A cross-section of recent ICGEB scientific publications.
From ICGEB PIs:
Published in Nature Reviews Bioengineering – co-author Jenny Molloy, Biomanufacturing Group: Building sustainable diagnostic ecosystems for global health. Access to diagnostic tests around the world is limited not only by their availability, but also by how they are produced and distributed. Many diagnostic technologies rely on expensive global supply chains that are concentrated in a small number of specialized biotechnology hubs. The authors argue that creating stronger and fairer diagnostic systems requires not only providing tests, but also combining decentralized diagnostic services with local manufacturing and research capabilities, so that communities can develop, produce, and use diagnostic tools more independently. This approach could make diagnostic systems more resilient, equitable, and sustainable in the long term.
Published in Science Advances – co-authors Davide Selvestrel and Giovanni Sorrentino, Advanced Disease Models Group, Andrés F. Muro, Mouse Molecular Genetics Group: S-Nitrosylation of glycogen phosphorylase regulates nuclear glycogenolysis and is impaired in metabolic liver disorders. The researchers have discovered how a build-up of glycogen, a stored form of sugar, inside the control centres of liver cells may contribute to liver problems in argininosuccinic aciduria, a rare inherited metabolic disorder, and metabolic dysfunction-associated steatotic liver disease, a common form of fatty liver disease. They found that nitric oxide helps an enzyme reach this compartment and break down glycogen, supporting the regulation of genes needed for healthy liver function. In animal experiments, supplementing nitric oxide restored the enzyme’s presence there.
Published in Cell Death & Disease – co-authors Davide Selvestrel, Caterina Da Rodda, Beatrice Anfuso, Suresh Velnati (Alumnus), Karin Hofmann and Giovanni Sorrentino, Advanced Disease Models Group: Human iPSC-derived liver organoid model multicellular tissue responses and therapeutic rescue in Wolman disease. Having developed miniature human liver models from stem cells, the researchers used them to study Wolman disease, a rare inherited disorder that causes harmful fat build-up and severe liver damage in infants. These models reproduced key features of the disease and showed how interactions between different liver cell types contribute to inflammation and scarring. Restoring the faulty gene’s function in the main liver cells reduced several signs of disease in both the models and animal experiments.
Published in PLOS Pathogens – authors Ifeoluwa D. Gbala, Tumour Virology Group, Om Basukala and Amira Zine El Abidine, Alumni of Tumour Virology Group, Michael P. Myers, Protein Networks Group, Rebecca Bertolio and Giannino Del Sal, Cancer Cell Signalling Group, Lawrence Banks, Tumour Virology Group: Phosphorylated HPV‑16 E7 disrupts planar cell polarity in cervical cancer cells through vangl1 dysregulation. A possible new target was identified for treating cervical cancer caused by HPV-16, a high-risk type of human papillomavirus. In laboratory experiments, a cancer-promoting protein made by the virus disrupted Vangl1, a protein that helps cells stay properly organised within tissues. Reducing Vangl1 made the cancer cells less able to invade surrounding tissue and more sensitive to chemotherapy. These findings suggest that treatments targeting Vangl1, or blocking the virus’s interaction with it, could potentially limit cancer spread and improve treatment response.
Published in the Journal of Drug Delivery Science and Technology – co-authors Serena Zacchigna and Yin Quan Tang, Alumnus of Cardiovascular Biology Group: Breast cancer homing peptide: A study of diagnostic efficacy across luminal, HER2+ and triple negative breast cancer. The researchers have developed MBC-P2, a small protein fragment that could help make several major types of breast cancer easier to detect, including triple-negative breast cancer. In laboratory tests and human tissue samples, it preferentially attached to cancer cells while showing little binding to normal breast cells. When linked to a fluorescent label, it made the cancer cells visible, suggesting potential for more precise imaging across breast cancer types that currently require different detection approaches.
Published in Bioorganic Chemistry – co-authored by Gizachew Muluneh Amera, Giulia Canarutto and Silvano Piazza, Computational Biology Group, and Stefano Cacciatore, Bioinformatics Group: Computational targeting of APE1-miRNA interactions in Cancer: Prioritization of candidate modulators. The researchers have identified compounds worth investigating as potential tools for studying how cancer cells adapt and resist treatment. Using computer screening and early laboratory tests, they explored whether these compounds could affect interactions between APE1, a protein involved in DNA repair and gene regulation, and a small RNA molecule linked to cancer. Two compounds showed preliminary signs of reducing the protein–RNA complex, but the tests do not yet establish how they work or whether they preserve APE1’s other important functions.
CRP Grant Awardee Publications:
Published in Cellular and Molecular Life Sciences – co-authored by Luciana Balboa, ICGEB CRP awardee: Lipid-mediated GPR32 signaling reprograms macrophage metabolism to impair anti-tuberculous immunity. A molecule was identified that may help tuberculosis bacteria survive by weakening the immune cells meant to destroy them. Studying fluid collected from around the lungs of people with TB, the researchers found that Resolvin D5 reduced these cells’ ability to use sugar for energy and control the infection. In laboratory experiments, blocking a signalling pathway involved in this response, or restoring a protein that supports the cells’ activity, counteracted some of these effects. The findings point to possible treatments that strengthen the body’s defences alongside antibiotics, although further research is needed to establish whether these approaches would be safe and effective in patients.