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Scientists at the University of Lausanne have identified a metabolic vulnerability in tumor cells linked to vitamin B7 (biotin). Cancer cells often depend on glutamine to sustain growth, but when this nutrient is limited, they can switch to alternative pathways involving pyruvate. This adaptive mechanism relies on the enzyme pyruvate carboxylase, which requires vitamin B7 to function.
The study found that without biotin, this enzyme becomes inactive, preventing cancer cells from compensating for glutamine loss and ultimately slowing their growth. Additionally, mutations in the FBXW7 gene—common in several cancers—further impair this pathway, increasing reliance on glutamine and exposing a potential therapeutic target.
These findings help explain why treatments targeting glutamine alone may fail, as cancer cells can adapt metabolically. The research suggests that future therapies could be more effective by simultaneously disrupting multiple metabolic pathways in tumor cells.
20-04-2026