This content is in French.
Cancer: when biotin becomes a therapeutic lever
27 février 2026
By Elodie Vaz | Published on February 27, 2026 | 3 min readCancer is characterized by uncontrolled cell proliferation, supported by profound metabolic reprogramming. Among the identified vulnerabilities, “glutamine dependence” plays a central role: many tumor cells require this amino acid to sustain protein and DNA synthesis and to maintain their energy cycle. In its absence, proliferation halts.
By Elodie Vaz | Published on February 27, 2026 | 3 min read
Cancer is characterized by uncontrolled cell proliferation, supported by profound metabolic reprogramming. Among the identified vulnerabilities, “glutamine dependence” plays a central role: many tumor cells require this amino acid to sustain protein and DNA synthesis and to maintain their energy cycle. In its absence, proliferation halts. Yet some tumors manage to circumvent this metabolic constraint.
A study published on February 25 in Molecular Cell by a team from the University of Lausanne highlights an unexpected mechanism involving vitamin B7 (biotin), revealing a new vulnerability in tumor cells deprived of this essential cofactor.
Cancer is characterized by uncontrolled cell proliferation, supported by profound metabolic reprogramming. Among the identified vulnerabilities, “glutamine dependence” plays a central role: many tumor cells require this amino acid to sustain protein and DNA synthesis and to maintain their energy cycle. In its absence, proliferation halts. Yet some tumors manage to circumvent this metabolic constraint.
A study published on February 25 in Molecular Cell by a team from the University of Lausanne highlights an unexpected mechanism involving vitamin B7 (biotin), revealing a new vulnerability in tumor cells deprived of this essential cofactor.
Sign in to read the rest
Reserved for healthcare professionals, free registration.
Scientific reference
University of Lausanne. Vitamins: a tool to exploit against cancer [press release]. EurekAlert!; 2026 Feb 25.
View the source
