Scientists from the Universities of Edinburgh and Cambridge in collaboration with a research center in Germany have analyzed a DNA-damaging chemical that has given scientists a better understanding of the cause of mutations within a cell’s DNA.
In a recent article in Genetic Engineering and Biotechnology News, one of the study’s group leaders commented that this finding may show how cancer cells build resistance to chemotherapy drugs.
Carcinogens, such as the chemicals in tobacco smoke, can cause damage to a cell’s genetic material and cause cancer. Nucleotides, the individual letters in the DNA code, are also modified.
For this study, researchers tracked the liver tumors in hundreds of mice. The tumors developed after inducing the mice with the diethylnitrosamine chemical.
It was estimated that the chemical caused approximately sixty thousand mutations in each cancer cell’s genome. The genome is the entire set of DNA and its genes.
Mutations affect essential genes that are known to be cancer drivers.
The next step for the researchers was to track tumors after induction of the diethylnitrosamine chemical.
About DNA Repair
The scientists found that when a cell divides, some of the lesions resulting from chemical damage are corrected through the DNA repair process.
However, many other lesions are not repaired and instead become permanent alterations in the DNA (mutations).
- The two strands of DNA that were damaged individually, become separated by the process of cell division. The result of this division is two “daughter” cells that develop their own unique mutations.
- During further replications of the lesions, the mutations form new combinations and select the best combination for the growth of tumors. This is referred to as “lesion segregation.” The end result is the formation within the tumor genome of complex mutation patterns.
The cycle of lesion segregation and DNA damage in cancer is often repeated, resulting in complex mutation patterns.
Dr. Duncan Odem, the research leader, said that the lesion segregation concept has given them a better understanding of the complexity of mutations and how they arise in cancer cells.
The researchers discovered that lesion segregation is a common feature in cancers and agree that this concept prompted them to revise their understanding of how DNA repair and clonal reproduction can define a cancer genome.
In conclusion, the scientists found that the cancer cells with favorable mutation patterns will win out. They can escape being affected by the immune system, grow faster, and have a better chance of surviving therapies.