Background: An increasing number of studies are indicating that the stemness phenotype is a critical determinant of the Lung adenocarcinoma (LUAD) patient's response. Thus, it is crucial to identify novel biomarkers for stemness determination.
Objective: Here, we aim to develop a robust LncRNAs based prognostic signature with a stemness association for the LUAD patients.
Methods: RNA-seq and clinical data were downloaded from the existing database. The data were analysed using Cox regression, KM-plot, GSEA, and T-test.
Results: Initially, we used the TCGA dataset to characterize the stemness phenotype in LUAD. The commonly expressed LncRNAs in TCGA and MCTP cohort were then used as input for the Cox-regression analysis. The top three LncRNAs were selected to build a prognostic model, which was the best prognosticator in multivariate analysis with stage and previously published prognosticators. The characterization of poor surviving patients using various analysis showed high stemness properties and low expression of differentiation markers. Furthermore, we validated the prognostic score in an independent MCTP cohort of patients. In the MCTP cohort, prognostic score significantly predicted survival independent of stage and previous prognosticators.
Conclusion: Taken together, in this study, we have developed and validated a new prognostic score associated with the stemness phenotype.
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http://dx.doi.org/10.3233/CBM-200687 | DOI Listing |
Theranostics
January 2025
Department of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
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October 2024
Department of Thoracic Surgery, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250012, China.
Hexavalent chromium Cr(VI), as a well-established carcinogen, contributes to tumorigenesis for many human cancers, especially respiratory and digestive tumors. However, the potential function and relevant mechanism of Cr(VI) on the initiation of esophageal carcinogenesis are largely unknown. Here, immortalized human esophageal epithelial cells (HEECs) were induced to be malignantly transformed cells, termed HEEC-Cr(VI) cells, via chronic exposure to Cr(VI), which simulates the progress of esophageal tumorigenesis.
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January 2025
Memorial Sloan Kettering Cancer Center, New York, New York, United States.
A mixed phenotype is characteristic of de novo Mixed Phenotype Acute Leukemia (MPAL) but can also be seen in other leukemias. It poses substantial classification and management dilemmas. Herein, we report a large cohort of acute leukemia with a mixed phenotype and define Acute Myeloid Leukemia with Mixed Phenotype (AML-MP) and MPAL as two distinct groups by characterizing the clinical, genetic, and transcriptomic features.
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January 2025
Department of Urology, Kidney and Urology Center, the Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.
Doublecortin-like kinase 1 (DCLK1) has been revealed to be involved in modulating cancer stemness and tumor progression, but its role in prostate cancer (PCa) remains obscure. Castration-resistant and metastatic PCa exhibit aggressive behaviors, and current therapeutic approaches have shown limited beneficial effects on the overall survival rate of patients with advanced PCa. This study aimed to investigate the biological role and potential molecular mechanism of DCLK1 in the progression of PCa.
View Article and Find Full Text PDFBlood
January 2025
Graduate School of Medicine and Frontier Biosciences, Osaka University, Japan.
The maintenance of cellular redox balance is crucial for cell survival and homeostasis and is disrupted with aging. Selenoproteins, comprising essential antioxidant enzymes, raise intriguing questions about their involvement in hematopoietic aging and potential reversibility. Motivated by our observation of mRNA downregulation of key antioxidant selenoproteins in aged human hematopoietic stem cells (HSCs) and previous findings of increased lipid peroxidation in aged hematopoiesis, we employed tRNASec gene (Trsp) knockout (KO) mouse model to simulate disrupted selenoprotein synthesis.
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