Background: Acute myeloid leukemia (AML) is a hematologic tumor with poor prognosis and significant clinical heterogeneity. By integrating transcriptomic data, single-cell RNA sequencing data and independently collected RNA sequencing data this study aims to identify key genes in AML and establish a prognostic assessment model to improve the accuracy of prognostic prediction.
Materials And Methods: We analyzed RNA-seq data from AML patients and combined it with single-cell RNA sequencing data to identify genes associated with AML prognosis. Key genes were screened by bioinformatics methods, and a prognostic assessment model was established based on these genes to validate their accuracy.
Results: The study identified eight key genes significantly associated with AML prognosis: SPATS2L, SPINK2, AREG, CLEC11A, HGF, IRF8, ARHGAP5, and CD34. The prognostic model constructed on the basis of these genes effectively differentiated between high-risk and low-risk patients and revealed differences in immune function and metabolic pathways of AML cells.
Conclusion: This study provides a new approach to AML prognostic assessment and reveals the role of key genes in AML. These genes may become new biomarkers and therapeutic targets that can help improve prognostic prediction and personalized treatment of AML.
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http://dx.doi.org/10.3389/fimmu.2024.1494106 | DOI Listing |
Neuromolecular Med
December 2024
Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, College of Physical Education, Hunan Normal University, Changsha, 410012, China.
Alzheimer's disease (AD) is the most common neurodegenerative disorder. The neuropathology of AD appears in the hippocampus. The purpose of this work was to reveal key differentially expressed genes (DEGs) in the hippocampus of AD patients and healthy individuals.
View Article and Find Full Text PDFClin Exp Med
January 2025
Medical Center of Hematology, Xinqiao Hospital of Army Medical University; Chongqing Key Laboratory of Hematology and Microenvironment; State Key Laboratory of Trauma and Chemical Poisoning, Army Medical University, Chongqing, No.83 Xinqiao Main Street, Shapingba District, 400037, China.
The aim of this study was to investigate the clinical features and outcomes of elderly patients with acute myeloid leukemia (AML) from a real word research. The clinical data of 223 consecutive elderly patients (aged ≥ 60 years) who were newly diagnosed with AML at our medical center between July 2017 and June 2022, including their clinical characteristics, genetic mutations, and survival outcomes, were retrospectively analyzed. Among the 223 patients (median age 67 years), 180 (80.
View Article and Find Full Text PDFFerroptosis, an iron-dependent form of programmed cell death driven by oxidative stress, plays a crucial role in the progression of Alzheimer's disease (AD). Aging diminishes antioxidant systems that maintain iron homeostasis, particularly affecting the glutathione peroxidase (GPX) system, leading to increased ferroptosis and exacerbated neurodegeneration and neuroinflammation in AD. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor regulating genes involved in antioxidant defense and ferroptosis.
View Article and Find Full Text PDFCell Mol Life Sci
January 2025
ENT Institute, Department of Otorhinolaryngology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Organoid is an ideal in vitro model with cellular heterogeneity and genetic stability when passaging. Currently, organoids are exploited as new tools in a variety of preclinical researches and applications for disease modeling, drug screening, host-microbial interactions, and regenerative therapy. Advances have been made in the establishment of nasal and olfactory epithelium organoids that are used to investigate the pathogenesis of smell-related diseases and cellular/molecular mechanism underlying the regeneration of olfactory epithelium.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Gladstone Institutes, UCSF, San Francisco, CA, USA.
Background: Cerebrovascular alterations and innate immune activation are key features of Alzheimer's disease (AD). However, the mechanisms that link blood-brain barrier disruption to neurodegeneration are poorly understood and well-defined druggable targets at the neurovascular interface are limited.
Method: By developing a multiomic and genetic loss-of-function pipeline, we reported the transcriptomic and global phosphoproteomic landscape of blood-induced microglia activation and the causal role for fibrin in induction of neurodegenerative genes and oxidative stress pathways in innate immune cells.
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