In a recent study, the research team of the National University of Singapore and the Singapore Science and Technology Research Bureau has made groundbreaking progress. These new findings reveal the relationship between cancer risk and poor eating habits and clarify the causal chain between common diseases such as diabetes induced by poor diet and the increased risk of cancer. The breakthrough results of this study are expected to provide strong support for the development of cancer prevention strategies aimed at promoting healthy aging.
The relevant research results were published online in the Cell journal, under the title “A glycolytic metabolite bypasses “two-hit” tumor suppression by BRCA2”. The corresponding author of the paper is Professor Ashok Venkitaraman, Director of the Singapore Cancer Research Institute.
Professor Venkitaraman explained, “Cancer is caused by the interaction between our genes and environmental factors such as diet, exercise, and pollution. It is not yet clear how these environmental factors increase the risk of cancer, but understanding the connections is crucial if we are to take preventive measures to help us stay healthy for a longer period.”
The research team first focused on those individuals who had a higher risk of breast cancer or ovarian cancer because they inherited a defective copy of the BRCA2 cancer gene. They found that cells derived from these patients are particularly sensitive to methylglyoxal, a compound generated in the process of cells decomposing glucose to produce energy, which is associated with diabetes, obesity, and bad eating habits.
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Research has revealed that this compound can cause DNA damage, which is precisely an early warning signal for cancer occurrence. The study also showed that even those individuals without genetic defect BRCA2 gene copies, such as diabetes or pre-diabetes patients (usually associated with obesity or poor eating habits) with high levels of acetaldehyde, would accumulate similar warning signals, indicating a higher risk of cancer.
Professor Venkitaraman further said, “Our research suggests that patients with high levels of acetaldehyde may have a higher risk of cancer. Acetaldehyde is easily detected by HbA1C in the blood, which may be used as a biomarker. In addition, high levels of acetaldehyde can usually be controlled through medication and good dietary habits, providing a pathway for taking proactive measures to prevent the occurrence of cancer.”
Dr. Li Ren Kong, the first author of the paper and a researcher at the Cancer Research Center of the National University of Singapore, added, “Our aim in starting this study was to understand which factors increase the risk of cancer in families, but ultimately revealed a deeper mechanism that closely links basic energy metabolism pathways to the process of cancer generation. These findings greatly enhance our understanding of the role of diet and weight management in regulating cancer risk.”
Interestingly, this study also revised long-standing theories about certain cancer prevention genes. This theory, known as the Knudsen “double strike” paradigm, was first proposed in 1971. The theory suggests that these genes must be permanently inactivated in our cells before cancer occurs.
These authors now find that acetaldehyde can temporarily inactivate these cancer prevention genes, which indicates that repeated bad eating habits or uncontrolled diabetes will “accumulate” over time, thus increasing the risk of cancer. This new knowledge is likely to change the future research direction in this field.
Based on these new findings, the authors plan to conduct further research to understand whether metabolic disorders (such as diabetes or poor diet) affect cancer risk in Singapore and other Asian countries.
They also hope to identify new mechanisms linking metabolism, diet, and cancer that they have discovered, to develop more effective methods to prevent or delay the occurrence of cancer.
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Reference
Li Ren Kong et al. A glycolytic metabolite bypasses “two-hit” tumor suppression by BRCA2. Cell, 2024, doi:10.1016/j.cell.2024.03.006.