11.01 - Lung cancer最新文献_第8页

Impact of the COVID-19 pandemic on suspected lung cancer referrals and subsequent lung cancer diagnosis at North Bristol NHS Trust COVID-19大流行对北布里斯托尔NHS信托公司疑似肺癌转诊和随后肺癌诊断的影响

11.01 - Lung cancer Pub Date : 2022-09-04 DOI: 10.1183/13993003.congress-2022.139

A. Ramos Pereira, C. Coombs, B. Masterman, A. Jeyabalan, M. Plummeridge, A. Bibby

引用次数: 0

Terminal effector Tregs in metastatic lymph nodes of lung cancer patients 肺癌患者转移性淋巴结终末效应物Tregs

11.01 - Lung cancer Pub Date : 2022-09-04 DOI: 10.1183/13993003.congress-2022.694

I. Kwiecień, E. Rutkowska, A. Raniszewska, J. Bednarek, R. Sokołowski, P. Rzepecki, J. Domagała-Kulawik

引用次数: 0

Pulmonary complications after surgical resection of lung cancer - analysis of thousands cases. 肺癌手术切除后肺部并发症数千例分析。

11.01 - Lung cancer Pub Date : 2022-09-04 DOI: 10.1183/13993003.congress-2022.320

A. Trojnar, J. Domagała-Kulawik, A. Sienkiewicz-Ulita, M. Zbytniewski, G. Gryszko, M. Cackowski, M. Dziedzic, K. Woznica, T. Orlowski, D. Dziedzic

引用次数: 0

Lung Cancer Screening Programme and Pandemic Influences on the Pattern of Referrals to a Thoracic Oncology Service 肺癌筛查计划和大流行对胸部肿瘤服务转诊模式的影响

11.01 - Lung cancer Pub Date : 2022-09-04 DOI: 10.1183/13993003.congress-2022.2271

S. Habib, M. Pittman

引用次数: 0

Detection of micrometastases in mediastinal lymph nodes by haematological analyser and flow cytometry-pilot study. 血液分析仪和流式细胞术检测纵隔淋巴结微转移的初步研究。

11.01 - Lung cancer Pub Date : 2022-09-04 DOI: 10.1183/13993003.congress-2022.699

I. Kwiecień, E. Rutkowska, J. Bednarek, R. Sokołowski, A. Raniszewska, K. Jahnz- Różyk, P. Rzepecki, J. Domagała-Kulawik

引用次数: 0

Prognostic factors in locally advanced non-small cell lung cancer 局部晚期非小细胞肺癌的预后因素分析

11.01 - Lung cancer Pub Date : 2022-09-04 DOI: 10.1183/13993003.congress-2022.2925

Y. Hadidene, H. Kamoun, H. Rejeb, D. Greb, I. Akrout, L. Fkih, H. Smadhi, M. L. Megdiche

引用次数: 0

Trans thoracic CT‑guided fine‑needle biopsy of pulmonary lesions, predictive factors for complications and accuracy of diagnosis 经胸CT引导下肺病变细针活检、并发症预测因素及诊断准确性

11.01 - Lung cancer Pub Date : 2022-09-04 DOI: 10.1183/13993003.congress-2022.3062

K. Piotkovskaya, E. Radeka, S. Nyrén, R. Karimi

引用次数: 0

cAMP response element-binding protein mediates immune-evasion of KRAS-mutant lung adenocarcinoma cAMP反应元件结合蛋白介导kras突变型肺腺癌的免疫逃避

11.01 - Lung cancer Pub Date : 2021-03-11 DOI: 10.1183/23120541.LSC-2021.84

Georgia A. Giotopoulou, G. Ntaliarda, A. Μarazioti, I. Lilis, N. Spiropoulou, F. Kalogianni, E. Tourkochristou, I. Giopanou, M. Spella, M. Iliopoulou, A. Korfiati, K. Theofilatos, S. Mavroudi, T. Mantamadiotis, T. Goldmann, S. Marwitz, G. Stathopoulos

{"title":"cAMP response element-binding protein mediates immune-evasion of KRAS-mutant lung adenocarcinoma","authors":"Georgia A. Giotopoulou, G. Ntaliarda, A. Μarazioti, I. Lilis, N. Spiropoulou, F. Kalogianni, E. Tourkochristou, I. Giopanou, M. Spella, M. Iliopoulou, A. Korfiati, K. Theofilatos, S. Mavroudi, T. Mantamadiotis, T. Goldmann, S. Marwitz, G. Stathopoulos","doi":"10.1183/23120541.LSC-2021.84","DOIUrl":"https://doi.org/10.1183/23120541.LSC-2021.84","url":null,"abstract":"Introduction: cAMP response element-binding protein (CREB) mediates proliferative and inflammatory transcription in neurodegeneration and cancer, but its role in malignant immune-evasion is obscure. Objectives: To discover the mechanisms underlying the oncogenic properties of CREB in KRAS-mutant lung adenocarcinoma (LUAD). Materials and Methods: We used conditional deletion, focal overexpression, and pharmacologic inhibition of CREB in different mouse and cellular models of early-stage and metastatic KRAS-mutant LUAD. We determined the neutrophil (ΝΦ) influx in the bronchoalveolar lavage (BAL) from LUAD-affected conditionally Creb1-deleted lungs. We employed The Cancer Genome Atlas, the GEO dataset GSE43458, and the human protein atlas to examine CREB and CXCR1 in human LUAD. Results: CREB is overexpressed in murine KRAS-mutant LUAD, pulmonary deletion of Creb1 (encoding murine CREB) inhibits LUAD development, and Creb1-overexpression augments the tumorigenicity of KRAS-mutant cells. Conditional Creb1 deletion in KRAS -mutant LUAD cells causes overexpression of CXCR1 ligands, and LUAD-bearing Creb1-deleted mice display increased pulmonary ΝΦ. Cxcr1-deficient mice are selectively permissive to KRAS-mutant tumor growth and show defective ΝΦ recruitment. The pro-tumor effects of CREB require intact host Cxcr1 and those of host Cxcr1 necessitate mutant KRAS in cancer cells. Pharmacologic CREB blockade prevents tumor growth and restores ΝΦ recruitment only when initiated before immune-evasion of KRAS-mutant LUAD. CREB and CXCR1 expression of human LUAD are compartmentalized to tumor and stromal cells, respectively, while CREB-controlled genes profoundly impact survival. Conclusions: CREB-mediated immune evasion of KRAS-mutant LUAD rests on signaling to ΝΦ CXCR1 and is actionable.","PeriodicalId":229516,"journal":{"name":"11.01 - Lung cancer","volume":"6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123812231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Mutational RNA signatures in environmentally-induced lung adenocarcinoma 环境诱导肺腺癌的突变RNA特征

11.01 - Lung cancer Pub Date : 2021-03-11 DOI: 10.1183/23120541.LSC-2021.34

Georgia A. Giotopoulou, S. Behrend, G. Ntaliarda, A. Lamort, M. Pepe, I. Lilis, M. Spella, G. Stathopoulos

{"title":"Mutational RNA signatures in environmentally-induced lung adenocarcinoma","authors":"Georgia A. Giotopoulou, S. Behrend, G. Ntaliarda, A. Lamort, M. Pepe, I. Lilis, M. Spella, G. Stathopoulos","doi":"10.1183/23120541.LSC-2021.34","DOIUrl":"https://doi.org/10.1183/23120541.LSC-2021.34","url":null,"abstract":"Introduction: Lung adenocarcinoma (LUAD) is the most frequent lung cancer in non-smokers. Although carcinogens other than smoking (i.e., radiation) likely cause LUAD, their molecular imprints are obscure. Objectives: To define the molecular imprints of smoking, its carcinogens, and radiation in LUAD RNA. Materials and Methods: FVB mice were exposed to tobacco smoke (500 mg/m3; 2 hrs/day; 5 months on/5 months off), its chemicals ethyl carbamate (1 g/Kg), diethylnitrosamine (20 mg/Kg), and methylnitrosourea (50 mg/Kg), or X-irradiation (15 Gy X-rays delivered to a 100 mm3 tissue voxel of the right upper lobe). Total lung tumor RNA was extracted using Trizol/RNAeasy, was analyzed on an Illumina HiSeq4000, and was interrogated employing STAR, DeSeqR, Pathvisio, GSEA, Samtools, SnpEff, and R*. Results: FVB mice developed LUAD in response to the carcinogens used. RNAseq of tumor tissues provided robust transcript abundance and sequence information, including single nucleotide variation at the mononucleotide, trinucleotide, gene, and chromosome levels, as well as insertions and deletions. The five different carcinogens produced markedly distinct mutational imprints on the exposed tissues. Interestingly, the signatures of smoking and its carcinogens were highly similar, contained KRAS and other point mutations, and were enriched in human KRAS-mutant LUAD, while the signatures of irradiated tissues displayed EGFR point mutations, a preponderance of transversions, and a distinct gene expression set. Conclusions: Bulk RNAseq of environmentally-induced mouse tumors can reveal carcinogenic exposures and causes. We are currently working to identify cellular origin-restricted signatures and to translate murine imprints to human LUAD.","PeriodicalId":229516,"journal":{"name":"11.01 - Lung cancer","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130858110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Regulation of PA200 in lung cancer PA200在肺癌中的调控作用

11.01 - Lung cancer Pub Date : 2021-03-11 DOI: 10.1183/23120541.LSC-2021.48

A. Yazgili, Vanessa Welk, T. Meul, Christina Lukas, I. Koch, E. Stacher-Priehse, M. Lindner, G. Stathopoulos, S. Meiners

{"title":"Regulation of PA200 in lung cancer","authors":"A. Yazgili, Vanessa Welk, T. Meul, Christina Lukas, I. Koch, E. Stacher-Priehse, M. Lindner, G. Stathopoulos, S. Meiners","doi":"10.1183/23120541.LSC-2021.48","DOIUrl":"https://doi.org/10.1183/23120541.LSC-2021.48","url":null,"abstract":"Lung cancer is the leading cause of death among all cancer types with the most common incidence and mortality rates. The proteasome is a well-identified therapeutic target for cancer treatment. It acts as the main protein degradation system in the cell and degrades key mediators of cell growth, migration and survival. In this study, we analyzed non-tumorous and tumor tissues of patients suffering from different types of lung cancers. We observed significant upregulation of proteasome activator 200 (PA200) in tumor tissues compared to non-tumor lung samples of the same patient (Mann-Whitney U test, n=6). We also analyzed tumor tissue sections of lung cancer patients by immunohistochemistry and showed that PA200 was strongly induced in cancer cells. However, neither tumor stroma nor necrotic areas indicated expression of the activator. Importantly, PA200 is significantly increased in lung adenocarcinoma (LUAD), squamous cell lung cancer (SQCLC) compared to small cell lung cancer (SCLC) and correlated with significantly diminished survival in non-small cell lung cancer patients. Silencing of PA200 in the lung adenoma cell line A549 resulted in concerted downregulation of invasion, proliferation and metastasis-related gene expression. Our future experiments will focus on the function of PA200 in lung cancer cell growth, migration and invasion using CRISPR/Cas9 PA200 depleted A549 and H1299 cell lines. We will investigate the cellular function of modified PA200/proteasome complexes by analyzing RNA and protein signatures via RNA sequencing and mass spectrometry, respectively. We will use the power of functional assays (migration and invasion assay, colony formation assay) and address the functional role of PA200 as an oncogenic regulator in lung tumor growth and metastasis in vitro.","PeriodicalId":229516,"journal":{"name":"11.01 - Lung cancer","volume":"200 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116156278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0