German scientists have come out with a new research that sheds light on the sleeping pattern in the night and the resultant cancer causing elements in the body before advising people to strive for sound sleep at night.
As we age, the decline in tissue function and the onset of cancer occur with the loss of stem cells, mainly driven by damage to the DNA of stem cells.
As the source of this DNA damage in stem cells has previously been unclear, the new research found that environmental stress is a major cause behind DNA damage in adult hematopoietic stem cells. Repeated exposure to such stress causes accelerated tissue aging and gradually leads to cancer, scientists said.
The study published in the journal Nature, shows that scientists at the Deutsches Krebsforschungszentrum (DKFZ) Heidelberg (German Cancer Research Center) and at the Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH) have explained that the stress caused by chronic blood loss or infection results in driving hematopoietic stem cells into a state of rapid cell division to produce new blood cells to overcome the damaged tissue.
Michael Milsom, lead author of the study, said that the state of dormancy protected hematopoietic stem cells from DNA damage and, hence protects them from premature aging as well.
The new model seeks to explain the gradual accumulation of DNA damage in stem cells with age and the associated decline in tissues repairing themselves in older persons.
Prof. Dr. Andreas Trumpp, director of HI-STEM and head of the Division of Stem Cells and Cancer at the DKFZ , hoped to find prevention or reduction in damaged cells which cause aging and the seed of cancer.
“The novel link between physiologic stress, mutations in stem cells and aging is very exciting,” says Trumpp. “By understanding the mechanism via which stem cells age, we can start to think about strategies to prevent or at least reduce the risk of damaged stem cells which are the cause of aging and the seed of cancer.”
In addition, the study examined how this stress response impacts on a mouse model of a rare inherited premature aging disorder that is caused by a defect in DNA repair. Patients with Fanconi anemia suffer a collapse of their blood system and have an extremely high risk of developing cancer.
Mouse models of Fanconi anemia have exactly the same DNA repair defect as found in human patients but the mice never spontaneously develop the bone marrow failure observed in nearly all patients. “This perfectly recapitulates what happens to Fanconi anemia patients and now gives us an opportunity to understand how this disease works and how we might better treat it,” commented Milsom,” he said.