In nature, bacteria have long found an unusual way to fight viruses. If an infection can no longer be stopped, some of them initiate a self-destruct program: a special enzyme destroys the infected cell's own DNA, preventing the virus from multiplying and spreading further through the bacterial population. Now, scientists are trying to turn this evolutionary mechanism into a high-precision weapon for treating oncological diseases.
NEWS AND VIEWS “DNA-shredding CRISPR enzyme takes aim at cancer cells” Mehran Takallo, Raymond H. J. Staals. Nature 2026-07-14. doi.org/10.1038/d41586… #CRISPR-Cas12a2 … A bacterial self-destruct mechanism has been repurposed as a potential therapy, selectively eliminating
This involves the protein Cas12a2, an unusual representative of the CRISPR system that works very differently from the well-known molecular scissors Cas9. Instead of precisely cutting a specific DNA segment, Cas12a2 remains inactive until it detects a pre-programmed RNA molecule. After that, the enzyme switches to a total destruction mode, cleaving the cell's DNA throughout the genome and causing its death.
In two studies published in the journal Nature in 2026, scientists showed that Cas12a2 can be programmed to recognize RNA characteristic of tumor cells with mutations in the TP53 or KRAS genes – some of the most common and simultaneously most challenging targets in modern oncology.
Mutations in these genes are found in almost half of all malignant tumors. For a long time, they were considered practically “inaccessible” to drug therapy, as damaged p53 and KRAS proteins lack suitable sites for conventional drug molecules to bind. The new approach completely changes the strategy. Instead of trying to restore the function of the mutant protein, Cas12a2 uses the tumor cell itself as a trigger: upon detecting specific RNA, the enzyme initiates irreversible destruction of its genome.
The results of the initial experiments appear promising. In one study, Cas12a2, programmed to recognize mutant KRAS, suppressed tumor cell growth by approximately 50% – the effectiveness was comparable to that of cisplatin, but with virtually no damage to healthy cells. In another study, the system destroyed over 90% of cells infected with the human papillomavirus (HPV), while preserving surrounding healthy tissues.
These findings have already attracted the attention of biotechnology companies. The German company Akribion Therapeutics is developing a therapy for HPV-related head and neck cancers. According to co-founder Paul Scholz, the first clinical trial data are expected by 2030.
However, researchers emphasize that the technology is still in its early stages of development. It is necessary to ensure its safety, confirm its effectiveness in clinical trials, and solve one of the most complex challenges in modern gene therapy – delivering Cas12a2 and the guide RNA exclusively to tumor cells without affecting healthy tissues. The delivery system remains one of the main obstacles to creating a drug today.
The story of Cas12a2 once again demonstrates how inventive evolution can be. A mechanism that has helped bacteria sacrifice individual cells to save the entire colony for millions of years may become the basis for a fundamentally new class of drugs for treating oncological diseases. Instead of correcting individual genes, it offers the possibility of selectively destroying cells based on their molecular “signature” by reading unique RNA markers of the disease.
It will likely be several more years before such methods become part of clinical practice. But the path, which once began with the study of bacterial defense systems, has already led to the creation of the first CRISPR drugs, and now opens up another direction – programmable destruction of pathological cells. If the technology proves safe and effective in humans, it could significantly expand the capabilities of modern oncology and offer hope to patients with tumors that were previously considered practically untreatable.
