The metabolic reprogramming that promotes tumorigenesis in glioblastoma is induced by dynamic alterations in the hypoxic tumor microenvironment, as well as in transcriptional and signaling networks, which result in changes in global genetic expression. The signaling pathways PI3K/AKT/mTOR and RAS/RAF/MEK/ERK stimulate cell metabolism, either directly or indirectly, by modulating the transcriptional factors p53, HIF1, and c-Myc. The overexpression of HIF1 and c-Myc, master regulators of cellular metabolism, is a key contributor to the synthesis of bioenergetic molecules that mediate glioma cell transformation, proliferation, survival, migration, and invasion by modifying the transcription levels of key gene groups involved in metabolism. Meanwhile, the tumor-suppressing protein p53, which negatively regulates HIF1 and c-Myc, is often lost in glioblastoma. Alterations in this triad of transcriptional factors induce a metabolic shift in glioma cells that allows them to adapt and survive changes such as mutations, hypoxia, acidosis, the presence of reactive oxygen species, and nutrient deprivation, by modulating the activity and expression of signaling molecules, enzymes, metabolites, transporters, and regulators involved in glycolysis and glutamine metabolism, the pentose phosphate cycle, the tricarboxylic acid cycle, and oxidative phosphorylation, as well as the synthesis and degradation of fatty acids and nucleic acids. This review summarizes our current knowledge on the role of HIF1, c-Myc, and p53 in the genic regulatory network for metabolism in glioma cells, as well as potential therapeutic inhibitors of these factors.

Glioblastoma (GBM) is the most common and aggressive primary brain tumor. Currently, treatment is ineffective and the median overall survival is 20.9 months. The poor prognosis of GBM is a consequence of several altered signaling pathways that favor the proliferation and survival of neoplastic cells. One of these pathways is the deregulation of phosphodiesterases (PDEs). These enzymes participate in the development of GBM and may have value as therapeutic targets to treat GBM. Methylxanthines (MXTs) such as caffeine, theophylline, and theobromine are PDE inhibitors and constitute a promising therapeutic anti-cancer agent against GBM. MTXs also regulate various cell processes such as proliferation, migration, cell death, and differentiation; these processes are related to cancer progression, making MXTs potential therapeutic agents in GBM.

Background/Objectives: Dental caries and periodontal diseases are the most common illnesses in the oral cavity and represent a public health concern globally. In recent decades, diverse studies showed that Kefir, a traditional beverage that can be milk- or water-based, contains a complex microbial community and has health benefits. The goal of this review was to update the current knowledge of kefir consumption and its impact on oral health. Methods: The search of a combination of keywords—kefir; dental caries; probiotics; microbiota; periodontal diseases; biofilm; and oral health—was conducted using PubMed, Google Scholar, and Web of Science databases for studies in human subjects. Discussion: The research suggests that kefir consumption may aid in decreasing counts of microorganisms typically associated with oral illness. Conclusions: Kefir has the potential to inhibit certain oral pathogens and reduce biofilm formation by promoting diversity within the oral microbiota, suggesting that kefir could be a promising adjuvant treatment for dental caries and periodontal diseases by improving oral health.

The aim of this study was the quantification of Sphingosine-1-phosphate (S1P) in periodontal pockets of patients with periodontitis. This is an observational, descriptive, case-control study. Thirty subjects were selected: 15 controls and 15 cases. A periodontal study was conducted following the parameters of AAP 2017 for the diagnosis of periodontal diseases. A sample of saliva and gingival crevicular fluid was obtained from each subject and then analyzed with the Human S1P Elisa kit (MyBioSource #MBS2516132) accordingly to the manufacturer's instructions, in order to verify the presence of S1P and quantify it´s concentration when founded. Results showed a significant difference (p=0.05) between cases and controls. In the case of saliva samples, the concentration of S1P was higher than the ones found in the control group (72.94 ng/mL and 45.12 ng/mL). For GCF, a higher amount of S1P was found in patients with POD (20.09 ng/mL and 15.20 ng/mL). This work raises a possible route of bone metabolism, inflammatory process, and identification of periodontitis through oral quantification of S1P, however, future studies are needed.

La salud bucal depende no solo de la higiene, sino también del equilibrio de los microorganismos que habitan nuestra boca. Cuando se altera, puede surgir la enfermedad periodontal, infección crónica de dientes y encías frecuente en el sur-sureste de México. En esta región, bebidas tradicionales como el pozol y la taberna contienen probióticos naturales, que además de favorecer la digestión, pueden contribuir a la salud bucal. Incorporar alimentos fermentados a la dieta, junto con buenos hábitos de higiene, ayuda a mantener equilibrada la microbiota y reduce el riesgo de enfermedades orales, integrando tradición y ciencia en la alimentación cotidiana.

P53 is a tumor suppressor involved in cell-cycle regulation and DNA repair. Studies have shown that altered p53 expression in oral squamous cell carcinoma (OSCC) is associated with a poor prognosis and increased tumor aggressiveness, suggesting it could be considered a potential prognostic marker. A search was performed using keywords such as oral squamous cell carcinoma, TP53, and p53 therapies in the PubMed and Web of Science databases, with a timeframe from 2020 to 2025. In this review, we examined various therapies targeting p53 that have been proposed in recent years. These therapies have been tested in vitro, in vivo, and in some cases, through clinical trials. Their goal is to restore the conformation and activity of mutated p53 by identifying small molecules that restore p53 function and eliminate mutated cells. Although some of these therapies show promising results, further clinical studies are needed to assess their efficacy and safety in OSCC patients.