by A research team at the National University of Singapore (NUS) has made a breakthrough in understanding the link between cancer risk and poor diet, shedding light on how common diseases like diabetes can also stem from dietary habits. Their findings, recently published in Cell, could pave the way for more effective cancer prevention strategies that promote healthy aging.
Led by Professor Ashok Venkitaraman, the study was carried out by scientists from the Cancer Science Institute of Singapore (CSI Singapore) and the NUS Center for Cancer Research (N2CR). Collaborating with researchers from the Agency for Science, Technology and Research (A*STAR), the team delved into the intricate relationship between genetic predisposition and environmental factors to uncover the mechanisms underlying cancer development.
Prof Venkitaraman highlighted the importance of understanding how environmental factors, including diet, exercise, and pollution, contribute to cancer risk. By studying patients with a high genetic risk of breast or ovarian cancers due to an inherited faulty copy of the BRCA2 gene, the team discovered that cells from these individuals were more sensitive to a compound called methylglyoxal. This compound, produced during the breakdown of glucose for energy, was found to induce DNA damage, serving as an early indicator of cancer development.
Moreover, the researchers observed that individuals without the faulty BRCA2 gene but with elevated levels of methylglyoxal, such as those with diabetes or pre-diabetes linked to obesity and poor diet, also displayed heightened cancer risk markers. Prof Venkitaraman emphasized that monitoring methylglyoxal levels through a simple blood test for HbA1C could serve as a potential marker for assessing cancer risk, with the possibility of managing these levels through medication and dietary interventions to mitigate cancer initiation.
Dr. Li Ren Kong, the study’s first author, underscored the significance of these findings in revealing a fundamental connection between energy metabolism and cancer progression, underscoring the role of diet and weight management in reducing cancer risks. Additionally, the team’s research challenged longstanding beliefs regarding cancer-preventing genes, showing that methylglyoxal could transiently inactivate these protective genes, suggesting that chronic exposure to poor diet and uncontrolled diabetes could accumulate over time, increasing cancer susceptibility.
By reshaping the understanding of how dietary factors influence cancer risk and utilizing biomarkers like methylglyoxal levels to guide preventive measures, the study poses implications for future research directions in cancer prevention and management. The findings signal a crucial step towards developing targeted strategies that leverage dietary interventions and metabolic control to curb the rising burden of cancer related to poor dietary habits.
