Compared to other types of lung cancer, lung adenocarcinoma patients with a history of smoking have a poor prognosis during the treatment of lung cancer. How lung adenocarcinoma-related genes are differentially expressed between smoker and non-smoker patients has yet to be fully elucidated. We performed a meta-analysis of four publicly available microarray datasets related to lung adenocarcinoma tissue in patients with a history of smoking using R statistical software. The top 50 differentially expressed genes (DEGs) in smoking vs. non‑smoking patients are shown using heat maps. Additionally, we conducted KEGG and GO analyses. In addition, we performed a PPI network analysis for 8 genes that were selected during a previous analysis. We identified a total of 2,932 DEGs (1,806 upregulated, 1,126 downregulated) and five genes (CDC45, CDC20, ANAPC7, CDC6, ESPL1) that may link lung adenocarcinoma to smoking history. Our study may provide new insights into the complex mechanisms of lung adenocarcinoma in smoking patients, and our novel gene expression signatures will be useful for future clinical studies.
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http://dx.doi.org/10.3892/or.2018.6197 | DOI Listing |
Nan Fang Yi Ke Da Xue Xue Bao
December 2024
Department of Thoracic Surgery, First Medical Center of Chinese PLA General Hospital, Beijing 100853, China.
Objectives: To examine how the glucose transporter SLC2A1 influences the proliferation and migration of lung adenocarcinoma (LUAD) and explore the underlying molecular mechanisms.
Methods: We examined the differential expression of SLC2A1 between normal and LUAD tissues in the TCGA database and its prognostic implications. Immunohistochemistry was used to detect SLC2A1 protein levels in clinical samples of LUAD and adjacent tissues, and the association of SLC2A1 expression levels with clinicopathological features of the patients was analyzed.
J Thorac Oncol
December 2024
Moores Cancer Center, University of California San Diego, La Jolla, CA 92037, USA; Department of Medicine, University of California San Diego, La Jolla, CA 92037, USA; Department of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Introduction: Copy-number (CN) loss of chromosome 9p, or parts thereof, impair immune response and confer ICT resistance by direct elimination of immune-regulatory genes on this arm, notably IFNγ genes at 9p24.1, and type-I interferon (IFN-I) genes at 9p21.3.
View Article and Find Full Text PDFJ Thorac Oncol
December 2024
Department of Medical Oncology, Shanghai Pulmonary Hospital, Cancer Institute, Tongji University School of Medicine, Shanghai, 200433, China. Electronic address:
Pyrotinib, a novel pan-HER tyrosine kinase inhibitor, has demonstrated substantial anti-tumor activity in non-small cell lung cancer (NSCLC) patients harboring HER2 mutations. However, the inevitable resistance to pyrotinib necessitates an in-depth understanding of the underlying mechanisms. In this study, potential resistance-associated mutations were identified through genomic sequencing of clinically paired samples and were validated using in vitro and in vivo models.
View Article and Find Full Text PDFPathol Res Pract
December 2024
Department of Pharmacy, Birla Institute of Technology and Science Pilani, Pilani Campus, Rajasthan 333031, India. Electronic address:
Long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript1 (MALAT1) has emerged as a crucial biomarker and therapeutic target for kidney diseases, including acute kidney injury (AKI), chronic kidney disease (CKD), diabetic kidney disease (DKD), lupus nephritis (LN), and renal cell carcinoma (RCC). LncRNAs are non-coding RNAs that have more than 200 nucleotides that play a crucial role in gene regulation at the post-translational stage, transcriptional, and epigenetic levels. LncRNA MALAT1 regulates gene expression and modulates cellular functions such as proliferation, inflammation, apoptosis, and fibrosis, which are key pathophysiology of kidney diseases.
View Article and Find Full Text PDFThorac Cancer
December 2024
Department of Pulmonary Oncology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Background: The cancer cell marker poliovirus receptor-like protein 4 (PVRL4) has been shown to be highly expressed in many cancers, including lung cancer. Myeloid-derived suppressor cells (MDSCs) are a population of immature myeloid cells with immunosuppressive roles that can attenuate the anticancer response. Here, the precise functions and the relationship between PVRL4 and MDSCs in lung adenocarcinoma (LUAD) progression were investigated.
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