Background: The glucose transporter protein 1 (Glut-1) overexpression is associated with poor overall survival (OS) in various malignant tumors. The aim of this study was to investigate prognostic significance of Glut-1 overexpression in patients with bone and soft-tissue sarcomas.
Methods: A total of 67 patients (mean age, 43 years; range, 8-79 years) with bone and soft tissue sarcomas were analyzed. Pathologic confirmation was observed from surgical specimens in all patients. Pathologic variables including tumor differentiation, necrosis, mitotic index, MIB-1 (Ki-67) grade and Glut-1 expression were assessed. Clinical characteristics and pathologic variables were determined by Kaplan-Meyer curve of OS after treatment.
Results: Glut-1 overexpression was found in 56 patients (83%). The patients with Glut-1 overexpression showed significantly poor OS compared with those without Glut-1 overexpression (P = 0.029). The presence of metastasis, treatment without surgical resection, tumor differentiation, necrosis, mitotic index and MIB-1 grade were also significantly negative prognostic factors. The presence of metastasis was independently associated with poor OS (P = 0.031).
Conclusions: Assessment of Glut-1 expression prior to treatment has a predictive potential effect in patients with bone and soft-tissue sarcomas.
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http://dx.doi.org/10.1093/jjco/hym125 | DOI Listing |
Mol Med
December 2024
Department of Ophthalmology, Ruijin Hospital Affiliated Medical School, Shanghai Jiaotong University, 197 Ruijin er Road, Shanghai, 200025, China.
Background: Glaucoma is a group of heterogeneous neurodegenerative diseases with abnormal energy metabolism and imbalanced neuroinflammation in the retina. Thioredoxin-interacting protein (TXNIP) is involved in glucose and lipid metabolism, and associated with oxidative stress and inflammation, however, not known whether to be involved in glaucoma neuropathy and its underlying mechanisms.
Methods: To establish the chronic ocular hypertension (COH) mice model.
Front Mol Biosci
November 2024
School of Interdisciplinary Engineering and Sciences (SINES), National University of Sciences and Technology (NUST), Islamabad, Pakistan.
Hypoxia-inducible factor-1 (HIF-1) regulates cell growth, protein translation, metabolic pathways and therefore, has been advocated as a promising biological target for the therapeutic interventions against cancer. In general, hyperactivation of HIF-1 in cancer has been associated with increases in the expression of glucose transporter type-1 (GLUT-1) thus, enhancing glucose consumption and hyperactivating metabolic pathways. The collective behavior of GLUT-1 along with previously known key players AKT, OGT, and VEGF is not fully characterized and lacks clarity of how glucose uptake through this pathway (HIF-1) probes the cancer progression.
View Article and Find Full Text PDFFront Bioeng Biotechnol
November 2024
Department of Ultrasound, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Malignant fibroblasts (MFs) are widely present in various diseases and are characterized by connective tissue proliferation; these cells act as a physical barrier that severely limits drug delivery and affects disease outcomes. Based on this, we constructed the smart, integrated, theranostic, targeted lipid nanoprobe HMME-RG3@PFH to overcome the bottleneck in the early diagnosis and treatment of MF-related diseases. The protein glucose transporter protein 1 (GLUT-1) is overexpressed on MFs, and its ideal substrate, ginsenoside RG3 (RG3), significantly enhances the targeted uptake of HMME-RG3@PFH by MFs in a hypoxic environment and endows the nanomaterial with stealthiness to prolong its circulation.
View Article and Find Full Text PDFJ Voice
November 2024
Department of Otolaryngology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, PR China.
J Cancer Res Clin Oncol
September 2024
Nano Bio Electronic Devices Lab, Cancer Electronics Research Group, School of Electrical and Computer Engineering, College of Engineering, University of Tehran, P.O. Box 14395/515, Tehran, Iran.
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