Alcohol has long been linked to cancer, but scientists are still figuring out just how a simple drink can quietly harm the body at its most fundamental level. New research from the Institute of Organic Chemistry and Biochemistry (IOCB) in Prague sheds light on what happens within our cells when alcohol is broken down— and why some people are more likely to get cancer than others. 

When alcohol is consumed, the body turns it into the harmful molecule acetaldehyde. This material is not just toxic in general; it can also directly assault DNA, the instruction handbook that teaches cells how to develop and reproduce. If DNA is broken and not repaired properly, cells might begin to act abnormally, eventually becoming malignant. 

The study, published in the Nature Portfolio journal Communications Biology, examines how cells routinely recover from this type of injury. Researchers focused on Fanconi anaemia, a rare genetic illness in which the body fails to repair specific forms of DNA damage. In some people, the two strands of DNA may become locked together, preventing normal cell division. The end outcome is severe genetic instability, which can cause cancer or cell death. 

According to Dr Jan Šilhán from IOCB Prague, this process does not only affect individuals with unusual genetic abnormalities. "Patients with Fanconi anaemia have abnormal blood formation and an increased risk of cancer. It appears that DNA damage produced by alcohol, specifically its toxic metabolite acetaldehyde, which reacts directly with DNA, can create similar problems in persons who do not have Fanconi anaemia." 

To further understand this process, the researchers reproduced alcohol-induced DNA damage in the lab. They discovered that a collection of enzymes known as the SXE complex can detect and cut off the damaged piece of DNA, allowing repair to begin. This repair system was more adaptable than previously thought, even repairing DNA damage induced by chemotherapy medicines and other hazardous compounds. 

According to the study's first author, PhD student Jana Havlíková, individual variances may be essential. "These findings could help explain why some people are more prone to alcohol-related cancers than others. The discrepancies may be due to how efficiently their DNA repair processes function." 

Previous experiments in the United Kingdom have provided supporting findings, with researchers studying mice that are unable to break down acetaldehyde and missing essential DNA repair pathways. The animals acquired serious blood problems and, often, malignant tumours. In one dramatic case, when a pregnant mouse was unable to absorb acetaldehyde, the developing embryo suffered significant harm. 

Taken together, the data show that those who have latent genetic defects in DNA repair, paired with a lower ability to detoxify acetaldehyde, may be at a much increased risk of cancer, even after consuming tiny amounts of alcohol. " The lesson is clear: drinking can destroy DNA. "We may have described the mechanism that cells use to repair this type of DNA damage, but our work is still basic research. There is no miracle pill," explains Šilhán. 

For public health experts, the study adds to a growing body of evidence showing the danger of cancer from alcohol is real, measurable, and based on fundamental biology.