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Objective: The prevalence of breast cancer and gynaecological cancers is high, and these cancer types can occur consecutively as secondary cancers. The aim of our study is to determine the genes commonly expressed in these cancers and to identify the common hub genes and drug components.

Materials And Methods: Gene intensity values of breast cancer, gynaecological cancers such as cervical, ovarian and endometrial cancers were used from the Gene Expression Omnibus database Affymetrix Human Genome U133 Plus 2.

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Objective: Triple negative breast carcinoma (TNBC) is characterized by the absence of estrogen receptor, progesterone receptor and human epidermal growth factor receptor-2 receptor expression. Carbonic anhydrase IX (CA IX) is a tumor-associated cell surface glycoprotein that is involved in adaptation to hypoxia-induced acidosis and plays a role in cancer progression. The aim of this study was to investigate CA IX expression in TNBC and its relationship with treatment effect.

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Background: Smooth muscle cells (SMCs) of the proximal thoracic aorta are derived from second heart field (SHF) and cardiac neural crest lineages. Recent studies, both in vitro and in vivo, have implied relevance of lineage-specific SMC functions in the pathophysiology of thoracic aortic diseases; however, whether 2 lineage-derived SMCs have any predisposed transcriptional differences in the control aorta remains unexplored.

Methods: Single-cell RNA sequencing and single-nucleus assay for transposase-accessible chromatin sequencing were performed on isolated cells from the aortic root and ascending aortas of 14-week-old SHF-traced () and cardiac neural crest-traced () male mice.

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PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.

Theranostics

January 2025

Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine and Institute of Brain and Brain-Inspired Science, Shandong University, Shandong, China.

Endothelial-to-mesenchymal transition (EndMT) is a cellular reprogramming mechanism by which endothelial cells acquire a mesenchymal phenotype. Endothelial cell dysfunction is the initiating factor of atherosclerosis (AS). Increasing evidence suggests that EndMT contributes to the occurrence and progression of atherosclerotic lesions and plaque instability.

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Glioblastoma IDH wild type (GBM IDH wt) has a poor prognosis and a strongly associated with inflammatory processes. Inflammatory molecules generate positive feedback with tumor cells fueling tumor growth as well as recruitment of immune cells that promote aggressiveness. Although the role of many inflammatory molecules is well known, there are many macromolecules, such as the S100A proteins, whose role is only now beginning to be established.

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