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<p>After the workshop conducted at one-north festival, we requested the public to participate in a survey. This survey was designed to gauge public interest and reservations about the use of Cas9 for therapeutic applications.</p> | <p>After the workshop conducted at one-north festival, we requested the public to participate in a survey. This survey was designed to gauge public interest and reservations about the use of Cas9 for therapeutic applications.</p> | ||
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<p>An overwhelmingly high number (85%) of participants is receptive to using a fully mature CRISPR/Cas9 technology – that is without any side effects. </p> | <p>An overwhelmingly high number (85%) of participants is receptive to using a fully mature CRISPR/Cas9 technology – that is without any side effects. </p> | ||
− | <img src="https://static.igem.org/mediawiki/2017/5/5a/Ntu_ihp_survey2.png" width=" | + | <img src="https://static.igem.org/mediawiki/2017/5/5a/Ntu_ihp_survey2.png" width="600" height="400"> |
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<p>When asked to consider whether they would be receptive to using CRISPR/Cas9 technology in the event of personal suffering to lung cancer – even when the issues of the treatment have yet to be fully worked out, more than half stated that they would, while 30% would consider the treatment. </p> | <p>When asked to consider whether they would be receptive to using CRISPR/Cas9 technology in the event of personal suffering to lung cancer – even when the issues of the treatment have yet to be fully worked out, more than half stated that they would, while 30% would consider the treatment. </p> | ||
− | <img src="https://static.igem.org/mediawiki/2017/b/bd/Ntu_ihp_survey3.png" width=" | + | <img src="https://static.igem.org/mediawiki/2017/b/bd/Ntu_ihp_survey3.png" width="600" height="400"> |
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<p>There are 61034 numbers of shared SNPs between F03 and F05 mice, that are not found in FVB mouse, and therefore are unique SNPs between F03 and F05 mice. In addition, there are 10837 SNPs between FVB and F05 mouse, and only 9236 number of SNPs shared between FVB and F03 mouse. The bar graphs below show the distribution of number of SNPs across different chromosomes.</p> | <p>There are 61034 numbers of shared SNPs between F03 and F05 mice, that are not found in FVB mouse, and therefore are unique SNPs between F03 and F05 mice. In addition, there are 10837 SNPs between FVB and F05 mouse, and only 9236 number of SNPs shared between FVB and F03 mouse. The bar graphs below show the distribution of number of SNPs across different chromosomes.</p> | ||
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<img src="https://static.igem.org/mediawiki/2017/2/2a/Cs1.png" > | <img src="https://static.igem.org/mediawiki/2017/2/2a/Cs1.png" > | ||
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<img src="https://static.igem.org/mediawiki/2017/3/33/Cs2.jpg" > | <img src="https://static.igem.org/mediawiki/2017/3/33/Cs2.jpg" > | ||
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+ | <p>This finding shows that CRISPR-Cas9 treated F03 and F05 mice share more common SNPs/variants than the control FVB mouse. As the author’s conclusion relies on the assumption that all three mice were genetically identical prior to treatment and that the mice were from a highly inbred strain, we would expect that most common variants existing prior to the treatment should be found in all three mice, not only at the two treated mice but at not the control mouse. Therefore, it suggests that F03 and F05 mouse had been more genetically related to each other than the FVB mouse prior to the treatment. The unexpected mutations identified in the original article simple represent pre-existing SNPs shared in common by the mice, and not due to of off-target mutations caused by CRISPR-Cas9. </p> | ||
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+ | <p>To reiterate, our analysis of the same set of data revealed that the FVB control mouse is very different from the sample mice F03 and F05 – suggesting that they are from different parents/lineages. FVB would have sufficient natural mutations to make them sorely inadequate as negative genetic controls. Mutations observed in CRISPR-Cas9 treated mice F03 and F05 when contrasted against the FVB control mouse is most likely not due to CRISPR-Cas9 treatment. </p> | ||
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+ | <p>Since then, a number of articles has been published to rebut this claim and the paper had received a second editorial. Although this paper has since been revised from publication, there are still some news article citing this paper while circulating claims that CRISPR-Cas9 causes unexpected mutations (as per 16 October 2017).</p> | ||
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+ | <p>Such inaccurate news might cause misinformation to the general public and make them more wary of new technologies. Even when provided access to the source papers, the public – even the news writers generally lack the specialized knowledge to critically analyse claims. In conclusion, these controversies caused by this article served as a reminder for the science community to perform safe and responsible work. </p> | ||
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+ | <p>Careful, safe and responsible experimental design and cross-checking of preliminary results before even considering publication is important in academia, even with peer-review system in place. This is especially so for topics that has high potential to be sensationalized – such as Cas9 technologies. This would aid in fostering trust and confidence in emerging technologies such as Crispr/Cas systems.</p> | ||
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+ | <p>Over-generalized conclusion is a concern in scientific research as it may lead to the generation of insignificant results. An example of such a publication will be the paper titled, “Unexpected mutations after CRISPR-Cas9 editing in-vivo”.</p> | ||
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+ | <p>In the paper, the authors conclude that CRISPR-Cas9 editing in blind mice that is supposed to only correct a mutation in the Pde6b gene, also causes a large number of mutations in untargeted regions. It is because they found an unexpectedly high number of indels and single nucleotide polymorphisms (SNPs) in the CRISPR-treated mice. This conclusion is based on the assumption that the 3 mice (1 control mouse and 2 CRISPR-Cas9 treated mice) used as the subjects of the experiment were genetically identical prior to the treatment. Since then, a number of articles has been published to rebut this claim and the paper had received a second editorial.</p> | ||
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<p>This finding shows that CRISPR-Cas9 treated F03 and F05 mice share more common SNPs/variants than the control FVB mouse. As the author’s conclusion relies on the assumption that all three mice were genetically identical prior to treatment and that the mice were from a highly inbred strain, we would expect that most common variants existing prior to the treatment should be found in all three mice, not only at the two treated mice but at not the control mouse. Therefore, it suggests that F03 and F05 mouse had been more genetically related to each other than the FVB mouse prior to the treatment. The unexpected mutations identified in the original article simple represent pre-existing SNPs shared in common by the mice, and not due to of off-target mutations caused by CRISPR-Cas9. Although this paper has since been revised from publication, there are still some news article circulating that claims that CRISPR-Cas9 causes unexpected mutations (as per 16 October 2017).</p> | <p>This finding shows that CRISPR-Cas9 treated F03 and F05 mice share more common SNPs/variants than the control FVB mouse. As the author’s conclusion relies on the assumption that all three mice were genetically identical prior to treatment and that the mice were from a highly inbred strain, we would expect that most common variants existing prior to the treatment should be found in all three mice, not only at the two treated mice but at not the control mouse. Therefore, it suggests that F03 and F05 mouse had been more genetically related to each other than the FVB mouse prior to the treatment. The unexpected mutations identified in the original article simple represent pre-existing SNPs shared in common by the mice, and not due to of off-target mutations caused by CRISPR-Cas9. Although this paper has since been revised from publication, there are still some news article circulating that claims that CRISPR-Cas9 causes unexpected mutations (as per 16 October 2017).</p> |
Revision as of 18:35, 1 November 2017