Renal cell carcinoma is the most common adult renal solid tumor and the deadliest urological cancer, with clear cell renal cell carcinoma (ccRCC) being the predominant subtype. The PI3K/AKT signaling pathway assumes a central role in ccRCC tumorigenesis, wherein its abnormal activation confers a highly aggressive phenotype, leading to swift resistance against current therapies and distant metastasis. Thus, treatment resistance and disease progression remain a persistent clinical challenge in managing ccRCC effectively. PTEN, an antagonist of the PI3K/AKT signaling axis, emerges as a crucial factor in tumor progression, often experiencing loss or inactivation in ccRCC, thereby contributing to elevated mortality rates in patients. Therefore, understanding the molecular mechanisms underlying PTEN suppression in ccRCC tumors holds promise for the discovery of biomarkers and therapeutic targets, ultimately enhancing patient monitoring and treatment outcomes. The present review aims to summarize these mechanisms, emphasizing their potential prognostic, predictive, and therapeutic value in managing ccRCC.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.bbcan.2024.189165 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Neuroendocrine Tumors in Horseshoe Kidneys: A Review of the Literature With Report of a Novel Finding Expanding Their Morphologic Spectrum.
Adv Anat Pathol
November 2024
Department of Radiology, School of Medical Sciences, State University of Campinas (Unicamp), Campinas, Brazil.
Horseshoe kidney is a rare congenital anomaly with an unusually higher frequency of neuroendocrine tumors. Symptoms are rare, and, in most of the cases, are incidentally diagnosed. The clinical behavior of these tumors is heterogeneous and can be difficult to predict based on histology alone.
View Article and Find Full Text PDFPurpose: The treatment landscape for metastatic renal cell carcinoma (mRCC) has evolved in recent years with the use of tyrosine kinase inhibitors (TKIs) and immuno-oncology (IO) therapies. This study examined patient characteristics, treatment patterns, health care resource utilization (HCRU), costs, and survival for individuals with mRCC who received either IO + IO or IO + TKI combinations as first-line (1L) regimens.
Methods: This retrospective cohort study used integrated claims and clinical data from a commercial health plan to study adults with mRCC who began 1L treatment between April 1, 2018, and January 31, 2023.
High glucose couples DJ-1 with PTEN to activate PDGFRβ for renal proximal tubular cell injury.
PLoS One
January 2025
VA Research, Education and Clinical Center, South Texas Veterans Health Care System, San Antonio, Texas, United States of America.
High glucose milieu in diabetes induces proximal tubular epithelial cells in the kidney to undergo hypertrophy and matrix protein expansion via Akt/mTORC1 signaling, leading to renal fibrosis. The familial Parkinson's disease protein DJ-1 acts as a driver of Ras-dependent tumorigenesis and protects dopaminergic neurons from apoptosis. But its function and mechanistic basis to regulate renal fibrosis is not clear.
View Article and Find Full Text PDFThe Oxidoreductase Retinol Saturase in Thyroid Gland Is Regulated by Hypothyroidism and Iodide Overload and Its Deletion Impairs Metabolic Homeostasis in Mice.
Antioxid Redox Signal
January 2025
Institute of Pharmacology, Max Rubner Center (MRC) for Cardiovascular Metabolic Renal Research, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany.
Thyroid hormones (TH) are major regulators of cell differentiation, growth, and metabolic rate. TH synthesis in the thyroid gland requires high amounts of HO to oxidize iodide for the iodination of thyroglobulin (TG). Retinol Saturase (RetSat) is an oxidoreductase implicated in dihydroretinol formation and cellular sensitivity toward peroxides and ferroptosis.
View Article and Find Full Text PDFSerum amyloid P (PTX2) attenuates hepatic fibrosis in mice by inhibiting the activation of fibrocytes and HSCs.
Hepatol Commun
November 2024
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!