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0.2%
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259
60.7%
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7.3%
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125
29.3%
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- Keio University School of Medicine is hosting the 11th Keio Healthcare Venture Contest, seeking new business ideas in the medical and healthcare fields from students, researchers, and entrepreneurs. - This year's student category features a dedicated "Mibyou (Pre-symptomatic) Measures" track, focusing on understanding health status at the pre-disease stage to drive lifestyle improvements and behavioral changes. - A lecture by physician-turned-VC Anna Nakayasu will address entrepreneurial strategies for converting clinical pain points into sustainable healthcare businesses, including monetization barriers and AI-era entry barriers. - Two additional lecturers, Masaya Sawafuji and Tao Cheng, will discuss field needs in preventive medicine and social implementation perspectives for Mibyou-focused healthcare businesses.
- Researchers at Keio University discovered recurrent COPA gene mutations as an independent driver of small intestinal tumorigenesis, published in Nature Genetics. - COPA mutations activate the Wnt signaling pathway without requiring APC mutations or the proteins R-spondin and Noggin, explaining a long-standing discrepancy in small intestinal cancer genetics. - The findings may inform updates to the WHO classification of digestive system tumors and open new avenues for diagnosis and treatment in patients lacking APC mutations. - Small intestinal cancers account for only 3% of gastrointestinal cancers, and this discovery provides a new molecular framework for understanding their malignant progression.
- Researchers at Keio University identified disease-associated CD4+ T cells that recognize the same Ro60 protein targeted by autoreactive B cells in Sjögren's disease, revealing a self-reinforcing immune loop. - The team used single-cell RNA sequencing and TCR analysis to identify 13 T-cell receptors that specifically recognized Ro60-derived peptides, with findings consistent across Japanese and Caucasian patients. - Anti-Ro60 antibodies form immune complexes that are taken up by antigen-presenting cells, which then activate Ro60-reactive CD4+ T cells, promoting further antibody production and sustaining chronic autoimmunity. - Interrupting this pathogenic loop could enable selective suppression of disease-causing autoimmune responses without impairing normal immune function, potentially reducing infection risks associated with current broad immunosuppressive therapies.
