Young adults who survived cancer when they were children develop age-related diseases earlier than others due to bacterial imbalances in the gut, perturbed immunity and damaged DNA, researchers have found.
An international team led by Hany Ariffin, a paediatric oncologist at the University of Malaya, revealed some of the molecular mechanisms involved in the susceptibility of childhood cancer survivors to age-related diseases as young adults, including diabetes and ischemic heart disease. Much of the research on this topic has focused on the relationship between the early onset of age-related diseases with the toxic effects of cancer treatments. But little has been known about what happens at the molecular level.
Over a series of studies involving Malaysian childhood cancer survivors, the team found that these young adults show chronic activation and accelerated age-related deterioration of the immune system. They also have higher markers of systemic inflammation than their healthy peers. Additionally, survivors showed evidence of specific immune responses to cytomegalovirus, a common virus that belongs to the herpes family and usually persists in the body in an inactive state following infection. These immune responses are similar to those found in the elderly.
Gut bacteria were less diverse in youngadult childhood cancer survivors compared to their healthy peers. Beneficial gut bacteria were also depleted. The researchers suggest that, while it is not clear why these changes occur, restoring ‘good’ gut bacteria to normal levels and increasing its diversity could mitigate the early onset of age-related diseases in this group.
One of the hallmarks of aging is the accumulation of damaged DNA and the shortening of caps, called telomeres, covering the ends of DNA strands. The researchers found that leukocyte telomere lengths in young adult survivors of childhood cancer were similar to individuals 20 to 30 years older.
As survival rates for most childhood cancers significantly improve, including in Malaysia, researchers and clinicians are aiming to “develop a more comprehensive treatment program with the goal of ensuring good quality of life for long-term survivors,” says Ariffin.
She and her team now plan to investigate how pharmacological and lifestyle interventions might reverse this aging process. They will continue investigating the molecular pathways that hasten aging in childhood cancer survivors in order to develop preventive and therapeutic strategies. They also hope to validate the use of
specific blood tests in the clinic to identify survivors who demonstrate premature aging and may benefit from early medical intervention.
Professor Hany Ariffin | E-mail: [email protected]
Faculty of Medicine
University of Malaya
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