According to researchers at Karolinska Institutet in Sweden, there are many challenges when it comes to using CRISPR gene editing as a part of medicine of the future. One challenge is how cells behave when subjected to DNA damage.
Damage to cells activates the protein p53. The technique is less effective when p53 is activated, but a lack of p53 allows cells to grow rapidly and become cancerous. The p53 protein gene is a tumor suppressor gene. If a person inherits only one copy of the p53 gene from their parents, they are predisposed to cancer and usually develop numerous tumors, Other linked genes with mutations can have a similar effect to p53 mutations. The transient inhibition of p53 is a strategy for preventing the advancement of mutated cells. The DNA damage response can potentially be a marker in development of more precise guide RNA sequences.
We have learned thus far in AP Biology that mutations are changes that occur in the DNA sequence of an organism or a change in a genetic sequence. Mutations can be caused by mistakes during cell division. They can be harmful, beneficial or have no effect.
The researchers plan to further conduct clinic-centered tests in order to understand how pertinent these mechanisms are. This study is largely focused on CRISPR screening experiments on isolated cells and analysis of the DepMap database.
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