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Anti-inflammatory and antinociceptive effects of LQFM275 - A new multi-target drug.
Int Immunopharmacol
December 2024
Laboratory of Pharmacology of Natural and Synthetic Products, Institute of Biological Sciences, Federal University of Goiás, Campus Samambaia, Goiânia, Brazil.
Compound (4-(3,5-di-tert-butyl-4-hydroxybenzylamine)benzenesulfonamide) (LQFM275) was designed and synthesized from darbufelone and sulfanilamide as a new multi-target for the treatment of inflammatory diseases. LQFM275 showed a great range of safe cytotoxicity profile (100-400 μM) evaluated by MTT assay, preventing damage induced by lipopolysaccharide (LPS) in EA.hy926 cell line.
View Article and Find Full Text PDFBRAFV600E/pTERT double mutated papillary thyroid cancers exhibit immune gene suppression.
Front Endocrinol (Lausanne)
December 2024
Division of Endocrinology, Mayo Clinic, Jacksonville, FL, United States.
Introduction: BRAFV600E mutation (BRAF) is common in papillary thyroid cancer (PTC), and most patients have an excellent outcome. However, a TERT-promoter mutation (pTERT) in the presence of BRAF (BRAFpTERT) has been demonstrated to confer a more aggressive behavior to PTC. Lymphocytic infiltration is often present in PTC.
View Article and Find Full Text PDFNon-Susceptibility Gene Variants in Head and Neck Paragangliomas.
Int J Mol Sci
November 2024
Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
Head and neck paragangliomas (HNPGLs) are rare neoplasms that, along with pheochromocytomas and extra-adrenal paragangliomas, are associated with inherited mutations in at least 12 susceptibility genes in approximately 40% of cases. However, due to the rarity of HNPGLs, only a series of small-scale studies and individual cases have reported mutations in additional genes that may be involved in tumorigenesis. Consequently, numerous disease-causing mutations and genes responsible for the pathogenesis of HNPGLs remain poorly investigated.
View Article and Find Full Text PDFThe absence of telomerase leads to immune response and tumor regression in zebrafish melanoma.
Cell Rep
December 2024
Institute for Research on Cancer and Aging of Nice (IRCAN), CNRS UMR7284, INSERM U1081, Université Côte d'Azur, 06107 Nice, France; Instituto Gulbenkian de Ciência, 2780-156 Oeiras, Portugal. Electronic address:
Most cancers re-activate telomerase to maintain telomere length and thus acquire immortality. Activating telomerase promoter mutations are found in many cancers, including melanoma. However, it is unclear when and if telomerase is strictly required during tumorigenesis.
View Article and Find Full Text PDFBeginning at the ends: telomere and telomere-based cancer therapeutics.
Mol Genet Genomics
December 2024
Department of Medical Genetics, School of Medicine, Iranshahr University of Medical Sciences, Iranshahr, Iran.
Telomeres, which are situated at the terminal ends of chromosomes, undergo a reduction in length with each cellular division, ultimately reaching a critical threshold that triggers cellular senescence. Cancer cells circumvent this senescence by utilizing telomere maintenance mechanisms (TMMs) that grant them a form of immortality. These mechanisms can be categorized into two primary processes: the reactivation of telomerase reverse transcriptase and the alternative lengthening of telomeres (ALT) pathway, which is dependent on homologous recombination (HR).
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