms. Cox regression analysis showed that the hazard ratio of the co-status was 0.14 (95% CI: 0.04-0.54), which was a good prognostic factor, and the prognostic effect of co-status was better than that of HRD score alone. The HRD status can be identified as an independent significance in NSCLC patients treated with first-line ICI-based therapy.

Investigate the relationship between Bacillus coagulans and its inhibition of chemotherapy-induced lung cancer resistance.

Lung cancer is a leading cause of death globally, with lung adenocarcinoma being the most common subtype. Despite advancements in targeted therapy, drug resistance remains a major challenge. This study investigated the impact of Bacillus coagulans on drug resistance in lung adenocarcinoma cells. The cells were pretreated with B. coagulans culture filtrate (BCCF), and functional assays were performed, including cell proliferation, cell cycle, apoptosis, and immunofluorescence staining. Results showed that BCCF induced cell cycle arrest at the S phase, reducing cell proliferation and suppressing drug resistance marker P-glycoprotein expression in BCCF-treated resistant cells rather than BCCF-treated control cells. Moreover, drug-resistant cells exhibited the ability for epithelial-mesenchymal transition, which could contribute to their necrosis through the iron-mediated cell death pathway upon BCCF treatment. Proteomic analysis identified downregulation of DNA mismatch repair protein PMS2 after BCCF treatment. These findings suggest that B. coagulans may modulate the DNA repair pathway, influencing drug resistance in lung adenocarcinoma cells. In conclusion, this study highlights the potential impact of B. coagulans on drug-resistant lung adenocarcinoma cells. Further investigation and understanding of the regulatory mechanisms by which B. coagulans modulates drug resistance in lung adenocarcinoma can aid in the development of more effective treatment strategies to improve the prognosis of lung cancer patients.

PRRX1-OLR1 axis supports CAFs-mediated lung cancer progression and immune suppression

ObjectiveTo investigate the mechanism by which cancer-associated fibroblasts (CAFs) affect the growth and immune evasion of lung cancer cells.MethodsInitially, datasets comparing CAFs with normal fibroblasts were downloaded from the GEO dataset GSE48397. Genes with the most significant differential expression were selected and validated using clinical data. Subsequently, CAFs were isolated, and the selected genes were knocked down in CAFs. Co-culture experiments were conducted with H1299 or A549 cells to analyze changes in lung cancer cell growth, migration, and immune evasion in vitro and in vivo. To further elucidate the upstream regulatory mechanism, relevant ChIP-seq data were downloaded from the GEO database, and the regulatory relationships were validated through ChIP-qPCR and luciferase reporter assays.ResultsOLR1 was significantly overexpressed in CAFs and strongly correlated with adverse prognosis in lung cancer patients. Knockdown of OLR1 markedly inhibited CAFs’ support for the growth and immune evasion of lung cancer cells in vitro and in vivo. ChIP-seq results demonstrated that PRRX1 can promote OLR1 expression by recruiting H3K27ac and H3K4me3, thereby activating CAFs. Knockdown of PRRX1 significantly inhibited CAFs’ function, while further overexpression of OLR1 restored CAFs’ support for lung cancer cell growth, migration, and immune evasion.ConclusionPRRX1 promotes OLR1 expression by recruiting H3K27ac and H3K4me3, activating CAFs, and thereby promoting the growth, migration, and immune evasion of lung cancer cells.

How General and Inflammatory Status Impacts on the Prognosis of Patients Affected by Lung Cancer: State of the Art.

Pulmonary cancer is often associated with systemic inflammation and poor nutritional status and these two aspects are strongly correlated and related to the scarce infiltration of a tumor by immune cells. We reviewed all English literature reviews from 2000 to 2024 from PubMed, Scopus and Google Scholar, including original articles, review articles, and metanalyses. We excluded non-English language articles and case reports/case series. Generally speaking, nutritional and inflammatory status largely affect medium and long-term prognosis in lung cancer patients. A correct stratification of patients could improve their preoperative general functional nutritional and inflammatory status, minimizing, therefore, possible treatment complications and improving long-term prognosis.

Unveiling the landscape of pathomics in personalized immunotherapy for lung cancer: a bibliometric analysis.

Pathomics has emerged as a promising biomarker that could facilitate personalized immunotherapy in lung cancer. It is essential to elucidate the global research trends and emerging prospects in this domain. The annual distribution, journals, authors, countries, institutions, and keywords of articles published between 2018 and 2023 were visualized and analyzed using CiteSpace and other bibliometric tools. A total of 109 relevant articles or reviews were included, demonstrating an overall upward trend; The terms "deep learning", "tumor microenvironment", "biomarkers", "image analysis", "immunotherapy", and "survival prediction", etc. are hot keywords in this field. In future research endeavors, advanced methodologies involving artificial intelligence and pathomics will be deployed for the digital analysis of tumor tissues and the tumor microenvironment in lung cancer patients, leveraging histopathological tissue sections. Through the integration of comprehensive multi-omics data, this strategy aims to enhance the depth of assessment, characterization, and understanding of the tumor microenvironment, thereby elucidating a broader spectrum of tumor features. Consequently, the development of a multimodal fusion model will ensue, enabling precise evaluation of personalized immunotherapy efficacy and prognosis for lung cancer patients, potentially establishing a pivotal frontier in this domain of investigation.

AMPK activation reduces cancer cell aggressiveness via inhibition of monoamine oxidase A (MAO-A) expression/activity

AimAMPK can be considered as an important target molecule for cancer for its unique ability to directly recognize cellular energy status. The main aim of this study is to explore the role of different AMPK activators in managing cancer cell aggressiveness and to understand the mechanistic details behind the process. Main methodsFirst, we explored the AMPK expression pattern and its significance in different subtypes of lung cancer by accessing the TCGA data sets for LUNG, LUAD and LUSC patients and then established the correlation between AMPK expression pattern and overall survival of lung cancer patients using Kaplan-Meire plot. We further carried out several cell-based assays by employing different wet lab techniques including RT-PCR, Western Blot, proliferation, migration and invasion assays to fulfil the aim of the study. Key findings•Expression of AMPK is correlated with survival and prognosis of lung cancer patients.•AMPK activators like Metformin and Phenformin downregulate A549 and HCT-116 cell proliferation and migration via repression of p38MAPK activity, subsequent augmentation of R1 repressor and corresponding downregulation of MAO-A expression/activity resulting reduction in the intracellular ROS.•SRT-1720 directly activates AMPK in LKB1 mutant A549 cells either alone or in combination with Metformin resulting regulation of cancer cell aggressiveness. SignificanceThis study identifies the importance of AMPK activators as a repurposing agent for combating lung and colon cancer cell aggressiveness. It also suggests SRT-1720 as a potent repurposing agent for cancer treatment especially in NSCLC patients where a point mutation is present in LKB1.

Mutant TP53 promotes invasion of lung cancer cells by regulating desmoglein 3

PurposeTargeted therapies have markedly improved the prognosis of lung cancer patients; nevertheless, challenges persist, including limited beneficiary populations and the emergence of drug resistance. This study investigates the molecular mechanisms of mutant TP53 in lung cancer, aiming to contribute to novel strategies for targeted therapy.MethodsThe TCGA database was employed to delineate the mutational landscape of TP53 in lung cancer patients. Differential gene expression between TP53-mutant and wild-type patients was analyzed, followed by functional enrichment. DSG3 protein expression in lung cancer patients was assessed using IHC, and its impact on prognosis was analyzed in the TCGA database. The influence of TP53 on the downstream gene DSG3 was investigated using qPCR, ChIP-qPCR, and luciferase reporter gene assays. Protein enrichment in the DSG3 promoter region was examined through IP-MS, and the regulatory role of the HIF1-α/TP53 complex on DSG3 was explored using Co-IP, luciferase assays, and ChIP-qPCR. Molecular interactions between TP53 (R273H) and HIF1-α were detected through immunoprecipitation and molecular docking. The effects and mechanisms of DSG3 on lung cancer phenotypes were assessed through WB, transwell, and wound healing assays.ResultsTP53 mutations were present in 47.44% of patients, predominantly as missense mutations. DSG3 exhibited high expression in TP53-mutant lung cancer patients, and this elevated expression correlated with a poorer prognosis. TP53 interference led to a reduction in DSG3 mRNA expression, with TP53 mutant P53 enriching at the P2 site of the DSG3 promoter region, a recruitment facilitated by HIF1-α. The DBD region of TP53 (R273H) demonstrated interaction with HIF1-α. DSG3, activated through Ezrin phosphorylation, played a role in promoting invasion and metastasis.ConclusionsMutant TP53 facilitates lung cancer cell invasion by modulating desmoglein 3.Graphical abstractThe regulation of TP53 on DSG3 in lung cancer cell

Analysis of clinical characteristics and prognosis of lung cancer patients with CPFE or COPD: a retrospective study

BackgroundLung cancer (LC) commonly occurs in patients with combined pulmonary fibrosis and emphysema (CPFE) and chronic obstructive pulmonary disease (COPD), but comparative research is limited. This study examines clinical characteristics, treatments, and prognosis in LC patients with CPFE or COPD.MethodsThe retrospective study involved 75 lung cancer patients with CPFE and 182 with COPD. It analyzed clinical features, tumor pathology, pulmonary function, laboratory parameters, and treatment responses.ResultsNotable differences were found between the CPFE + LC and COPD + LC groups. Both groups were mostly elderly, male smokers. The CPFE + LC group had higher BMI and more adenocarcinoma and squamous cell carcinoma, while COPD + LC had predominantly squamous cell carcinoma. CPFE + LC tumors were mostly in the lower lobes; COPD + LC’s were in the upper lobes. The CPFE + LC group showed higher tumor metastasis rates, more paraseptal emphysema, and elevated levels of TG, CEA, NSE, and Killer T Cells. In advanced stages (IIIB-IV), the CPFE + LC group receiving first-line treatment had shorter median progression-free survival (PFS) and a higher risk of progression or death than the COPD + LC group, regardless of whether it was non-small cell lung cancer (NSCLC) or small cell lung cancer (SCLC). No significant PFS difference was found within CPFE + LC between chemotherapy and immunotherapy, nor in immune-related adverse events between groups, with interstitial pneumonia being common.ConclusionThis study emphasizes distinct lung cancer characteristics in CPFE or COPD patients, highlighting the need for tailored diagnostic and treatment approaches. It advocates for further research to improve care for this high-risk group.

Ferroptosis: emerging roles in lung cancer and potential implications in biological compounds.

Lung cancer has high metastasis and drug resistance. The prognosis of lung cancer patients is poor and the patients' survival chances are easily neglected. Ferroptosis is a programmed cell death proposed in 2012, which differs from apoptosis, necrosis and autophagy. Ferroptosis is a novel type of regulated cell death which is driven by iron-dependent lipid peroxidation and subsequent plasma membrane ruptures. It has broad prospects in the field of tumor disease treatment. At present, multiple studies have shown that biological compounds can induce ferroptosis in lung cancer cells, which exhibits significant anti-cancer effects, and they have the advantages in high safety, minimal side effects, and less possibility to drug resistance. In this review, we summarize the biological compounds used for the treatment of lung cancer by focusing on ferroptosis and its mechanism. In addition, we systematically review the current research status of combining nanotechnology with biological compounds for tumor treatment, shed new light for targeting ferroptosis pathways and applying biological compounds-based therapies.

Exploring Synergistic Interactions between Natural Compounds and Conventional Chemotherapeutic Drugs in Preclinical Models of Lung Cancer.

In the current work, the synergy between natural compounds and conventional chemotherapeutic drugs is comprehensively reviewed in light of current preclinical research findings. The prognosis for lung cancer patients is poor, with a 5-year survival rate of 18.1%. The use of natural compounds in combination with conventional chemotherapeutic drugs has gained significant attention as a potential novel approach in the treatment of lung cancer. The present work highlights the importance of finding more effective therapies to increase survival rates. Chemotherapy is a primary treatment option for lung cancer but it has limitations such as reduced effectiveness because cancer cells become resistant. Natural compounds isolated from medicinal plants have shown promising anticancer or chemopreventive properties and their synergistic effect has been observed when combined with conventional therapies. The combined use of an anti-cancer drug and a natural compound exhibits synergistic effects, enhancing overall therapeutic actions against cancer cells. In conclusion, this work provides an overview of the latest preclinical research on medicinal plants and plant-derived compounds as alternative or complementary treatment options for lung cancer chemotherapy and discusses the potential of natural compounds in treating lung cancer with minimal side effects.

Association of preexisting anti-thyroid antibodies and body mass index with prognosis of lung cancer patients treated with PD-1/PD-L1 inhibitors

Abstract Objectives Immune checkpoint inhibitors are a new beneficial medication in the treatment of cancer. Whether preexisting TPOAb was related to longer overall survival (OS) is controversial. This retrospective study analyzed the OS and progression-free survival (PFS) of patients with lung cancer, and explored predictive factors associated with the efficacy of PD-1/PD-L1 inhibitors treatment. Methods Patients with lung cancer who were hospitalized in the First Affiliated Hospital of Wenzhou Medical University between January 1, 2020 and December 30, 2020 were enrolled. Thyroid function, TPOAb, TGAb, and prognostic nutritional index levels and body mass index were analyzed. Supervising physicians independently assessed patient staging, OS, and PFS. Demographic data, pathological type, and previous treatment history were also collected. Results In total, this study enrolled 69 patients, with ages of 46–80 years old. Patients with lower weight showed reduced OS and PFS rates relative to those with normal weight and overweight (p&lt;0.05). The single patient with large cell neuroendocrine carcinoma (LCNEC) exhibited a 1-, 1.5- and 2-year OS rate lower than that of the patients diagnosed with squamous cell carcinoma, small cell lung cancer, or adenocarcinoma (p&lt;0.05). This LCNEC patient also had lower 1-, 1.5-, and 2-year PFS rates compared to adenocarcinoma patients (p&lt;0.05). TPOAb and TGAb levels were unrelated to OS or PFS. Multivariate Cox regression analyses revealed a positive association between body mass index, OS, and PFS. Conclusions Patients with lower body weight were predictive of poorer survival outcomes when receiving PD-1/PD-L1 inhibitors treatment as compared to patients with normal weight and overweight. However, positive baseline TGAb and TPOAb levels were not associated with increased OS or PFS in patients with lung cancer.

Research Progress of the Effect of Mediterranean Diet on the Correlation of Lung Cancer

Lung cancer is one of the top 10 causes of death in the world today, and it is a great concern worldwide for its high mortality rate. Currently, the researchers are digging into various factors influencing the occurrence and development of lung cancer in order to increase the odds for curing lung cancer, improve the prognosis of lung cancer patients as well as reduce its morbidity. The Mediterranean diet (MD) is a special dietary structure that is based on eating vegetables, fruits, coarse grains, legumes and low-fat fish, which have anti-inflammatory, antioxidant and lipid-lowering effects. Recent studies have revealed that the MD may prevent lung cancer occurrence to some extent and inhibit its development. The purpose of this paper is to summarize and analytically discuss the effects of the MD on the oncogenesis and development of lung cancer through a review of the relevant literatures, thus to provide references for MD to prevent and treat lung cancer. .