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The researchers discovered a mechanism by which a common oncogene activated by cancer patients affects how fast cells grow
.
Researchers focused on the effects of MYC tumor genes have revealed new insights
into the factors that regulate the growth of cancer cells.
In healthy tissues, cell growth and proliferation are tightly controlled processes
.
The researchers found genomic binding sites of the MYC oncogene in the regulatory region of the target gene and showed that removing these binding sites from DNA slows down cell growth
.
Pihlajamaa confirmed that our results show that very small changes in a cell's DNA, such as modifications of a single gene regulatory element, can have a significant impact on
the proliferation rate of cells.
These findings are likely to benefit
many cancer patients in the future.
Pihlajamaa said a better understanding of the mechanisms that control cell growth could help identify targets that may be suppressed by new cancer drugs
.
The new method facilitates further research
Another major impact of the study comes from a new method developed by the researchers
.
Professor Jussi Taipale, head of the research group, explained that the method is very beneficial for future research as it can be used to study how various mutations affect proliferation and other cellular properties
.
The method is based on the so-called gene scissors, the CRISPR-Cas9 system, which has become an important tool
for biomedical research in recent years.
However, the genome editing process induces a DNA damage response and affects cell growth
.
"Our method solves this problem by using an experimental strategy in which cells that have undergone genome editing are directly compared to each other, while unedited wild-type cells are discarded
from analysis," Taipale said.
Taipale concludes that this is a powerful method that could have a significant impact
on the process of elucidating controlled cell growth in the future.
essay
A competitive precision CRISPR method to identify the fitness effects of transcription factor binding sites