CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) technology’s origin stems from a 1987 discovery of specific genetic sequences inside the genome of Escherichia Coli; however, it wasn’t until 2007 which introduced practical usages of CRISPR. While CRISPR is seemingly a natural phenomenon, scientists quickly acknowledged its potential and began researching practical usages of it. Scientists discovered that certain bacteria, such as E. Coli, use CRISPR as an antiviral mechanism. CRISPR’s capabilities intrigue scientists because it offers a different approach that is more precise, quicker, and cheaper for altering an organism’s genome to better suit it for survival. Whether CRISPR is being used to treat genetic mutations that lead to cancer or drought-resistant plants, CRISPR’s applications can be applied nearly anywhere on the genetic level. CRISPR-Cas9 works by combining a protein that can snip DNA strands with a molecule that guides it to the site of concern. “When bacteria survive a viral attack, they incorporate snippets of the virus’s DNA into their genomes. Those stolen segments are called ‘CRISPR.’ If the virus attacks again, the bacteria use those CRISPR segments as a template to create strands of RNA that home in on the corresponding sequence in the virus’s genome. The CRISPR RNA carries along a protein called Cas9 to the target location on the DNA. The protein disarms the virus by cutting its DNA at that spot” (c&en.org).
One particular area of concern where CRISPR technology may provide some aid is the p53 and associated genes. According to Cancer.gov, the “p53 gene makes a protein found inside the nucleus of cells and plays a key role in controlling cell division and cell death. Mutations (changes) in the p53 gene may cause cancer cells to grow and spread in the body” (Cancer.gov). Cells that have this mutated p53 gene lack the ability to control cell division and death. We’ve learned in AP Biology that the interphase cells go through before undergoing mitosis, and cytokinesis is extremely important to ensure that they divide and grow properly. But if something goes wrong during G1, S, or G2, that could lead to uncontrolled cell growth and division and cancer. Targeting p53 using CRISPR technology has some limitations, though. CRISPR is much less effective against p53 that is active, but both inactivated and mutated p53 allow for uncontrolled growth, leading to cancer. So, the scientists at Karolinska Institute propose that p53 inhibition is the most effective way to manipulate p53 to be better suited for CRISPR treatments. Preventing further mutation of p53 became the key concern because this leads to extra complexities and danger to associated genes.
Preventing similar genes from DNA damage is key to preventing uncontrolled cell growth. The researchers “identified a network of linked genes with mutations that have a similar effect to p53 mutations, and shown that the transient inhibition of p53 is a possible pharmaceutical strategy for preventing the enrichment of cells with such mutations” (Karolinska Institute). Furthermore, the scientists studied the DNA damage response as a possible answer in developing a more accurate guide to RNA sequences, which are used to guide CRISPR where a DNA sequence requires editing. The scientists claim that “We believe that the up-regulation of genes involved in the DNA damage response can be a sensitive marker for how much unspecific (‘off-target’) activity a guide RNA has, and can thus help in the selection of ‘safer’ guide RNAs.”
Cancer has been a seemingly unsolvable problem for generations. Any step taken to further our capabilities for handling cancer is a good step, and eventually, we will reach a point where cancer is hopefully a disease of the past. Utilizing CRISPR to its fullest potential will take time, but scientists are hopeful that it will be an absolute game-changer in the fight against cancer and other genetic diseases.