Singapore , May 9, 2024 In a groundbreaking study, scientists have uncovered a previously unknown link between diet, metabolism, and cancer risk, shedding light on why unhealthy dietary habits and unmanaged metabolic conditions like diabetes may increase susceptibility to cancer.

Conducted by researchers from Singapore and the UK, the study utilized mouse models, human tissue samples, and lab-grown human breast organoids to unveil a mechanism by which changes in glucose metabolism can temporarily deactivate tumor-suppressing genes, such as BRCA2.

Lead author Li Ren Kong, a cancer pharmacologist from the Cancer Science Institute of Singapore (CSI Singapore), highlights the significance of these findings in understanding cancer risk factors and management strategies.

Contrary to the long-standing ‘two-hit’ paradigm proposed by Knudson in 1971, which suggests both copies of a tumor suppressor gene must be permanently inactivated for cancer initiation, this study reveals that mutations in just one copy of the BRCA2 gene can increase susceptibility to cancer when exposed to environmental stresses.

One of the key findings suggests that methylglyoxal (MGO), a byproduct of glucose metabolism, can impair the tumor-suppressing functions of BRCA2, leading to mutations associated with cancer development. This effect was observed in both noncancerous cells and patient-derived tissue samples, indicating a potential link between glucose metabolism, diabetes, and cancer progression.

While these findings provide valuable insights, further research using larger clinical studies or animal models is needed to explore the intricate connections between dietary factors, metabolic disorders, and cancer risk.

Nevertheless, understanding how MGO disrupts BRCA2 function may pave the way for innovative cancer prevention and early detection strategies. Monitoring MGO levels through routine blood tests and adopting interventions to control glucose metabolism could offer proactive measures against cancer initiation and progression.