Researchers have discovered a link between diet and the occurrence of cancer. The disease could be prevented with a simple test

Researchers have discovered a mechanism that helps explain why cancer risk is associated with an unhealthy diet or untreated metabolic conditions, Science Alert reports.

Researchers in Singapore and the UK have found that changes in glucose metabolism could help cancer cells grow by temporarily turning off a gene that protects us against tumors, called BRCA2.

“These findings raise awareness of the impact of diet and weight control in managing cancer risk,” says lead author of the new study, pharmacologist Li Ren Kong of the Cancer Science Institute in Singapore.

“We started the study with the goal of understanding what factors increase the risk in cancer-susceptible families, but we ended up discovering a deeper mechanism related to the development of cancer,” he adds.

The finding also casts doubt on an older theory about genes protecting against cancer. Knudson’s “double hit” paradigm, first proposed in 1971, states that both copies of a tumor suppressor gene must be permanently inactivated in our cells for cancer cells to develop.

Recent studies have found that a mutation in one of the two BRCA2 genes in cells is involved in various types of cancer. Interestingly, mice and human cells with this mutation do not show the usual signs of genetic instability seen in cells with both copies of the mutated gene.
In mice, a single affected copy of BRCA2 does not appear to cause major problems in organ development or DNA repair in most tissues. But cells with this mutation appear more vulnerable to stress, such as exposure to environmental toxins, which can reduce BRCA2 protein levels, which in turn leads to functional problems.

“It is not yet very clear how such environmental factors increase cancer risk, but it is vital to understand the connection if we are to take preventive measures to help us stay healthy for longer,” says oncologist and CSI Singapore’s Ashok Venkitaraman .

The team first examined people who had inherited a faulty copy of BRCA2. They found that these people’s cells are more sensitive to methylglyoxal (MGO), which is produced when cells break down glucose in the process of glycolysis.

Glycolysis generates more than 90 percent of the MGO in cells, which a pair of enzymes usually keep at minimal levels. If they can’t keep up, high levels of MGO can lead to the formation of harmful compounds that damage DNA and proteins. In diseases such as diabetes, where MGO levels are elevated due to high blood sugar, these harmful compounds contribute to the complications of the disease.

The researchers found that MGO can temporarily disable the functions of the tumor suppressor protein BRCA2, leading to mutations linked to cancer development.

Because BRCA2 function is not permanently inactivated, it can later return to normal levels. But cells repeatedly exposed to MGO can continue to accumulate cancer-causing mutations.

Overall, this suggests that changes in glucose metabolism may disrupt BRCA2 function, contributing to cancer development and progression.

These results come from laboratory tests done on small samples, so researchers say more larger studies are needed to look at possible links between dietary factors, diabetes and other metabolic disorders.

This new information may lead to strategies for cancer prevention or early detection.

“MGO can be easily detected by a blood test. Additionally, high levels of methylglyoxal can usually be controlled with medication and a balanced diet,” says Venkitaraman.

Publisher: MB

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