Osteosarcoma is an aggressive bone cancer characterized by high rate of recurrence and metastasis. In a new study, researchers show that restoring the RNA-editing enzyme adenosine deaminase acting on RNA 2 (ADAR2) slows tumor growth, reduces invasion, promotes bone-like differentiation, and improves chemotherapy sensitivity in cell and mouse models. The findings identify IGFBP7 RNA editing as a key mechanism underlying these effects, highlighting a potential differentiation-based treatment strategy for pediatric patients with bone cancer.

The Universitat Jaume I of Castelló has secured nearly one million euros for five projects under the competitive call for grants aimed at strengthening research careers, within the Human Resources programme of the 2024–2027 State Plan for Scientific, Technical and Innovation Research. This achievement places the UJI fourth nationally and first in the Valencian Community in terms of funding obtained in this call, behind only the Spanish National Research Council (CSIC), the University of Barcelona and the Universitat Politècnica de Catalunya, and ahead of larger universities.

The 2025 call awarded a total of 130 grants worth almost 25 million euros. Its aim is to support the consolidation of the professional careers of national and international researchers within the Spanish System for Science, Technology and Innovation (SECTI), through the creation of permanent positions and by facilitating the launch or strengthening of research lines via funding for R&D&I projects and the improvement of laboratories, facilities and scientific equipment.

With global life expectancy steadily increasing, the growing gap between lifespan and healthspan has placed the aging of the female reproductive system at the forefront of biomedical research. This process, which profoundly impacts fertility, quality of life, and long-term health, is no longer viewed simply through the lens of chronological age or menopause. Instead, a paradigm shift is underway, where aging is understood as a distinct biological process best quantified by multi-omics technologies and computational models known as "aging clocks." These tools—encompassing epigenetics, transcriptomics, proteomics, metabolomics, and microbiomics—provide a powerful, integrated framework to measure biological age, reveal tissue-specific vulnerabilities, and elucidate systemic aging patterns that chronological metrics fail to capture. While this research area is still evolving, the growing availability of high-quality datasets offers unprecedented opportunities to advance our understanding of reproductive aging, infertility, and pregnancy complications, moving towards more personalized and predictive healthcare.

Paligenosis defines a tightly controlled program through which terminally differentiated cells re‑enter the cell cycle and contribute to tissue repair after injury. This review systematically introduces the concept, the three sequential stages of paligenosis—mTORC1 suppression with autophagy initiation, followed by mTORC1 reactivation and stemness gene induction, and finally proliferation with lineage restoration—as well as the underlying molecular networks involving autophagy, metabolic rewiring, and epigenetic remodeling. The article then compares paligenosis with other forms of cellular plasticity such as dedifferentiation, transdifferentiation, epithelial‑mesenchymal transition, and induced pluripotency, highlighting its unique stepwise, reversible and intralineage nature. A major focus is the dual role of paligenosis: while it ensures efficient regeneration in tissues like the stomach and pancreas, its persistent or dysregulated activation under chronic stress or oncogenic signals can drive metaplasia, tumor initiation, metastasis and therapy resistance. The review closes by discussing biomarker prospects for distinguishing adaptive repair from malignant drift, and the therapeutic potential of modulating paligenotic pathways for regenerative medicine and cancer treatment.