Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4836596 | PMC |
Publication Analysis
Top Keywords
Similar Publications
NOTCH1 regulates the DNA damage response and sorafenib resistance by activating ATM in hepatocellular carcinoma.
Am J Transl Res
December 2024
Department of Pharmacy, Shanghai Fifth People's Hospital, Fudan University 801 Heqing Road, Shanghai 200240, China.
Objective: This study investigates the mechanism underlying sorafenib resistance in hepatocellular carcinoma cells (HCC), focusing on DNA damage repair (DDR) pathways to develop targeted therapeutic strategies.
Methods: Bioinformatics analysis was used to screen genes associated with sorafenib resistance, which was further demonstrated by western blotting. Cell proliferation was determined using the EdU assay.
Targeting EGFR-binding protein SLC7A11 enhancing antitumor immunity of T cells via inducing MHC-I antigen presentation in nasopharyngeal carcinoma.
Cell Death Dis
January 2025
Department of Pathology, The Xiangya Hospital, Central South University, 410008, Changsha, Hunan, China.
Approximately 80% of nasopharyngeal carcinoma (NPC) patients exhibit EGFR overexpression. The overexpression of EGFR has been linked to its potential role in modulating major histocompatibility complex class I (MHC-I) molecules. We discovered that EGFR, operating in a kinase-independent manner, played a role in stabilizing the expression of SLC7A11, which subsequently inhibited MHC-I antigen presentation.
View Article and Find Full Text PDFAdvanced hepatocellular carcinoma treatment strategies: Are transarterial approaches leading the way?
World J Gastrointest Oncol
January 2025
Department of General and Pediatric Surgery, Bolzano Central Hospital - SABES, Bolzano 39100, Trentino-Alto Adige, Italy.
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, with advanced stages posing significant treatment challenges. Although hepatic arterial infusion chemotherapy (HAIC) has emerged as a promising modality for treating advanced HCC, particularly in Asian clinical practice, its adoption in Western medicine remains limited due to a lack of large-scale randomized controlled trials. This editorial reviews and comments on the meta-analysis conducted by Zhou , which evaluates the efficacy and safety of HAIC and its combination strategies for advanced HCC.
View Article and Find Full Text PDFConstruction of a prognostic model for gastric cancer based on immune infiltration and microenvironment, and exploration of MEF2C gene function.
BMC Med Genomics
January 2025
Department of Oncology, The First People's Hospital of Yibin, No.65, Wenxing Street, Cuiping District, Yibin, 644000, China.
Background: Advanced gastric cancer (GC) exhibits a high recurrence rate and a dismal prognosis. Myocyte enhancer factor 2c (MEF2C) was found to contribute to the development of various types of cancer. Therefore, our aim is to develop a prognostic model that predicts the prognosis of GC patients and initially explore the role of MEF2C in immunotherapy for GC.
View Article and Find Full Text PDFSynthesis and biological evaluation of 4-((3-(tetrahydro-2H-pyran-4-yl)-1H-pyrazol-4-yl)oxy)quinoline derivatives as novel potential transforming growth factor-β type 1 receptor inhibitors for hepatocellular carcinoma.
Bioorg Chem
February 2025
Department of General Surgery, the Second Xiang-Ya Hospital, Central South University, Changsha 410011 China. Electronic address:
The transforming growth factor β (TGF-β) type 1 receptor (ALK5) plays a key role in tumor microenvironment. Small-molecule inhibitors of TGFβR1 provides a prospective approach for the treatment of malignant tumors. In this study, a series of 4-((3-(tetrahydro-2H-pyran-4-yl)-1H-pyrazol-4-yl)oxy)quinoline derivatives were identified as novel, potential TGFβR1 inhibitors.
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!