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Clinical relevance of midkine as a biomarker predicting atherosclerotic risk factors in individuals with type-2 diabetes mellitus: a cross-sectional study.
J Diabetes Metab Disord
June 2025
Iraqi Ministry of Health, Baghdad, Iraq.
Objective: Midkine (MK) is a member of a small protein family that includes pleiotrophin. MK levels are elevated in obese patients and have a pro-arthrogenic effect through various pathophysiological processes including vascular inflammation and atherogenesis. This study aimed to investigate the association between serum MK levels and several atherosclerotic risk factors in patients with type 2 diabetes mellitus (T2DM).
View Article and Find Full Text PDFBioinformatics study of bortezomib resistance-related proteins and signaling pathways in mantle cell lymphoma.
Transl Cancer Res
September 2024
Department of Hematology, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing, China.
Background: The bortezomib (BTZ) resistance mechanisms in mantle cell lymphoma (MCL) are complex, involving various genes and signaling pathways. This study used bioinformatical tools to identify and analyze differentially expressed genes (DEGs) associated with BTZ resistance.
Methods: Gene chip datasets containing MCL BTZ-resistant and normal control cohorts (GSE20915 and GSE51371) were selected from the Gene Expression Omnibus (GEO) database.
Midkine links aging with breast cancer-A new predictor of cancer risk.
Cancer Cell
November 2024
Cancer Biology and Stem Cells Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, VIC 3050, Australia. Electronic address:
Despite aging being one of the strongest risk factors for cancer, little is known about the biological mechanisms that promote tumor initiation. In this issue of Cancer Cell, Yan et al. address this fundamental question in the context of breast cancer and report that midkine is upregulated during the aging process and can promote tumorigenesis.
View Article and Find Full Text PDFUCHL1 Overexpression Is Related to the Aggressive Phenotype of Non-small Cell Lung Cancer.
Tuberc Respir Dis (Seoul)
October 2024
Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.
Background: Ubiquitin C-terminal hydrolase L1 (UCHL1), which encodes thiol protease that hydrolyzes a peptide bond at the C-terminal glycine residue of ubiquitin, regulates cell differentiation, proliferation, transcriptional regulation, and numerous other biological processes and may be involved in lung cancer progression. UCHL1 is mainly expressed in the brain and plays a tumor-promoting role in a few cancer types; however, there are limited reports regarding its role in lung cancer.
Methods: Single-cell RNA (scRNA) sequencing using 10X chromium v3 was performed on a paired normal-appearing and tumor tissue from surgical specimens of a patient who showed unusually rapid progression.
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