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Purpose: To compare tumor perfusion on cone-beam computed tomography (CBCT) after hepatic artery infusion port implantation with the tumor response to hepatic arterial infusion chemotherapy (HAIC) in patients with hepatocellular carcinoma (HCC).
Methods: This retrospective study was conducted in patients with advanced HCC treated with HAIC from 2015 to 2020. We performed CBCT with contrast injection via a port on the day following implantation. We classified tumor perfusion on CBCT into three groups: hyperperfusion, isoperfusion, and hypoperfusion. We also evaluated tumor response to HAIC on follow-up images using RECIST 1.1 and compared it with tumor perfusion on CBCT.
Results: This study included 206 tumors in 193 patients (mean: 60.5 years) with HCC. There were 100 hyperperfusion tumors (48.5%), 92 isoperfusion tumors (44.7%), and 14 hypoperfusion tumors (6.8%). The tumor response to HAIC included 10 tumors with a complete response (CR) (4.9%), 66 tumors with a partial response (32%), 60 tumors with stable disease (29.1%), and 70 tumors with progressive disease (34%). Hyperperfusion tumors had a 65% objective response rate (ORR) and a 92% disease control rate (DCR). Isoperfusion tumors had a 12% ORR and a 46.8% DCR, while hypoperfusion tumors had a 0% ORR and a 7.1% DCR. A CR was shown only in hyperperfusion tumors. The ORR and DCR of the three groups were different, with statistical significance ( < 0.001).
Conclusion: Hyperperfusion tumors on CBCT showed a better tumor response to HAIC, with a 65% ORR in patients with HCC. Tumor perfusion on CBCT after implantation of the hepatic arterial infusion port was associated with the tumor response to HAIC.
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http://dx.doi.org/10.4274/dir.2023.232311 | DOI Listing |
Cell Mol Biol (Noisy-le-grand)
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Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Despite significant advancements in the treatment of non-small cell lung cancer (NSCLC) using conventional therapeutic methods, drug resistance remains a major factor contributing to disease recurrence. In this study, we aimed to explore the potential benefits of combining PI3K inhibition with Cisplatin in the context of NSCLC-derived A549 cells. Human non-small cell lung cancer A549 cells were cultured and treated with BKM120, cisplatin, or their combination.
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Department of Gastroenterology, The Second Hospital of Shandong University, Jinan, China.
Metabolic associated steatohepatitis (MASH) is a severe form of metabolic dysfunction-associated steatotic liver disease (MASLD) characterized by hepatocellular injury, inflammation, and fibrosis. Despite advances in understanding its pathophysiology, the molecular mechanisms driving MASH progression remain unclear. This study investigates the role of long non-coding RNA Linc01271 in MASLD/MASH pathogenesis, ant its involvement in the miR-149-3p/RAB35 axis and PI3K/AKT/mTOR signaling pathway.
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September 2025
Roche Products India Pvt. Ltd, Mumbai, India.
Introduction: Trastuzumab emtansine (T-DM1), an antibody-drug conjugate, targets tumor cells overexpressing human epidermal growth factor receptor 2 (HER2). This single-arm, phase IV study assessed the safety and efficacy of T-DM1 in Indian patients with HER2-positive, locally advanced, or metastatic breast cancer previously treated with trastuzumab and a taxane.
Methods: Patients received T-DM1 (3.
Cancer Immunol Res
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Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States.
Antibody-based therapies have revolutionized cancer treatment but have several limitations. These include: down-regulation of the target antigen; mutation of the target epitope; or in the case of antibody drug conjugates (ADCs), resistance to the chemotherapy warhead. Since TROP2-targeted therapy with ADCs yields responses in TROP2+ solid tumors but lacks the durability observed with other immunotherapy-based approaches, we developed novel TROP2-targeting chimeric antigen receptor (CAR) T cells as an alternative.
View Article and Find Full Text PDFCancer Immunol Res
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University of Pennsylvania, Philadelphia, PA, United States.
Pancreatic ductal adenocarcinoma (PDA) is defined by a myeloid-enriched microenvironment and has shown remarkable resistance to immune checkpoint blockade (e.g., PD-1 and CTLA-4).
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