Research conducted by the Ontario Institute for Cancer Research (OICR) in Toronto has shed light on how smoking triggers cancer by inhibiting the creation of protective proteins designed to control cell growth.
The study, led by University of Toronto PhD student Nina Adler, uncovered that smoking leads to “stop-gain” mutations in DNA, which signal the body to halt the production of crucial protective proteins. As a result, cells are no longer shielded, enabling uncontrolled growth and potentially fostering the development of cancer.
Adler, who conducted the research during her postgraduate studies in Dr. Jüri Reimand’s lab at OICR, emphasized the association between smoking and disruptions in the formation of tumor suppressors. According to Adler, these mutations allow abnormal cells to proliferate unhindered by the body’s natural defenses, potentially facilitating the onset of cancer.
The investigation, comparing the genetic imprints left by smoking in the DNA of 12,000 tumor samples across 18 different cancer types, revealed a strong correlation between smoking and these stop-gain mutations, making individuals more susceptible to cancer.
Moreover, the study found that the duration and intensity of smoking had a proportional relationship with the prevalence of stop-gain mutations in tumors.
Dr. Reimand highlighted the profound damage inflicted by tobacco on DNA, impacting the cellular functions. He stressed the study’s significance in revealing how smoking deactivates crucial proteins, compromising the body’s cellular building blocks and posing potential threats to long-term health.
Reimand further suggested that other lifestyle factors like alcohol consumption and an unhealthy diet might also contribute to these stop-gain mutations, although further research is required for conclusive evidence.
Adler emphasized the significance of understanding how smoking operates at a molecular level, noting this as an essential step in comprehending the impact of lifestyle on cancer risk.
Published in the journal Science Advances on November 3, the study’s findings provide crucial insights into the molecular mechanisms underlying smoking-induced cancer development.