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Objective To explore the gene mutation characteristics and the relationship between gene mutations and long-term prognosis in clinical stage Ⅰ A lung adenocarcinoma patients. Methods A retrospective analysis was conducted on 63 clinical stage Ⅰ A lung adenocarcinoma patients who underwent surgical resection at the Cancer Hospital of the Chinese Academy of Medical Sciences from January 2007 to October 2012, with documented postoperative recurrence or metastasis, as well as those who had a follow-up duration of 10 years or more without recurrence or metastasis. Whole exome sequencing (WES) technology was used to analyze the gene mutation profiles in tumor tissues and univariate and multivariate Cox regression analysis were used to clarify the influencing factors for patient prognosis. Results After long term follow-up, 13 out of the 63 patients (21%) experienced recurrence or metastasis. WES technology analysis revealed that the most common tumor related gene mutations occurred in epidermal growth factor receptor (EGFR), with a mutation rate of 65.1% (41/63), followed by tumor protein p53 (TP53), fatatypical cadherin 1 (FAT1), low density lipoprotein receptor-related protein 1B (LRP1B), mechanistic target of rapamycin (MTOR), phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit gamma (PIK3CG), and SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4 (SMARCA4), with mutation rates of 30.2% (19/63), 20.6% (13/63), 15.9% (10/63), 15.9% (10/63), 15.9% (10/63), and 15.9% (10/63), respectively. Multivariate Cox regression analysis showed that PIK3CG mutations (HR=21.52, 95% CI: 3.19-145.01), smoothened (SMO) mutations (HR=35.28, 95% CI: 3.12-398.39), catenin beta 1 (CTNNB1) mutations (HR= 332.86, 95% CI: 15.76-7 029.05), colony stimulating factor 1 receptor (CSF1R) mutations (HR= 8 109.60, 95% CI: 114.19-575 955.17), and v-Raf murine sarcoma viral oncogene homolog B (BRAF) mutations (HR=23.65, 95% CI: 1.86-300.43) were independent risk factors affecting the prognosis of clinical stage Ⅰ A lung adenocarcinoma patients. Conclusions PIK3CG, SMO, CTNNB1, CSF1R, BRAF gene mutations are closely related to long-term recurrence or metastasis in clinical stage ⅠA lung adenocarcinoma. Patients with these gene mutations should be given closer clinical attention. [ABSTRACT FROM AUTHOR]

Objective: The study aimed to develop and evaluate a clinical diagnostic model that combined computer tomography (CT) radiomic features with a nomogram for predicting invasiveness in subsolid pulmonary nodules. Methods: This retrospective study analyzed both clinical and imaging data from patients at our institution who were diagnosed with pathologically confirmed subsolid pulmonary nodules at our institution based on thin-slice CT images. Radiomic features were extracted from these CT images, and LASSO regression with K-fold cross-validation was used to select the most informative features. Three predictive models were constructed via multivariate logistic regression: the first incorporated clinical parameters and conventional imaging features; the second relied solely on radiomic characteristics; and the third was a hybrid clinical-radiomics model. The logistic regression results were visually represented using a nomogram. Receiver operating characteristic curves were utilized to compare the classification predictive performance of the three models for distinguishing ground-glass opacity lung adenocarcinoma IA and non-IA cases. Decision curve analysis (DCA) was employed to assess the clinical utility of these models across different cohorts. Results: A total of 204 subsolid pulmonary nodules from 192 patients were included. They were divided into invasive (n=114) and non-invasive groups (n=90) based on pathological typing. These nodules were divided into a training set (n=143, IA:non-IA 77∶66) and a test set (n=61, IA:non-IA 38∶23). A total of 1316 features were initially extracted from each subsolid nodule. Subsequently, two independent clinical predictors (mean CT value and maximum diameter) and three radiomic features were selected through feature selection and logistic regression for model building. The combined clinical-radiomics model demonstrated superior discriminative capability (AUC=0.920, 95%CI: 0.818~0.931) in distinguishing IA from non-IA within the training set compared to the radiomics model and the clinical model independently (AUC=0.907, 95%CI: 0.792~0.914; AUC=0.822, 95%CI: 0.764~0.895). In the test set, the inclusion of clinical data improved the diagnostic efficacy of the radiomics model. DCA demonstrated that the combined model generally provided greater clinical benefits in most scenarios. Conclusion: The developed clinical-radiomics joint model showed promising performance in predicting the subsolid pulmonary nodule invasiveness.

Early diagnosis of anal canal cancer is important because the degree of progression greatly affects prognosis and quality of life. We reviewed the current status and problems of definitive diagnosis in 47 cases of malignant tumors of the anal canal diagnosed at our hospitals. The chief complaints were bleeding in 21 cases, anal pain in 20, tumor in 17, disordered defecation in 4, abdominal symptoms in 3, and itching in 2. The duration from symptom onset to consultation was 6 months or longer in 16 cases. Histological diagnoses included adenocarcinoma in 22 cases, squamous cell carcinoma in 18, basal cell carcinoma in 2, malignant melanoma in 2, and endocrine cell carcinoma, Paget􀁠s disease and malignant lymphoma in 1 each. Definitive diagnosis was made by digital examination in 24 cases, endoscopy in 10, examination under anesthesia in 9, and pathology of surgical specimens in 4. Eight cases required more than 1 month for definitive diagnosis. By histological type, most adenocarcinomas were mass lesions with ulceration and could be diagnosed by digital examination at the first visit. On the other hand, squamous cell carcinoma presented a variety of macroscopic findings and definitive diagnosis tended to be delayed. For early diagnosis of malignant tumors of the anal canal, anorectal examination should always be performed with the possibility of malignant disease in mind. In addition, aggressive tissue biopsy, endoscopy and examination under anesthesia should be considered in case of atypical findings. [ABSTRACT FROM AUTHOR]

Lung cancer is the malignant tumor with the highest incidence and mortality rate worldwide. For lung adenocarcinoma, identifying specific gene mutations, fusions, and giving corresponding targeted drugs can greatly improve the survival time of the patients. Among them, anaplastic lymphoma kinase (ALK) fusion occurs in 3%-7% of non-small cell lung cancer (NSCLC). In clinical practice, a variety of detection methods can be used to determine the ALK fusion status, but false negative test results are possible. This paper retrospectively analyzed the diagnosis and treatment of a patient with lung adenocarcinoma, judged the ALK fusion status by various detection methods. Among them, immunohistochemistry (IHC)(Ventana D5F3), RNA based next-generation sequencing (RNA-based NGS) confirmed positive echinoderm microtubule associated protein like 4 (EML4)-ALK fusion, while DNA-based NGS was negative. This paper analyzed the detection methods of ALK fusion, in order to clarify which detection method is the most accurate and simple to choose in different clinical cases and guide the subsequent treatment. [ABSTRACT FROM AUTHOR]

Background and purpose: Lung adenocarcinoma has the characteristics of difficult early detection, rapid tumor progression and low surgical resection rate. Although studies on immunotherapy alone and immunotherapy combined with chemotherapy have shown initial success in improving prognosis and overcoming drug resistance, the majority of lung adenocarcinoma patients still receive limited benefits. Therefore, there is an urgent need to identify novel biomarkers with relatively high sensitivity and specificity to improve the prognosis of lung adenocarcinoma. Cell division cycle protein 20 (CDC20) is involved in the occurrence and development of various tumors, but its biological role and mechanism in lung adenocarcinoma remain unclear. The aim of this study was to investigate the expression of CDC20 in lung adenocarcinoma and its predictive value for the prognosis of patients with lung adenocarcinoma, and to further explore the effects of CDC20 on the proliferation and invasion capabilities of lung adenocarcinoma cells. Methods: Utilizing immunohistochemistry (IHC) to detect the expression of CDC20 in lung adenocarcinoma tissues, we analyzed its correlation with poor prognosis in combination with bioinformatics and clinicopathological parameters. Kaplan-Meier survival curves were employed to illustrate the impact of CDC20 on postoperative survival rates in lung adenocarcinoma patients. COX multivariate regression analysis was conducted to identify independent prognostic factors influencing postoperative survival rates. Additionally, receiver operating characteristic (ROC) curves were applied to assess the diagnostic value of CDC20 expression in lung adenocarcinoma patients. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) and Western blot were used to measure the expression levels of CDC20 in normal human lung epithelial cells (BEAS-2B) and human lung adenocarcinoma cells (A549 and H1299). In cellular experiments, CDC20 was knocked down in lung adenocarcinoma cells, which were divided into three groups: si-NC (control group), si-CDC20#1 (knockdown group 1) and si-CDC20#2 (knockdown group 2). Cell counting kit-8 (CCK-8), colony formation, transwell and wound healing assays were conducted to assess cell proliferation, migration and invasion capabilities. Functional enrichment analysis using Geng Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways was conducted to explore the biological roles of CDC20 in lung adenocarcinoma. Finally, gene set enrichment analysis (GSEA) was employed to investigate potential regulatory pathways of CDC20 in lung adenocarcinoma. This study was approved by the Ethics Committee of Hebei Chest Hospital (Number: 2022051). Results: The results of both bioinformatics analysis and IHC demonstrated a significantly high expression of CDC20 in lung adenocarcinoma tissues (P 0.05). Both bioinformatics analysis and clinical parameter evaluation revealed a correlation between high CDC20 expression and poor patient prognosis. Kaplan-Meier survival analysis and COX regression analysis consistently indicated a significant negative correlation between CDC20 expression and postoperative survival rates in patients (P0.05). Additionally, the expression levels of CDC20 were higher in human lung adenocarcinoma cell lines A549 and H1299 compared with BEAS-2B (P0.05). Knockdown of CDC20 effectively inhibited the proliferation, migration and invasion of lung adenocarcinoma cells (P0.05). The results of GO, KEGG pathways and GSEA consistently pointed to a relationship between CDC20 and cell cycle regulation. Conclusion: CDC20 is highly expressed in lung adenocarcinoma. High expression of CDC20 is an independent risk factor for poor prognosis of lung adenocarcinoma patient. CDC20 can promote the proliferation, migration and invasion of lung adenocarcinoma cells. [ABSTRACT FROM AUTHOR]

Background and objective With further understanding and research into non-small cell lung cancer with tumours ≤2 cm in maximum diameter, segmental lung resection is able to achieve the same long-term prognosis as lobectomy. However, there are few studies on the prognostic effect of wedge resection on small volume invasive lung adenocarcinoma with an invasion depth of 0.5 to 1.0 cm. Therefore, this study focuses on the clinical efficacy and prognosis of wedge resection in patients with small-volume invasive lung adenocarcinoma. Methods A retrospective analysis of the medical records of 208 patients who underwent surgery in the Department of Thoracic Surgery of the Affiliated Provincial Hospital of Anhui Medical University from February 2016 to December 2017 was made, and the postoperative pathological results confirmed small volume invasive lung adenocarcinoma. According to their surgical methods, they were divided into lobectomy group (n=115), segmentectomy group (n=48) and wedge resection group (n=45). Kaplan-Meier survival curve estimation and Cox proportional risk regression model were used to explore the influence of different surgical methods on the prognosis of patients with small volume invasive lung adenocarcinoma. Results The wedge resection group had better perioperative outcomes compared with the segmentectomy group and lobectomy group, with statistically significant differences in intraoperative bleeding (P=0.036), postoperative drainage (P<0.001), operative time (P=0.018), postoperative time with tubes (P=0.001), and postoperative complication rate (P=0.006). There were no significant differences when comparing the three groups in terms of survival rate (lobectomy group vs segmentectomy group, P=0.303; lobectomy group vs wedge resection group, P=0.742; and segmentectomy group vs wedge resection group, P=0.278) and recurrence-free survival rate (lobectomy group vs segmentectomy group, P=0.495; lobectomy group vs wedge resection group, P=0.362; segmentectomy group vs wedge resection group, P=0.775). Univariate and multivariate survival analyses showed that consolidation tumor ratio (CTR) was the prognostic factor of overall survival and revurrence-free survival for patients with small-volume invasive lung adenocarcinoma (P<0.05). Conclusion Wedge resection in patients with small volume invasive lung adenocarcinoma can achieve long-term outcomes similar to segmentectomy and lobectomy. When the CTR≤0.5, wedge resection is preferred in such patients. [ABSTRACT FROM AUTHOR]

Background and objective Lung adenocarcinoma (LUAD) is a highly morbid and fatal cancer. Despite advancements in modern medical treatment, the 5-year survival rate of patients remains suboptimal. Our previous study revealed that zinc finger SWIM-type containing 1 (ZSWIM1), a novel protein, promotes the proliferation, migration, and invasion of LUAD cells. The aim of this study is to investigate the impact of E3 ubiquitin ligase tripartite motif protein 21 (TRIM21) on ZSWIM1-mediated cell proliferation and migration. Methods The interaction and co-localization between TRIM21 and ZSWIM1 were verified using co-immunoprecipitation (Co-IP) and immunofluorescence (IF). The effects of TRIM21 and ZSWIM1 on the proliferation and migration of LUAD cells were assessed through MTT and Transwell assays, respectively. Western blot (WB) analysis was conducted to evaluate the impact of TRIM21 and ZSWIM1 on the expression of epithelial- mesenchymal transition (EMT) markers in LUAD cells. The influence of TRIM21 on the ubiquitination of ZSWIM1 was examined using Co-IP combined with WB. Results TRIM21 was found to interact and co-localize with ZSWIM1. Overexpression of TRIM21 inhibited the proliferation and migration of LUAD cells. Overexpression of TRIM21 reduced the promoting effect of ZSWIM1 on the proliferation, migration, and invasion of lung adenocarcinoma cells, and reversed the impact of ZSWIM1 on the expression of E-cadherin and Vimentin. Conversely, knockdown of TRIM21 further enhanced the promoting effect of ZSWIM1 on the proliferation and migration of LUAD cells. Mechanistically, we observed that overexpression of TRIM21 significantly enhanced the ubiquitination level of ZSWIM1, leading to a decrease in ZSWIM1 protein expression. Conclusion TRIM21 binds to and promotes the ubiquitination of ZSWIM1, resulting in reduced protein expression of ZSWIM1, which leads to the inhibition of ZSWIM1-mediated promotion of proliferation, migration, and invasion in LUAD cells. [ABSTRACT FROM AUTHOR]

Objective: To study, through bioinformatics analysis and cellular biology experiments, the effects of keratin 6A (KRT6A) on the diagnosis, prognosis and immune microenvironment of pancreatic ductal adenocarcinoma (PDAC) and biological behaviors of PDAC PANC1 cells, such as proliferation and apoptosis. Methods: The GEPIA platform was used to integrate the data from the TCGA (The Cancer Genome Atlas) and the GTEx (Genotype-Tissue) to analyze the KTRT6A expression in PDCA tissues. CIBERSORT software was then used to analyze the correlation between KRT6A expression and immune cell infiltration in PDCA tissues, and GSEA analysis was used to study the signaling pathway related to KRT6A gene expression. Immunohistochemical analysis was performed on cancer and adjacent tissue samples from 60 PDAC patients preserved in the Department of Pathology of Changhai Hospital to verify the expression of KRT6A in tumor tissues. The expression of KRT6A gene in PANC1 cells was inhibited by interfering with siRNA. The effects of KRT6A on the proliferation and apoptosis of PDAC cells were detected by CCK-8 assay and flow cytometry. Results: Data analysis of the TCGA and the GTEx found that KRT6A was highly expressed in human PDAC tissues and was significantly correlated with poor survival period of patients (P=0.015). CIBERSORT software and GSEA analysis showed that the infiltration of M2-type macrophages in PDCA tissues with high KRT6A expression was increased (P=0.034), and there was a significant correlation between high KRT6A expression and the up-regulation of Wnt pathway (NES: 1.7359272, P<0.05), pentose phosphate pathway (PPP) (NES: 1.5613053, P<0.05) and other signaling pathways (P<0.05 or P<0.01). Immunohistochemical results further verified the high expression of KRT6A in PDCA tissues (P<0.001). Proliferation and apoptosis experiments showed that interfering with KRT6A gene could significantly inhibit the proliferation (P<0.05) and apoptosis (P<0.001) of PANC1 cells. Conclusion: KRT6A is highly expressed in human PDAC tissues, and knocking down its expression can inhibit the proliferation and apoptosis of PANC1 cells, and has the potential to be a new target for PDAC diagnosis and prognosis. [ABSTRACT FROM AUTHOR]

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Non-small cell lung cancer (NSCLC) is a prevalent tumour type in our country, with lung squamous carcinoma being a commonly observed NSCLC subtype besides lung adenocarcinoma. Epidermal growth factor receptor (EGFR) is a significant driver gene in lung cancer, and EGFR mutation frequency is considerably lower in lung squamous carcinoma in comparison to lung adenocarcinoma. Although targeted therapy against EGFR has demonstrated significant advancements in lung adenocarcinoma, while progress in lung squamous carcinoma has been relatively sluggish. This paper reviews recent studies on molecular targeted therapy for EGFR-mutated lung squamous carcinoma and summarises the efficacy of EGFR-tyrosine kinase inhibitors (TKIs) in treating squamous carcinoma of the lung, in order to provide a reference for treating patients with EGFR-mutated squamous carcinoma of the lung. [ABSTRACT FROM AUTHOR]

Background and objective Cystic lung cancer, a special type of lung cancer, has been paid more and more attention. The most common pathological type of cystic lung cancer is adenocarcinoma. The invasiveness of cystic lung adenocarcinoma is vital for the selection of clinical treatment and prognosis. The aim of this study is to analyze the multiple clinical features of cystic lung adenocarcinoma, explore the independent risk factors of its invasiveness, and establish a risk prediction model. Methods A total of 129 cases of cystic lung adenocarcinoma admitted to the Department of Thoracic Surgery of the First Affiliated Hospital of Nanjing Medical University from January 2021 to July 2022 were retrospectively analyzed and divided into pre-invasive group [atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (AIS) and minimally invasive adenocarcinoma (MIA)] and invasive group [invasive adenocarcinoma (IAC)] according to pathological findings. There were 47 cases in the pre-invasive group, including 19 males and 28 females, with an average age of (51.23±14.96) years. There were 82 cases in the invasive group, including 60 males and 22 females, with an average age of (61.27±11.74) years. Multiple clinical features of the two groups were collected, including baseline data, imaging data and tumor markers. Univariate analysis, LASSO regression and multivariate Logistic regression analysis were used to screen out the independent risk factors of the invasiveness of cystic lung adenocarcinoma, and the risk prediction model was established. Results In univariate analysis, age, gender, smoking history, history of emphysema, neuron-specific enolase (NSE), number of cystic airspaces, lesion diameter, cystic cavity diameter, nodule diameter, solid components diameter, cyst wall nodule, smoothness of cyst wall, shape of cystic airspace, lobulation, short burr sign, pleural retraction, vascular penetration and bronchial penetration were statistically different between the pre-invasive group and invasive groups (P<0.05). The above variables were processed by LASSO regression dimensionality reduction and screened as follows: age, gender, smoking history, NSE, number of cystic airspaces, lesion diameter, cystic cavity diameter, cyst wall nodule, smoothness of cyst wall and lobulation. Then the above variables were included in multivariate Logistic regression analysis. Cyst wall nodule (P=0.035) and lobulation (P=0.001) were found to be independent risk factors for the invasiveness of cystic lung adenocarcinoma (P<0.05). The prediction model was established as follows: P=e^x/(1+e^x), x=-7.927+1.476* cyst wall nodule+2.407* lobulation, and area under the curve (AUC) was 0.950. Conclusion Cyst wall nodule and lobulation are independent risk factors for the invasiveness of cystic lung adenocarcinoma, which have certain guiding significance for the prediction of the invasiveness of cystic lung adenocarcinoma. [ABSTRACT FROM AUTHOR]

Background and objective Bone is a common site for metastasis in lung adenocarcinoma, but the mechanism behind lung adenocarcinoma bone metastasis is still unclear. And currently, there is a lack of easily traceable and stable lung adenocarcinoma bone metastasis cell models, which limits the research on the mechanism of lung adenocarcinoma bone metastasis. The establishment of human lung adenocarcinoma cell line that are highly metastatic to bone, labeled with green fluorescent proteins (GFP) and fireflies luciferase (LUC), along with transcriptomic characterization, would be beneficial for research on lung adenocarcinoma bone metastasis and provide new experimental methods. Methods The human lung adenocarcinoma cell line A549-GFP-LUC was injected into nude mice via the left ventricle to construct a bone metastasis model, and was domesticated in vivo for three consecutive times to obtain the human high bone metastasis lung adenocarcinoma cell line A549-GFP-LUC-BM3; cell counting kit-8 (CCK-8), colony formation assay, scratch wound assays, Transwell assay and Western blot were used to compare the proliferation and invasion abilities of A549-GFP-LUC-BM3 with the parental cells. A549-GFP-LUC-BM3 cells and parental cells were further analyzed by transcriptomic sequencing. Results Human high-bone metastatic lung adenocarcinoma cells A549-GFP-LUC-BM3 was successfully established. Compared to parental cells, this cells exhibited a significantly higher incidence of bone metastasis and enhanced in vitro proliferation, migration, and invasion abilities. Transcriptomic sequencing results revealed that the A549-GFP-LUC-BM3 cell line had 2954 differentially expressed genes compared to the parental cells, with 1021 genes up-regulated and 1933 genes down-regulated. Gene Ontology (GO) functional enrichment analysis indicated that the differentially expressed genes were primarily localized in cellular components such as the cell periphery. The molecular functions identified as significantly enriched included signaling receptor activity, calcium ion binding, and extracellular matrix structural constituent. Additionally, the biological processes found to be enriched were cell adhesion and biological adhesion. The enrichment analysis conducted using the Kyoto Encyclopedia of Genes and Genomes (KEGG) revealed that the differentially expressed genes were primarily involved in the metabolism of xenobiotics by cytochrome P450, retinol metabolism, drug metabolism-cytochrome P450, cell adhesion molecules, steroid hormone biosynthesis, and the nuclear factor kappa B (NF-B) signaling pathway. Conclusion The highly bone-metastatic human lung adenocarcinoma cell line with GFP and luciferase double labeling was successfully established. The biological behavior and transcriptome sequencing of the cell line suggest that it has a high bone-metastatic potential. [ABSTRACT FROM AUTHOR]

Background and objective Tumor microenvironment (TME) is one of the important factors in tumorigenesis and progression, in which tumor-associated macrophages (TAMs) play an important role in non-small cell lung cancer (NSCLC) progression. However, the mechanism of TAMs in NSCLC progression remains unclear, so this study aimed to investigate the role of TAMs in NSCLC progression and to find potential therapeutic targets. Methods Gene Expression Profiling Interactive Analysis (GEPIA) database was used to analyze the expression of prostaglandin E2 receptor 4 (EP4) mRNA in NSCLC and normal lung tissues; the protein expression levels of cyclooxygenase-2 (COX-2), EP4, cluster of differentiation 86 (CD86), CD163 and CD31 were detected by immunohistochemistry (IHC) in 120 NSCLC tissues and 24 paracancerous tissues specimens. The nude mouse lung adenocarcinoma cell A549 and macrophage RAW264.7 co-transplanted tumor model was established. And the samples were collected by gavage with EP4 inhibitor E7046, and then stained with hematoxylin-eosin (HE), IHC, and immunofluorescence (IF), and then detected by Western blot for the epithelial mesenchymal transformation (EMT) of the tumor tissues of the nude mice in each group. Western blot was used to detect the expressions of EMT related protiens in each group of nude mice; full-length transcriptome sequencing was used to screen the key genes causing liver metastasis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was performed. Results EP4 mRNA expression level in NSCLC tissues was generally lower than that in normal lung tissues (P<0.05); COX-2, EP4, CD163, CD31 proteins were differentially expressed in NSCLC tissues and adjacent tissues, and differences were observed in many clinicopathological parameters of NSCLC patients; RAW264.7 shortened the latency period of tumorigenesis of A549 and promoted the proliferation of tumors and liver metastasis of tumors, and E7046 could reduce tumor cell proliferation activity, tumor tissue vascular density and M2-type macrophage infiltration in nude mice; IF staining showed that macrophages were mainly distributed around the metastatic foci of tumors; Western blot results showed that compared with A549 alone transplantation group, the relative expression of E-cadherin protein in tumor tissues of mice in A549 and RAW264.7 co-transplantation group was significantly decreased, and the difference was statistically significant (P<0.05), while the relative expression of N-cadherin protein was up-regulated, but the difference was not statistically significant (P>0.05); the main pathways enriched in the differential genes of the full-length transcriptome were the PI3K-AKT and MAPK signaling pathways. Conclusion During NSCLC development, the COX-2/PGE2/EP4 axis may promote tumor progression by inducing macrophage functional activation, and EP4 may be a potential new target for tumor immunotherapy. This study provides new perspectives and ideas for in-depth exploration of the mechanisms of NSCLC development, as well as a theoretical basis for the development of new therapeutic strategies for NSCLC. [ABSTRACT FROM AUTHOR]

With the continuous innovation of genomics, proteomics and molecular biological detection technology, the treatment of non-small cell lung cancer (NSCLC) has changed from traditional chemotherapy to immunotherapy and targeted therapy. Among them, molecular tumor markers targeting tyrosine kinase pathways play more important roles in clinical practice. For advanced NSCLC patients with positive epidermal growth factor receptor (EGFR) mutations, there are many first-line drugs on the market and they could bring significant efficacy, thus completely subverting the treatment pattern of advanced NSCLC. Common mutations of EGFR in Chinese patients are located on exons 19, 20 and 21, of which exons 19 and 21 mutations are the more common types. Besides, there is also a subtype of EGFR mutations, known as EGFR 20 exon insertion (EGFR 20ins) mutation. The authors summarized the treatment of a lung adenocarcinoma patient with EGFR 20ins mutation accepting Furmonertinib mesylate, in order to provide effective references for clinical diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Intravascular large B-cell lymphoma (IVLBCL) is an aggressive extranodal large B-cell lymphoma, cocurrence in the same organ with other malignancies is very rare, especially in the lung. Here, we report a rare case of lung adenocarcinoma with IVLBCL. The patient was admitted to the hospital due to diarrhea associated with fever and cough. A computed tomography (CT) scan of the chest showed an irregular patchy high-density shadow in the upper lobe of the right lung with ground-glass opacity at the margin. After admission, the patient was given anti-infection treatment, but still had intermittent low fever (up to 37.5 oC). The pathological diagnosis of percutaneous lung biopsy (PLB) was lepidic-predominant adenocarcinoma with local infiltration, which was proved to be invasive nonmucinous adenocarcinoma of the lung with IVLBCL after surgery. This paper analyzed the clinicopathological characteristics and reviewed the relevant literature to improve the knowledge of clinicians and pathologists and avoid missed diagnosis or misdiagnosis. [ABSTRACT FROM AUTHOR]

Fetal adenocarcinoma of the lung (FLAC) is a rare tumor. Due to its different clinicopathological features, biological behavior and clinical outcome, FLAC is classified into low-grade FLAC (L-FLAC) and high-grade FLAC (HFLAC). Most patients with H-FLAC are middle-aged heavy smokers. Here, we describe an extremely rare case of a young male patient who denies smoking and initially presents with a mass on the top of the head and is eventually diagnosed with H-FLAC. The aim of this article is to improve the understanding and awareness of FLAC, and increase the attention to the disease, so as to prevent the underdiagnosis and misdiagnosis of the disease, strengthen early identification and accurate diagnosis, and promote subsequent effective treatment and improve prognosis. [ABSTRACT FROM AUTHOR]

Background and objective The pathological types of lung ground glass nodules (GGNs) show great significance to the clinical treatment. This study was aimed to predict pathological types of GGNs based on computed tomography (CT) quantitative parameters. Methods 389 GGNs confirmed by postoperative pathology were selected, including 138 cases of precursor glandular lesions [atypical adenomatous hyperplasia (AAH) and adenocarcinoma in situ (AIS)], 109 cases of microinvasive adenocarcinoma (MIA) and 142 cases of invasive adenocarcinoma (IAC). The morphological characteristics of nodules were evaluated subjectively by radiologist, as well as artificial intelligence (AI). Results In the subjective CT signs, the maximum diameter of nodule and the frequency of spiculation, lobulation and pleural traction increased from AAH+AIS, MIA to IAC. In the AI quantitative parameters, parameters related to size and CT value, proportion of solid component, energy and entropy increased from AAH+AIS, MIA to IAC. There was no significant difference between AI quantitative parameters and the subjective CT signs for distinguishing the pathological types of GGNs. Conclusion AI quantitative parameters were valuable in distinguishing the pathological types of GGNs. [ABSTRACT FROM AUTHOR]

Background and objective Lung cancer is a leading cause of cancer-related deaths. Non-small cell lung cancer (NSCLC) is the most common pathological subtype, with adenocarcinoma being the predominant type. FAT atypical cadherin 1 (FAT1) is a receptor-like protein with a high frequency of mutations in lung adenocarcinoma. The protein encoded by FAT1 plays a crucial role in processes such as cell adhesion, proliferation, and differentiation. This study aims to investigate the expression of FAT1 in lung adenocarcinoma and its relationship with immune infiltration. Methods Gene expression levels and relevant clinical information of 513 lung adenocarcinoma samples and 397 adjacent lung samples were obtained through The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data. The mRNA expression levels of the FAT1 gene in lung adenocarcinoma tissues were analyzed, along with its association with the prognosis of lung adenocarcinoma patients. Pathway enrichment analysis was conducted to explore the signaling pathways regulated by the FAT1 gene. Immunoblotting was used to detect the differential expression of FAT1 in lung epithelial cells and various lung cancer cell lines, while immunohistochemistry was employed to assess FAT1 expression in lung cancer and adjacent tissues. Results FAT1 gene mutations were identified in 14% of lung adenocarcinoma patients. TCGA database data revealed significantly higher FAT1 mRNA expression in lung adenocarcinoma tissues compared to adjacent lung tissues. Kaplan-Meier analysis indicated lower survival rates in lung adenocarcinoma patients with higher FAT gene expression. Pathway enrichment analysis suggested the involvement of FAT1 in tumor development pathways, and its expression was closely associated with immune cell infiltration. Immunohistochemical validation demonstrated significantly higher expression of FAT1 in cancer tissues compared to adjacent lung tissues. Conclusion FAT1 mRNA is highly expressed in lung adenocarcinoma tissues, and elevated FAT1 mRNA expression is associated with poor prognosis in lung adenocarcinoma patients. FAT1 may serve as a potential biomarker for lung cancer. [ABSTRACT FROM AUTHOR]

Background and objective Cough is one of the main complications after pulmonary surgery, which seriously affects the postoperative quality of life. Preserving the pulmonary branch of vagus nerve may reduce the incidence of postoperative cough. Therefore, the aim of this study was to investigate whether preserving the pulmonary branch of the vagus nerve could reduce the incidence of postoperative chronic cough in patients with stage I peripheral lung adenocarcinoma. Methods A total of 125 patients who underwent single-port thoracoscopic radical resection for lung cancer in the Department of Thoracic Surgery, The First Affiliated Hospital of University of Science and Technology of China from June 2022 to June 2023 were retrospectively selected, and divided into two groups according to whether the vagopulmonary branch was preserved during the operation, namely, the vagopulmonary branch group (n=61) and the traditional group (n=64). The general clinical data, perioperative conditions, lymph node dissection, Mandarin Chinese version of The Leicester Cough Questionnaire (LCQ-MC) scores before and 8 weeks after operation were recorded in the two groups. Both the two groups were divided into tamponade group and non-tamponade group according to whether autologous fat or gelatin sponge was tamponade after lymph node dissection. LCQ-MC scores and postoperative chronic cough of both groups were calculated. Results The LCQ-MC score of the traditional group was significantly lower than that of the vagopulmonary branch group in physiological, psychological, social and total scores at 8 weeks after surgery, and the difference was statistically significant (P<0.05). There were more cough patients in the traditional group than the vagopulmonary branch group at 8 weeks after surgery, with significant difference (P=0.006). Subgroup analysis was conducted separately for the vagopulmonary branch group and the traditional group. Among the patients in the vagopulmonary branch group and the traditional group, the LCQ-MC scores of the non-tamponade group 8 weeks after surgery were lower than those of the tamponade group (P<0.05). There were more patients with cough in the group 8 weeks after surgery than in the tamponade group (P=0.001, P=0.024). Conclusion For patients with stage I peripheral lung adenocarcinoma, the preservation of the pulmonary branch of vagus nerve is safe and effective, which can reduce the incidence of postoperative chronic cough and improve the postoperative quality of life of the patients. [ABSTRACT FROM AUTHOR]

Background and objective Radiation therapy is one of the most common treatments for non-small cell lung cancer (NSCLC). However, the insensitivity of some tumor cells to radiation is one of the major reasons for the poor efficacy of radiotherapy and the poor prognosis of patients, and exploring the underlying mechanisms behind radioresistance is the key to solving this clinical challenge. This study aimed to identify the molecules associated with radioresistance in lung adenocarcinoma (LUAD), identified thyroid hormone receptor interactor 13 (TRIP13) as the main target initially, and explored whether TRIP13 is related to radioresistance in LUAD and the specific mechanism, with the aim of providing theoretical basis and potential targets for the combination therapy of LUAD patients receiving radiotherapy in the clinic. Methods Three data-sets, GSE18842, GSE19188 and GSE33532, were selected from the Gene Expression Omnibus (GEO) database and screened for differentially expressed genes (/log FC/>1.5, P<0.05) in each of the three datasets using the R 4.1.3 software, and then Venn diagram was used to find out the differentially expressed genes common to the three datasets. The screened differential genes were then subjected to protein-protein interaction (PPI) analysis and module analysis with the help of STRING online tool and Cytoscape software, and survival prognosis analysis was performed for each gene with the help of Kaplan-Meier Plotter database, and the TRIP13 gene was identified as the main molecule for subsequent studies. Subsequently, the human LUAD cell line H292 was irradiated with multiple X-rays using a sub-lethal dose irradiation method to construct a radioresistant cell line, H292DR. The radioresistance of H292DR cells was verified using cell counting kit-8 (CCK-8) assay and clone formation assay. The expression levels of TRIP13 in H292 and H292DR cells were measured by Western blot. Small interfering RNA (siRNA) was used to silence the expression of TRIP13 in H292DR cells and Western blot assay was performed. The clone formation ability and migration ability of H292DR cells were observed after TRIP13 silencing, followed by the detection of changes in the expression levels of proteins closely related to homologous recombination, such as ataxia telangiectasia mutated (ATM) protein. Results Screening of multiple GEO datasets, validation of external datasets and survival analysis revealed that TRIP13 was highly expressed in LUAD and was associated with poor prognosis in LUAD patients who had received radiation therapy. And the results of gene set enrichment analysis (GSEA) of TRIP13 suggested that TRIP13 might be closely associated with LUAD radioresistance by promoting homologous recombination repair after radiation therapy. Experimentally, TRIP13 expression was found to be upregulated in H292DR, and silencing of TRIP13 was able to increase the sensitivity of H292DR cells to radiation. Conclusion TRIP13 is associated with poor prognosis in LUAD patients treated with radiation, possibly by promoting a homologous recombination repair pathway to mediate resistance of LUAD cells to radiation. [ABSTRACT FROM AUTHOR]

Background and objective Invasive mucinous adenocarcinoma (IMA) was a rare and specific type of lung adenocarcinoma, which was often characterized by fewer lymphatic metastases. Therefore, it was difficult to evaluate the prognosis of these tumors based on the existing tumor-node-metastasis (TNM) staging. So, this study aimed to develop Nomograms to predict outcomes of patients with pathologic N0 in resected IMA. Methods According to the inclusion criteria and exclusion criteria, IMA patients with pathologic N0 in The Affiliated Lihuili Hospital of Ningbo University (training cohort, n=78) and Ningbo No.2 Hospital (validation cohort, n=66) were reviewed between July 2012 and May 2017. The prognostic value of the clinicopathological features in the training cohort was analyzed and prognostic prediction models were established, and the performances of models were evaluated. Finally, the validation cohort data was put in for external validation. Results Univariate analysis showed that pneumonic type, larger tumor size, mixed mucinous/non-mucinous component, and higher overall stage were significant influence factors of 5-year progression-free survival (PFS) and overall survival (OS). Multivariate analysis further indicated that type of imaging, tumor size, mucinous component were the independent prognostic factors for poor 5-year PFS and OS. Moreover, the 5-year PFS and OS rates were 62.82% and 75.64%, respectively. In subgroups, the survival analysis also showed that the pneumonic type and mixed mucinous/non-mucinous patients had significantly poorer 5-year PFS and OS compared with solitary type and pure mucinous patients, respectively. The C-index of Nomograms with 5-year PFS and OS were 0.815 (95%CI: 0.741-0.889) and 0.767 (95%CI: 0.669-0.865). The calibration curve and decision curve analysis (DCA) of both models showed good predictive performances in both cohorts. Conclusion The Nomograms based on clinicopathological characteristics in a certain extent, can be used as an effective prognostic tool for patients with pathologic N0 after IMA resection. [ABSTRACT FROM AUTHOR]

Background and objective Transcription factor (TF) can bind specific sequences that either promotes or represses the transcription of target genes, and exerts important effects on tumorigenesis, migration, invasion. Staphylococcal nuclease-containing structural domain 1 (SND1), which is a transcriptional co-activator, is considered as a promising target for tumor therapy. However, its role in lung adenocarcinoma (LUAD) remains unclear. This study aims to explore the role of SND1 in LUAD. Methods Data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), Clinical Proteomic Tumor Analysis Consortium (CPTAC), and Human Protein Atlas (HPA) database was obtained to explore the association between SND1 and the prognosis, as well as the immune cell infiltration, and subcellular localization in LUAD tissues. Furthermore, the functional role of SND1 in LUAD was verified in vitro. EdU assay, CCK-8 assay, flow cytometry, scratch assay, Transwell assay and Western blot were performed. Results SND1 was found to be upregulated and high expression of SND1 is correlated with poor prognosis of LUAD patients. In addition, SND1 was predominantly present in the cytoplasm of LUAD cells. Enrichment analysis showed that SND1 was closely associated with the cell cycle, as well as DNA replication, and chromosome segregation. Immune infiltration analysis showed that SND1 was closely associated with various immune cell populations, including T cells, B cells, cytotoxic cells and dendritic cells. In vitro studies demonstrated that silencing of SND1 inhibited cell proliferation, invasion and migration of LUAD cells. Besides, cell cycle was blocked at G1 phase by down-regulating SND1. Conclusion SND1 might be an important prognostic biomarker of LUAD and may promote LUAD cells proliferation and migration. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Ground-glass nodule (GGN) lung cancer often progresses slowly in clinical and there are few clinical studies on long-term follow-up of patients with operable GGN lung cancer treated with stereotactic body radiation therapy (SBRT). We present a successful case of GGN lung cancer treated with SBRT, but a new GGN was found in the lung adjacent to the SBRT target during follow-up. The nodule progressed rapidly and was confirmed as lung adenocarcinoma by surgical resection. No significant risk factors and related driving genes were found in molecular pathological findings and genetic tests. It deserves further study whether new GGN is related to the SBRT. This case suggests that the follow-up after SBRT should be vigilant against the occurrence of new rapidly progressive lung cancer in the target area and adjacent lung tissue. [ABSTRACT FROM AUTHOR]

Background and objective In China, lung cancer remains the cancer with the highest incidence and mortality rate. Among early-stage lung adenocarcinomas (LUAD), the micropapillary (MPP) component is prevalent and typically exhibits high aggressiveness, significantly correlating with early metastasis, lymphatic infiltration, and reduced five-year survival rates. Therefore, the study is to explore the similarities and differences between MPP and non-micropapillary (non-MPP) components in malignant pulmonary nodules characterized by GGOs in early-stage LUAD, identify unique mutational features of the MPP component and analyze the relationship between the ZNF469 gene, a member of the zinc-finger protein family, and the prognosis of early-stage LUAD, as well as its correlation with immune infiltration. Methods A total of 31 malignant pulmonary nodules of LUAD were collected and dissected into paired MPP and non-MPP components using microdissection. Whole-exome sequencing (WES) was performed on the components of early-stage malignant pulmonary nodules. Mutational signatures analysis was conducted using R packages such as maftools, Nonnegative Matrix Factorization (NMF), and Sigminer to unveil the genomic mutational characteristics unique to MPP components in invasive LUAD compared to other tumor tissues. Furthermore, we explored the expression of the ZNF469 gene in LUAD using The Cancer Genome Atlas (TCGA) database to investigate its potential association with the prognosis. We also investigated gene interaction networks and signaling pathways related to ZNF469 in LUAD using the GeneMANIA database and conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Lastly, we analyzed the correlation between ZNF469 gene expression and levels of immune cell infiltration in LUAD using the TIMER and TISIDB databases. Results MPP components exhibited a higher number of genomic variations, particularly the 13th COSMIC (Catalogue of Somatic Mutations in Cancer) mutational signature characterized by the activity of the cytidine deaminase APOBEC family, which was unique to MPP components compared to non-MPP components in tumor tissues. This suggests the potential involvement of APOBEC in the progression of MPP components in early-stage LUAD. Additionally, MPP samples with high similarity to APOBEC signature displayed a higher tumor mutational burden (TMB), indicating that these patients may be more likely to benefit from immunotherapy. The expression of ZNF469 was significantly upregulated in LUAD compared to normal tissue, and was associated with poor prognosis in LUAD patients (P<0.05). Gene interaction network analysis and GO/KEGG enrichment analysis revealed that COL6A1, COL1A1, COL1A2, TGFB2, MMP2, COL8A2 and C2CD4C interacted with ZNF469 and were mainly involved in encoding collagen proteins and participating in the constitution of extracellular matrix. ZNF469 expression was positively correlated with immune cell infiltration in LUAD (P<0.05). Conclusion The study has unveiled distinctive mutational signatures in the MPP components of early-stage invasive LUAD in the Asian population. Furthermore, we have identified that the elevated expression of mutated ZNF469 impacts the prognosis and immune infiltration in LUAD, suggesting its potential as a diagnostic and prognostic biomarker in LUAD. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

To screen out the key genes affecting lung adenocarcinoma (LUAD) through bioinformatics methods, and to analyze their biological functions and the influences on the LUAD prognosis. Methods The GSE118370 and GSE136043 chip data were downloaded from the Gene Expression Omnibus(GEO) Database. The LUAD-related data were selected from the The Cancer Genome Atlas(TCGA) Database. R software was used to analyze the co-expressed differentially expressed genes (DEGs)； clusterProfile R package was utilized for Gene Ontology (GO) functional enrichment analysis； DAVID Database was used for the Kyoto Gene and Genome Encyclopedia (KEGG) signaling pathway enrichment analysis； STRING Database was used to construct the protein-protein interaction (PPI) network； Cytoscape was used to screen out the top 10 key genes； GEPIA Database and Human Protein Atlas(HPA) Database were used to analyze the expressions of key genes mRNA and protein in normal lung tissue and LUAD tissue, and their expressions in LUAD tissues with different stages；immune infiltration analysis and survival analysis were used to analyze the correlation between the expressions of key genes and the survival time of the patients. Results In total, 428 DEGs were screened out. The GO functional analysis results showed that the DEGs of LUAD were mainly enriched in biological process(BP) such as epithelial-mesenchymal transition (EMT), cellular component(CC) such as the cell base, and molecular function(MF) such as extracellular matrix (ECM) structure formation.The KEGG signaling pathway analysis results showed that the DEGs of LUAD were mainly enriched in the pathways like cytokine receptor interactions.topoisomerase Ⅱ alpha(TOP2A), abnormal spindle microtubule assembly(ASPM), cyclin B1, (CCNB1), cell division cycle associated 8(CDCA8), baculoviral IAP repeat containing 5(BIRC5), aurora A(AURKA), kinesin family member 20A(KIF20A), centrosomal protein 55(CEP55), centromere protein F(CENPF), and targeting protein for xklp2(TPX2) were selected as the key genes. Compared with normal lung tissue, the expression levels of TOP2A, CCNB1, CDCA8, BIRC5, AURKA, KIF20A, CEP55, CENPF, and TPX2 mRNA in lung tissue of the LUAD patients were increased (P<0.01), and the expression levels of TOP2A, CCNB1, CDCA8, BIRC5, AURKA, KIF20A, CEP55, CENPF, and TPX2 proteins were increased. There were significant differences in the expression levels of CCNB1, CDCA8, BIRC5, AURKA, KIF20A, CEP55, and TPX2 mRNA in the LUAD tissue with different stages (P<0.01). Compared with the LUAD patients with stage Ⅰ, stage Ⅱ, and stage Ⅲ, the expression levels of CCNB1, CDCA8, AURKA, KIF20A, CEP55, and TPX2 mRNA in lung tissue of the LUAD patients with stage Ⅳ were increased(P<0.01)； compared with the LUAD patients with stage Ⅰ, stage Ⅱ, and stage Ⅳ, the expression level of BIRC5 mRNA in lung tissue of the LUAD patients with stage Ⅲ was increased (P<0.01). The expressions of 10 key genes were negatively correlated with the B-lymphocyte infiltration (－0.253≤r≤－0.014, P<0.01)； the expressions of TOP2A, ASPM, CDCA8, BIRC5, CEP55, CENPF, and TPX2 were positively correlated with the neutrophil infiltration (0.049≤r≤0.165, P<0.01)； the expressions of CCNB1 and AURKA were negatively correlated with the CD4 T lymphocyte, macrophage, and dendritic cell infiltration -0.210≤r≤－0.100, P<0.01). The high expression of CDCA8 increased the risk of LUAD deterioration (P<0.01), and the high expressions of TOP2A, CCNB1, CDCA8, BIRC5, AURKA, KIF20A, CEP55, CENPF, and TPX2 increased the death risk of the patients(P<0.01). Conclusion TOP2A, ASPM, CCNB1, CDCA8, BIRC5, AURKA, KIF20A, CEP55, CENPF, and TPX2 are the key genes involved in the development and progression of LUAD. They may promote the development of LUAD by accelerating the EMT process, and their high expressions suggest the poor prognosis and elevate the death risk of the LUAD patients. [ABSTRACT FROM AUTHOR]

AA2 on ferroptosis index of LUAD cells. The concentration of lipid ROS (L-ROS) in LUAD ceBackground and objective Lung adenocarcinoma (LUAD) is the most common type of non-small cell lung cancer, and any change of miRNAs expression will affect the degree of target regulation, thus affecting intracellular homeostasis. This study verified that miR-186-5p could inhibit the proliferation, migration and invasion of LUAD cells by regulating PRKAA2. Methods Previous investigations found that the expression of miR-186-5p was markedly suppressed in LUAD. Bio-informatics method is used to predict the target protein related to ferroptosis downstream and inquire about its expression level in LUAD and its influence on the survival of patients. Double luciferase verified the binding site of PR^AA2 and miR-186-5p. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to detect the expression of PR^AA2. The effects of miR-186-5p of LUAD cells as well as the mechanism by which miR-186-5p inhibits Fer-1's sensitivity to ferroptosis were confirmed by EdU, Transwell, and scratch assays. The effect of miR-186-5p on the amount of reactive oxygen species (ROS) in LUAD cells was discovered using ROS experiment. Malondialdehyde (MDA) and glutathione (GSH) experiments were used to detect the effects of miR-186-5p and PR^lls were measured using the L-ROS tests to determine the effects of miR-186-5p and PRAA2. Resuits The expression of PR^AA2 is up-regulated, and a high level of PR^AA2 expression was associated with a poor prognosis for patients with LUAD. Overexpression of miR-186-5p decreased the gene and protein expression of PRAA2. By promoting ferroptosis, miR-186-5p overexpression prevented lung cancer cells from proliferating, invading, and migrating. ROS could be produced in higher amounts in LUAD cells due to miR-186-5p. Overexpression of miR-186-5p and knockdown PRAA2 up-regulated MDA content and reduced GSH content in LUAD cells, respectively. miR-186-5p could increase the content of L-ROS and promote the ferroptosis sensitivity of LUAD cells by targeting PRAA2. Conclusion miR-186-5p promotes ferroptosis of LUAD cells through targeted regulation of PRAA2, thus inhibiting the proliferation, invasion and migration of LUAD. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Sichuan University (Medical Science Edition) is the property of Editorial Board of Journal of Sichuan University (Medical Sciences) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

AIM: To explore the effect of chromobox 4 （CBX4） silencing on the proliferation, migration and invasion of esophageal and gastric junction adenocarcinoma cells. METHODS: RT-qPCR was used to detect the expression level of CBX4 mRNA in cancer tissues and adjacent tissues of patients with esophageal and gastric junction adenocarcinoma who underwent surgery in Shanxi Provincial Cancer Hospital from June 2017 to June 2019, and in esophageal and gastric junction adenocarcinoma cell lines. Taking the esophageal and gastric junction adenocarcinoma cells AGS and SKGT-4 as the research objects, negative control （NC） and CBX4 siRNAs were transfected into the cells. Cell proliferation was detected by CCK-8 assay, cell migration was detected by scratch test, and cell invasion was detected by Transwell test. Western blot was used to detect CBX4, β-catenin, c-MYC and cyclin D1 protein expression levels. RESULTS: Compared with adjacent normal tissues, the expression of CBX4 in esophageal and gastric junction adenocarcinoma was significantly up-regulated. Compared with normal gastric epithelial cells, the level of CBX4 mRNA in esophageal and gastric junction adenocarcinoma cells was significantly increased （P<0. 05）. After down-regulation of CBX4 expression, the proliferation, migration and invasion of AGS and SK-GT-4 cells decreased significantly, and the expression of β-catenin, c-MYC and cyclin D1 protein also decreased （P<0. 05）. CONCLUSION: CBX4 is highly expressed in esophageal and gastric junction adenocarcinoma cells. Silencing of CBX4 may regulate Wnt/β-catenin signaling pathway to inhibit the proliferation, migration and invasion of esophageal and gastric junction adenocarcinoma cells. [ABSTRACT FROM AUTHOR]

Epidermal growth factor receptor (EGFR) mutations are the most common driver genes in the development of non-small cell lung cancer (NSCLC), of which mutations in exons 18-21 are frequent, especially the loss of exon 19 and exon 21 L858R mutation are the most frequent. Other rare gene mutations are rare. Simultaneous occurrence of two or more rare EGFR mutations are extremely rare in lung cancer, and the incidence of EGFR L833V/H835L rare gene compound mutations is very low, and there is little clinical data and evidence of relevant treatment methods. Some EGFR-tyrosine kinase inhibitors (EGFR-TKIs) are effective in treating lung cancer patients with rare gene mutations. In this article, we reported a case of NSCLC patient with a rare gene compound mutation EGFR L833V/H835L, who responded to Afatinib in combination with Anilotinib treatment well after 5 months of treatment, and computed tomography (CT) showed shrinkage of lung lesions. Meanwhile, we also compiled previously reported NSCLC patients with EGFR L833V/H835L rare gene compound mutation and summarized the characteristics of this group of patients and the effect of applying different kinds of EGFR-TKIs treatment. [ABSTRACT FROM AUTHOR]

Background and objective Lung adenocarcinoma (LUAD) is a major subtype of lung cancer, and its treatment and diagnosis remain a hot research topic. Targeting protein for Xenopus kinesin-like protein 2 (TPX2) is highly expressed in a variety of cancer cells and may be associated with the progression of LUAD. This study aimed to investigate the effect of TPX2 on the malignant progression of LUAD cells and the regulatory mechanisms. Methods The expression of gene TPX2 in LUAD tissues from The Cancer Genome Atlas (TCGA) database was analyzed by bioinformatics analysis techniques. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression levels of TPX2 and miR-218-5p in human lung normal cell lines and human LUAD cell lines. Western blot was used to detect TPX2 protein expression in cell lines and its effect on the expression of key proteins in the p53 signaling pathway. The relationship between TPX2 and miR-218-5p was predicted using bioinformatics and verified by dual luciferase reporter gene assay. Cell counting kit-8 (CCK-8) assay, cell clone formation, cell scratching, Transwell assay, and flow cytometry were used to detect the effects of miR-218-5p and TPX2 on LUAD cell function. Results TPX2 was significantly overexpressed in LUAD cells, and knockdown of TPX2 inhibited LUAD cell proliferation, migration, and invasion, promoted apoptosis and induced G2/M phase block, and promoted the expression of key proteins in the p53 signaling pathway. miR-218-5p, an upstream regulator of TPX2, could inhibit its expression. Overexpression of miR-218-5p eliminated the malignant development caused by high expression of TPX2, inhibited the malignant processes of LUAD cells such as proliferation and migration as well as promoted the p53 signaling pathway. Conclu- sion miR-218-5p targets and inhibits TPX2 expression and exerts an inhibitory effect on the malignant progression of LUAD cells via p53. [ABSTRACT FROM AUTHOR]

A pulmonary nodule(PN) is characterized by a round or irregular lesion in the lung with a diameter W3 cm. PN is characterized by the following features upon imaging: heightened density, clear or unclear boundaries, without atelectasis, hilar lymph node enlargement, and pleural effusion. However, the pathogenesis of PN remains unclear, and the current treatment measures have failed to meet the clinical demands. Therefore, animal models of PN are of great significance for investigating its pathogenesis and discovering or optimizing effective drugs and methods for its prevention and treatment. This paper summarizes the widely used animal models of PNs. Previous research has shown that the most common animal models were used for granulomas, lung adenomas, atypical adenomatous hyperplasia(AAH), and adenocarcinomas. The experimental animals utilized were A/J mice, C57BL/6 mice, and mice with predominantly EGFR and Kras mutations. Moreover, the chief inducers included carcinogenic compounds, such as benzo (a) pyrene and 4-(methylnitrosamino)-1-(3-pyridyl)・1・butanone (NNK). Furthermore, the preparation methods and model characteristics of PNs were systematically and comprehensively reviewed to provide a strong basis and a valuable reference for the rational selection of animal models for basic research and drug dev elop ent. [ABSTRACT FROM AUTHOR]

Background and objective Idiopathic pulmonary fibrosis (IPF) is an idiopathic chronic, progressive interstitial lung disease with a diagnosed median survival of 3-5 years. IPF is associated with an increased risk of lung cancer. Therefore, exploring the shared pathogenic genes and molecular pathways between IPF and lung adenocarcinoma (LUAD) holds significant importance for the development of novel therapeutic approaches and personalized precision treatment strategies for IPF combined with lung cancer. Methods Bioinformatics analysis was conducted using publicly available gene expression datasets of IPF and LUAD from the Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis was employed to identify common genes involved in the progression of both diseases, followed by functional enrichment analysis. Subsequently, additional datasets were used to pinpoint the core shared genes between the two diseases. The relationship between core shared genes and prognosis, as well as their expression patterns, clinical relevance, genetic characteristics, and immune-related functions in LUAD, were analyzed using The Cancer Genome Atlas (TCGA) database and single-cell RNA sequencing datasets. Finally, potential therapeutic drugs related to the identified genes were screened through drug databases. Results A total of 529 shared genes between IPF and LUAD were identified. Among them, SULF1 emerged as a core shared gene associated with poor prognosis. It exhibited significantly elevated expression levels in LUAD tissues, concomitant with high mutation rates, genomic heterogeneity, and an immunosuppressive microen-vironment. Subsequent single-cell RNA-seq analysis revealed that the high expression of SULF1 primarily originated from tumor-associated fibroblasts. This study further demonstrated an association between SULF1 expression and tumor drug sensitivity, and it identified potential small-molecule drugs targeting SULF1 highly expressed fibroblasts. Conclusions This study identified a set of shared molecular pathways and core genes between IPF and LUAD. Notably, SULF1 may serve as a potential immune-related biomarker and therapeutic target for both diseases. [ABSTRACT FROM AUTHOR]

Background and objective The biological and molecular characteristics of spread through air spaces (STAS), a newly recognized invasive mode of lung cancer, remain controversial. The aim of this study was to investigate the clinicopathological features and molecular characteristics of STAS in patients with pulmonary adenocar-cinoma. Methods A total of 694 resected invasive non-mucinous lung adenocarcinomas diagnosed by clinicopathology from July 2019 to March 2021 in the First Affiliated Hospital of Guangzhou Medical University were collected, and the relationship between STAS and clinicopathological factors was analyzed. The state of protein expression of anaplastic lymphoma kinase (ALK) was detected by immunohistochemical method. Epidermal growth factor receptor (EGFR) was detected by amplification refractory mutation system-polymerase chain reaction (ARMS-PCR). ROS proto-onco-gene 1-receptor (ROS1) was detected by reverse transcription-PCR (RT-PCR). Results A total of 344 STAS positive cases and 350 STAS negative cases were collected. By univariate analysis, STAS positivity was statistically associated with tumor maximum diameter (P<0.001), pleural invasion (P<0.001), lymphovascular invasion (P<0.001), nerve invasion (P=0.013), lymph node metastasis (P<0.001), clinical stage (P<0.001) and histological type (P<0.001). There was a statistical correlation between STAS and ALK protein expression (P=0.001). Multivariate analysis showed that STAS positive was correlated with pleural invasion (P=0.001), vascular invasion (P<0.001), lymph node metastasis (P=0.005)and ALK protein expression (P=0.032). Conclusion STAS is associated with highly aggressive biological behavior of lung adenocarcinoma, suggesting a poor prognosis. [ABSTRACT FROM AUTHOR]

Cervical mucinous adenocarcinoma is a rare and special histological type of cervical malignant tumor, which mainly includes adenocarcinoma of the cervix gastric type, adenocarcinoma of the cervix and intestines, and primary cervical signet-ring cell carcinoma. Due to the uncertainty between the pathogenesis of cervical mucinous adenocarcinoma and human papillomavirus (HPV) infection makes it difficult to be suggested by routine cervical cancer screening. Meanwhile, the etiology and pathogenesis of cervical mucinous adenocarcinoma are not clear, and there is a lack of typical clinical manifestations and early diagnosis methods, and the clinicopathological features and treatment are different from those of cervical common adenocarcinoma, resulting in patients being prone to miss the best treatment time, so the prognosis of cervical mucinous adenocarcinoma is worse than that of cervical common adenocarcinoma. In recent years, due to the popularization of HPV vaccine, the relative incidence of cervical mucinous adenocarcinoma has slightly increased compared with before, and the research on cervical mucinous adenocarcinoma has received more and more attention. The relevant research on cervical mucinous adenocarcinoma at home and abroad is reviewed, and the relevant pathogenesis, clinical features and treatment of cervical mucinous adenocarcinoma are discussed, in order to provide a reference for the clinical diagnosis and treatment of cervical mucinous adenocarcinoma. [ABSTRACT FROM AUTHOR]

Background and objective Lung cancer is the most common malignant tumor in China, lung adenocarcinoma (LUAD) is the main type of lung cancer, which is a serious threat to people's life and health. At present, there are fewer studies on the role of Dikkopf1 (DKKl) in lung adenocarcinoma. The aim of this study was to investigate the role and potential prognostic value of DKKl in the development of lung adenocarcinoma by bioinformatics methods. Methods Several databases, such as genotype-tissue expression (GTEx), The Cancer Genome Atlas (TCGA) and tumor-immune system interactions database (TISIDB), were used to analyze the expression, clinicopathological features, immune cell infiltration, prognosis and methylation of DKKl in lung adenocarcinoma. Then, linked immune cell infiltration Omics database was used to analyze the co-expressed genes of DKKl and their functional enrichment. Finally, 59 pathological samples of paraffin-embedded lung adenocarcinoma patients who underwent surgery at the Affiliated Cancer Hospital of Xinjiang Medical University between 2016 and 2017 were collected for the validation of the prognostic value of expression by immunohistochemistry (IHC) test. Results The results of bioconfidence analysis showed that the expression level of DKKl in lung adenocarcinoma tissues was higher than that in normal tissues, the expression in advanced cancers was higher than that in early stages, and the experimental validation revealed that among 59 cases of lung adenocarcinoma, there were 15 cases of negative expression (25.4%), 18 cases of weakly positive expression (30.5%), and 26 cases of strongly positive expression (44.1%). The different expression of DKKl is related to methylation, prognosis and the activities of various immune cells. Functional enrichment shows that DKKl may be involved in skin development and cell-substrate junction, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis shows that DKKl is related to ABC transporters. Bioinformatics analysis and clinical case specimens showed that high DKKl expression was associated with poorer prognosis in patients with lung adenocarcinoma. Conclusion High expression of DKKl in lung adenocarcinoma is associated with poor prognosis. DKKl is closely associated with tumor immune cell infiltration and pathways. DKKl can be considered as a potential prognostic marker and a novel target for immunotherapy of lung adenocarcinoma. [ABSTRACT FROM AUTHOR]

Background and objective Lung cancer is one of the most common malignant tumors in the world, and the current lung cancer screening and treatment strategies are constantly improving, but its 5-year survival rate is still very low, which seriously endangers human health. Therefore, it is critical to explore new biomarkers to provide personalized treatment and improve the prognosis. Cuproptosis is a newly discovered type of cell death, which is due to the accumulation of excess copper ions in the cell, eventually leading to cell death, which has been suggested by studies to be closely related to the occurrence and development of lung adenocarcinoma (LUAD). Based on The Cancer Genome Atlas (TCGA) database, this study explored the association between cuproptosis-related genes (CRGs) and LUAD prognosis, established a prognostic risk model, and analyzed the interaction between CRGs and LUAD immune cell infiltration. Methods The RNA-seq data of LUAD tissue and paracancerous or normal lung tissue were downloaded from the TCGA database; the RNA-seq data of normal lung tissue was downloaded from the Genotype-tissue Expression (GTEx) database, and the data of 462 lung adenocarcinoma cases were downloaded from the Gene Expression Omnibus repository (GEO) as verification. T the risk score model to assess prognosis was constructed by univariate Cox and Lasso-Cox regression analysis, and the predictive ability of the model was evaluated by receiver operating characteristic (ROC) curve and calibration curve. Immune-related and drug susceptibility analysis was further performed on high- and low-risk groups. Results A total of 1656 CRGs and 1356 differentially expressed CRGs were obtained, and 13 CRGs were screened out based on univariate Cox and Lasso-Cox regression analysis to construct a prognostic risk model, and the area under the curves (AUCs) of ROC curves 1-, 3- and 5- year were 0.749, 0.740 and 0.689, respectively. Further study of immune-related functions and immune checkpoint differential analysis between high- and low-risk groups was done. High-risk groups were more sensitive to drugs such as Savolitinib, Palbociclib, and Cytarabine and were more likely to benefit from immunotherapy. Conclusion The risk model constructed based on 13 CRGs has good prognostic value, which can assist LUAD patients in individualized treatment, and provides an important theoretical basis for the treatment and prognosis of LUAD. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Simultaneous multiple primary tumors on the same side of the lung with Tropheryma whipplei (TW) infection are rare. We reviewed the clinical data, imaging manifestations, pathological results, diagnosis and treatment of a primary pulmonary mucinous adenocarcinoma (PPMA) patient with bronchial squamous cell papilloma (BSCP) and TW infection, and discussed our treatment experience. The patient mainly presented with chronic cough and sputum, and computed tomography (CT) showed inflammatory changes with multiple nodular shadows. Biopsy of the lower lobe of the right lung showed PPMA, and right lung sub-branchial nodules discovered during bronchoscope revealed BSCP. Metagenomics next generation sequencing (mNGS) of bronchoalveolar lavage fluid showed mixed infection of Streptococcus pneumoniae and TW with a poor anti-infective effect. No clear genetic mutation was detected, and the patient was treated with chemotherapy and regularly followed up. We should improve the awareness of multiple pulmonary pathologies during clinical practice, avoid missed diagnosis and misdiagnosis, and carry out comprehensive treatment after clarifying the diagnosis as soon as possible. [ABSTRACT FROM AUTHOR]

Background and objective Myocyte enhancer factor 2D (MEF2D) can participate in the process of tumor lesions by regulating the transcription of oncogenes. In a previous study, MEF2D was demonstrated to enhance the proliferation and metastasis of lung adenocarcinoma cells A549 and H1299 by promoting the transcription of NUSAP1. The research aimed to explore the expression level and clinical significance of MEF2D in lung adenocarcinoma. Methods A total of 199 patients with lung adenocarcinoma were collected. Immunohistochemical staining was used to detect MEF2D expression levels in cancer and adjacent tissues. After the clinical and follow-up data were collated, the correlation between MEF2D expression level and clinical characteristics and prognosis of the patients was analyzed. Results In the lung adenocarcinoma, the high expression rate of MEF2D in cancer tissues was significantly higher than that in adjacent tissues (P<0.05). According to immunohistochemical score, MEF2D expression level in lung adenocarcinoma tissues was correlated with tumor differentiation, N stage, M stage and intrapulmonary metastasis (P<0.05). Kaplan-Meier analysis showed that patients with low MEF2D expression had significantly better prognosis than patients with high MEF2D expression (P<0.05). Cox multivariate analysis showed that MEF2D expression level, M stage, N stage and bone metastasis of lung cancer were independent risk factors for prognosis of lung adenocarcinoma patients. Conclussion MEF2D expression level is closely related to the metastasis of lung adenocarcinoma and other clinical characteristics, and can be used as an independent risk factor for the prognosis of patients with lung adenocarcinoma, which has the potential to be developed as a clinical diagnosis and treatment target of lung adeno-carcinoma. [ABSTRACT FROM AUTHOR]

Background and objective More early-stage non-small cell lung cancer (NSCLC) are diagnosed in time and treated surgically, but systematic lymph node dissection can not bring enough survival benefits for them, and even increase the probability of postoperative complications. This study aims to analyze the risk factors and evaluate mediastinal lymph node metastasis sites in different lung lobes for NSCLC with diameter <2 cm, so as to provide reference for surgery. Methods We collected 1051 patients with pulmonary nodule diameter <2 cm who were treated by pulmonary lobectomy with lymph node sampling/dissection in Department of Thoracic Surgery of the First .Affiliated Hospital with Nanjing Medical University from December 2009 to December 2019. SPSS 26.0 statistical software was used for statistical analysis, to explore the risk factors and evaluate mediastinal lymph node metastasis sites in different lung lobes. Results 95 of 1051 (9.04%) patients presented lymph node metastasis. Male, pathological non-adenocarcinoma, 1 cm0.05). Lymph nodes in group N1 were significantly correlated with lymph node metastasis in groups #2R, #4R, #5, #6, #7 and #9 (P<0.01). Conclusion Lobe-specific lymph node dissection (LSND) can be performed for early-stage NSCLC. Male, pathological non-adenocarcinoma, 1 cm

Background and objective Venous thromboembolism (VTE) as the most common cancer-associated complication has become the second death-causing reason among cancer patients. The management of VTE in patients with lung adenocarcinoma should focus on early and timely detection of risk factors. The aim of the study is to investigate the current situation of VTE in patients with lung adenocarcinoma treated with anti-tumor therapy and then explore the risk factors associated with the occurrence of VTE during anti-tumor therapy for early detection and screening of VTE. Methods The present study included patients diagnosed as lung adenocarcinoma undergoing anti-tumor therapy in First Affiliated Hospital of Nanjing Medical University between December 2019 and May 2021. The risk factors were identified via univariate and multivariate Cox analysis. The incidence of independent risk factors were investigated through Kaplan-Meier curves combined with Log-rank test. Results The results of univariate and multivariate Cox regression showed that history of VTE, targeted therapy and radiotherapy were risk factors for VTE in patients with lung adenocarcinoma treated with anti-tumor therapy (P<0.05). Furthermore, the results of Kaplan-Meier curves and Log-rank tests indicated the incidences of VTE in patients with history of VTE, targeted therapy and radiotherapy were higher (P<0.05). Conclusion History of VTE, radiotherapy and targeted therapy are found as independent risk factors for the occurrence of VTE, which should be identified and monitored for reduction of VTE incidence. [ABSTRACT FROM AUTHOR]

Background and objective Pre-operative accuracy of subcentimeter ground glass nodules (SGGNs) is a difficult problem in clinical practice, but there are few clinical studies on the benign and malignant prediction model of SGGNs. The aim of this study was to help identify benign and malignant lesions of SGGNs based on the imaging features of high resolution computed tomography (HRCT) and the general clinical data of patients, and to build a risk prediction model. Methods This study retrospectively analyzed the clinical data of 483 patients with SGGNs who underwent surgical resection and were confirmed by histology from the First Affiliated Hospital of University of Science and Technology of China from August 2020 to December 2021. The patients were divided into the training set (n=338) and the validation set (n=145) according to 7:3 random assignment. According to the postoperative histology, they were divided into adenocarcinoma group and benign lesion group. The independent risk factors and models were analyzed by univariate analysis and multivariate Logistic regression. The receiver operator characteristic (ROC) curve was constructed to evaluate the model differentiation, and the calibration curve was used to evaluate the model consistency. The clinical application value of the decision curve analysis (DCA) evalua-tion model was drawn, and the validation set data was substituted for external verification. Results Multivariate Logistic analysis screened out patients' age, vascular sign, lobular sign, nodule volume and mean-CT value as independent risk factors for SGGNs. Based on the results of multivariate analysis, Nomogram prediction model was constructed, and the area under ROC curve was 0.836 (95%CI: 0.794-0.879). The critical value corresponding to the maximum approximate entry index was 0.483. The sensitivity was 76.6%, and the specificity was 80.1%. The positive predictive value was 86.5%, and the negative predictive value was 68.7%. The benign and malignant risk of SGGNs predicted by the calibration curve was highly consistent with the actual occurrence risk after sampling 1,000 times using Bootstrap method. DCA showed that patients showed a positive net benefit when the predictive probability of the predicted model probability was 0.2 to 0.9. Conclusion Based on preoperative medical history and preoperative HRCT examination indicators, the benign and malignant risk prediction model of SGGNs was established to have good predictive efficacy and clinical application value. The visualization of Nomogram can help to screen out high-risk groups of SGGNs, providing support for clinical decision-making. [ABSTRACT FROM AUTHOR]