Epigenetic modifications have emerged into one of the cancer hallmarks, replacing the concept of malignant pathologies as being solely genetic-based conditions. The epigenetic landscape is responsible for normal development but also for the heterogeneity among tissues in terms of gene expression patterns. Dysregulation in these mechanisms has been associated with disease stage, and increased attention is now granted to cancer in order to take advantage of these modifications in terms of novel therapeutic strategies or diagnosis/prognosis tools. Oral cancer has also been subjected to epigenetic analysis with numerous studies revealing that the development and progression of this malignancy are partially induced by an altered epigenetic substrate together with genetic alterations and prolonged exposure to environmental risk factors. The present review summarizes the most important epigenetic modifications associated with oral cancer and also their potential to be used as new therapeutic targets.
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http://dx.doi.org/10.3390/ijms19030670 | DOI Listing |
Adv Sci (Weinh)
January 2025
Institute of Biomedicine and Translational Medicine, University of Tartu, Ravila 14B, Tartu, 50411, Estonia.
In triple-negative breast cancer (TNBC), pro-tumoral macrophages promote metastasis and suppress the immune response. To target these cells, a previously identified CD206 (mannose receptor)-binding peptide, mUNO was engineered to enhance its affinity and proteolytic stability. The new rationally designed peptide, MACTIDE, includes a trypsin inhibitor loop, from the Sunflower Trypsin Inhibitor-I.
View Article and Find Full Text PDFJ Oral Microbiol
January 2025
Integrative Microecology Clinical Center, Shenzhen Clinical Research Center for Digestive Disease, Shenzhen Technology Research Center of Gut Microbiota Transplantation, The Clinical Innovation & Research Center, Shenzhen Key Laboratory of Viral Oncology, Department of Clinical Nutrition, Shenzhen Hospital, Southern Medical University, Shenzhen, China.
Background: This study aims to develop an oral microbiota-based model for gastric cancer (GC) risk stratification and prognosis prediction.
Methods: Oral microbial markers for GC prognosis and risk stratification were identified from 99 GC patients, and their predictive potential was validated on an external dataset of 111 GC patients. The identified bacterial markers were used to construct a Deep Neural Network (DNN) model, a Random Forest (RF) model, and a Support Vector Machine (SVM) model for predicting GC prognosis.
Iran J Med Sci
December 2024
Department of Oral and Maxillofacial Radiology, School of Dentistry, Tehran University of Medical Sciences, Tehran, Iran.
Fibrous dysplasia is a slow-progressing benign condition characterized by abnormal bone formation that leads to some skeletal disorders. Although some of the fibrous dysplasia have unusual clinical and radiographic features that can lead to a challenging diagnosis, most lesions reveal an expansile bone defect due to cortex thinning. This report presented a case of monostotic fibrous dysplasia of a 43-year-old woman with involvement of the right maxillary jaw and sinuses, which indicated unusual histopathological features.
View Article and Find Full Text PDFFront Mol Biosci
January 2025
Vienna Metabolomics Center (VIME), University of Vienna, Vienna, Austria.
Cancer is ranked as the top cause of premature mortality. Volatile organic compounds (VOCs) are produced from catalytic peroxidation by reactive oxygen species (ROS) and have become a highly attractive non-invasive cancer screening approach. For future clinical applications, however, the correlation between cancer hallmarks and cancer-specific VOCs requires further study.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Otolaryngology, The Affiliated Ganzhou Hospital of Nanchang University, Ganzhou, Jiangxi, China.
Oral cancer is a highly malignant disease characterized by recurrence, metastasis, and poor prognosis. Autophagy, a catabolic process induced under stress conditions, has been shown to play a dual role in oral cancer development and therapy. Recent studies have identified that autophagy activation in oral epithelial cells suppresses cancer cell survival by inhibiting key pathways such as the mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK), while activating the adenosine monophosphate-activated protein kinase (AMPK) pathway.
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