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This technology can be used to disrupt and destroy targeted genes in the genomes of cells. To achieve their goals, the team refined a CRISPR-Cas9 technique to efficiently disrupt all genes in the leukaemia cell genome individually.. This allowed them to identify those genes whose disruption was http://justlillianortiz.techno-rebels.com/2016/08/04/some-basic-guidelines-on-vital-criteria-of-interview-body-language detrimental to the growth and survival of AML cells. Dr Kosuke Yusa, joint project leader from the Sanger Institute, said: “Previous studies showed proof of principle, but this is one of the first systematic attempts to identify the genetic vulnerabilities of AML. We have improved and applied CRISPR-Cas 9 technology to look at what actually kills cells. CRISPR is becoming a powerful technique in cancer research because it overcomes some of the limitations of earlier tools.” The human genome contains around 20,000 genes, by refining CRISPR-Cas9 technology and using it to screen the leukaemia genome the team uncovered a catalogue of approximately 500 genes that are essential for cancer cell survival, including more than 200 genes for which drugs could be designed. Whilst a handful of these genes including DOT1L, BCL2 and MEN1 are already established therapeutic targets, most of them are novel and open up many new possibilities for developing effective treatments against the disease. The researchers chose the KAT2A gene for further research and in order to demonstrate the validity of their findings. By inhibiting KAT2A using genetic and drug-based techniques, they showed that disruption of the gene reduced the growth and survival of AML cells, but not of normal blood cells. Dr Konstantinos Tzelepis, a first author on the paper from the Sanger Institute, said: “This is an exciting finding, as KAT2A inhibition worked on a number of primary AML cells with diverse genotypes. Whilst the gene needs to be studied in greater depth to understand its potential for use in the clinic, we show that targeting KAT2A destroyed AML cells in the laboratory while sparing healthy blood cells.” The team then validated this finding, by disrupting the KAT2A gene from leukaemia cells in transgenic mice, and observing the effect on the cancer.
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