Abstract
Simple SummaryIt is widely believed that cancer is developed due to changes in the genetic codes of our DNA, leading to abnormal growth of cells. In the past few years scientists have discovered a system which is used as an immune mechanism by bacteria in order to cleave the invading viruses, called CRISPR/Cas9. Exploiting this system in humans will allow scientists to attempt to edit genetic errors that lead to cancer. This scientific breakthrough has a lot of potential for treating a variety of diseases, including cancer. It has already been successfully used in treatment of some types of blood cancer. In this article, we discuss the opportunities and limitations of CRISPR/Cas9 in treatment of solid cancer.Cancer is considered by not only multiple genetic but also epigenetic amendments that drive malignant cell propagation and consult chemo-resistance. The ability to correct or ablate such mutations holds enormous promise for battling cancer. Recently, because of its great efficiency and feasibility, the CRISPR-Cas9 advanced genome editing technique has been extensively considered for therapeutic investigations of cancers. Several studies have used the CRISPR-Cas9 technique for editing cancer cell genomic DNA in cells and animal cancer models and have shown therapeutic potential in intensifying anti-cancer protocols. Moreover, CRISPR-Cas9 may be used to correct oncogenic mutations, discover anticancer drugs, and engineer immune cells and oncolytic viruses for immunotherapeutic treatment of cancer. We herein discuss the challenges and opportunities for translating therapeutic methods with CRISPR-Cas9 for clinical use and suggest potential directions of the CRISPR-Cas9 system for future cancer therapy.
Highlights
What Is Clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9?Our DNA is constantly being damaged by internal and external sources
It is set to revolutionize the use of Chimeric antigen receptor (CAR)-T and adaptive cell therapies by overcoming some hurdles such as graft versus host disease (GVHD)
Manufacturing timeline, high cost of manufacturing, off-tumor effects, CAR-T delivery, trafficking and tumor infiltration, and associated safety and toxicities are a few examples of the major challenges ahead
Summary
Our DNA is constantly being damaged by internal and external sources. It is widely accepted that genomic instability and accumulation of driver aberrations lead to clonal cancer evolution. Following pairing of sgRNA with the target sequence Cas nuclease domains makes site specific double-stranded breaks off-target cleavage and the mode of the delivery of TALEN to cells is limited due to its long DNA recognition sequence [3,4,5]. Following induction of DSB, cell repair machinery is close to a section of sgRNA called proto-spacer adjacent motif (PAM) located at the 30 end activated to repair and restore the genome through NHEJ or HRR pathways, as explained of sgRNA [7]. Multiple sgRNA sequences can, in principle, allow gene editing at multiple locations [8] This ability provides the potential for scientists to speculate as to the possibility of simultaneous multiple deletions and insertions of base pairs, which has huge potential to enable treatment for some inherited disorders that have previously been deemed incurable. Can we exploit such a flexible and high-fidelity repair mechanism to correct mutational errors and treat cancer? Gene editing and, in particular, CRISPR/Cas technology has turned into an area of interest for many scientists and clinicians alike in order to study its potential in cancer research and treatment
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