blue double-helix models in the background (Credit: iStock)
Game-changing DNA-editing technology intended to get rid of patients of diseases can cause cancer, on the basis of two studies.
The danger with the CRISPR program for the editing happens especially when CRISPR-Cas9 is used to replace a disease-causing gene with a healthy child.
A study from the Karolinska Institutet and another by Novartis, both published on Monday in the journal Nature Medicine, shows that a successful CRISPR-Cas9 editing can indicate that the modified cell is missing a cancer-suppressing protein, causing a patient’s risk.
The protein, called p53, acts as the body’s cellular “first aid” kit and also the causes of some CRISPR operations to fail. Since CRISPR-Cas9 works as a scissors to cut strands of DNA, the cut can also lead to p53 to swoop in and repair of defective cell — or self-destruct.
“By picking the cells that repaired the damaged gene, we were planning to fix, we may accidentally also pick cells without functional p53,” said Emma Haapaniemi, co-author of the Karolinska Institutet study.
“If administered to a patient, as in the field of gene therapy for hereditary diseases, such as cells that can give rise to cancer, the concern for the safety of CRISPR-based gene therapies.”
P53 dysfunction causes significant risk of cancer. It is responsible for almost half of ovarian cancers, 43 percent of colorectal cancers and a substantial number of the lung, pancreas, stomach, liver and breast cancer, according to Stat News.
Does CRISPR-Cas9 do more harm than good?
Although p53 mutations greatly increase the risk of cancer, the findings are a reason to be careful, and not for full-blown alarm.
Bernhard Schmierer, a researcher at the Karolinska Institutet, called CRISPR-Cas9, a “powerful tool with a massive therapeutic potential,” before the stress of the possible risks.
“Like all medical treatments, however, CRISPR-Cas9-based therapies can have side effects, which patients and health care providers need to be aware of. Our study suggests that future work on the mechanisms that lead to p53 in response to CRISPR-Cas9 will be crucial in improving the safety of CRISPR-Cas9-based therapies,” he said in a statement.
Schmierer told the Naples News that “it is unclear whether the findings translate in the cells actually used in the current clinical studies.”
The type of genetic modification examined in the studies, known as gene correction, is also one of the CRISPR-Cas9 capabilities.
It can also be used to edit genes by interference, instead of a direct replacement, even when p53 is functioning properly. This type of gene disruption — the so-called non-homologous end join — is used in sickle cell and thalassemia tests.
This story was previously published in the New York Post.