New study finds link between diet, metabolism, and cancer risk
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NEW YORK, May 6: In a groundbreaking study, researchers from Singapore and the UK have uncovered a previously unknown mechanism that sheds light on why an unhealthy diet and unmanaged metabolic conditions like diabetes are associated with an increased risk of cancer.
Utilizing mouse models, human tissue, and lab-grown human breast organoids, the research team discovered that alterations in glucose metabolism could facilitate cancer growth by temporarily deactivating a gene called BRCA2, known for its tumor-suppressing properties.
Lead author of the study, cancer pharmacologist Li Ren Kong from the Cancer Science Institute of Singapore (CSI Singapore), highlighted the implications of the findings, stating, “These findings raise awareness of the impact of diet and weight control in the management of cancer risks.”
Initially aiming to investigate factors contributing to cancer risk in susceptible families, the researchers stumbled upon a deeper mechanism linking energy consumption pathways to cancer development.
The discovery challenges the long-established ‘two-hit’ paradigm proposed by Knudson in 1971, which posits that both copies of a tumor suppressor gene must be permanently inactivated for cancer to initiate. Recent studies revealed that a mutation in just one copy of the BRCA2 gene can predispose individuals to various cancers.
Further examinations unveiled that cells with a mutated BRCA2 gene were more sensitive to methylglyoxal (MGO), a compound produced during glucose breakdown. High levels of MGO, often seen in conditions like diabetes, can impair DNA and protein function, potentially leading to cancer development.
The study also highlighted the link between glucose metabolism, MGO, and BRCA2 function, suggesting that changes in glucose metabolism could disrupt BRCA2 activity, contributing to cancer progression.
While these findings provide critical insights into cancer development, the researchers emphasize the need for additional studies using larger clinical cohorts or animal models to explore the relationship between dietary factors, metabolic disorders, and cancer risk.
The discovery of MGO’s role in temporarily disabling BRCA2 function opens avenues for potential cancer prevention or early detection strategies. Venkitaraman, the oncologist and cancer researcher from CSI Singapore, suggests that HbA1C blood tests could serve as markers for detecting MGO levels, allowing for proactive measures against cancer initiation.
This groundbreaking research, published in Cell, offers promising prospects for understanding and addressing the intricate interplay between metabolism and cancer development.
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