When an adult under 50 is diagnosed with colorectal cancer, it is referred to as early onset colorectal cancer. Previously thought of as an age-related illness, colorectal cancer is alarmingly on the rise in younger persons worldwide, with an annual incidence increase of 1.4%.
Research indicates that in many regions, the incidence of colorectal cancer is rising in younger adults more quickly than in older ones, with around 1 in 5 diagnoses occurring in people under 55. Additionally, studies show that among men and women under 50, colon cancer is currently the most common cause of cancer-related death.
The causes of the rising incidence of early-onset colorectal cancer are still not well understood. The exposome may play a role, according to earlier studies. This phrase describes all of the exposures that an individual encounters over their lifetime and the ways in which those exposures impact their health.
The increased frequency of early-onset colorectal cancer may be explained by epigenetic modifications, or “molecular imprints,” linked to eating habits, smoking, and pesticide exposure, according to a recent study published in Nature MedicineTrusted Source.
Important conclusions of the research
The Vall d’Hebron Institute of Oncology (VHIO) researchers concentrated on the potential link between colorectal cancer and the exposome. But instead of evaluating exposures directly, the team looked at epigenetic modifications, particularly DNA methylation (Trusted Source).
These are chemical changes that affect how genes are expressed without changing the DNA sequence. Experts frequently liken epigenetic markers to annotations in a book; they affect how the material is read but do not alter the content itself.
DNA methylation patterns in individuals with colorectal cancer diagnosed before and after age 50 were examined in this study. Next, based on exposure to different environmental factors, the researchers developed epigenetic risk ratings.
They discovered unique epigenetic fingerprints associated with environmental exposures, tobacco use, and dietary habits.
The head of the VHIO Computational Biology Group and lead study author José Seoane, PhD, told Medical News Today that risk scores and epigenetic fingerprints are helpful tools for examining the exposome.
For a long time, epidemiologists have been researching how the environment affects our methylation. Numerous EWAS (epigenetic broad association studies) have been conducted to identify methylation loci linked to exposures, according to Seoane.
He explained, “We are able to reconstruct a type of ‘history’ of exposure from the methylation data because we obtain this information and build profiles of how this signal is changing in tumor tissues.”
In addition to confirming established risk variables, the study discovered a novel correlation with a common agricultural chemical.
Even after controlling for socioeconomic characteristics and other pesticides, the researchers found that counties with increased picloram use also had higher incidences of early onset colorectal cancer using U.S. population data.
A potential novel risk factor for colorectal cancer
Subsequent investigation indicated distinct genetic traits in cancers associated with increased picloram exposure. The APC gene, a crucial gene in the development of colorectal cancer, has less alterations.
This implies that environmental exposures may have a role in the development of cancer through pathways other than conventional genetic changes.
The researchers stress that these results demonstrate a connection rather than evidence of causation. Therefore, more research is required to determine whether picloram directly causes the development of early-onset colorectal cancer.
“We anticipated having it in our hits because epidemiological studies have already shown the relationship between smoking and food and early onset colorectal cancer,” Seoane told MNT.