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Week13 cancer+aging

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&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Firstly, if the specific gene which can cause cancer is found, it is much easier to develop a drug. By gathering plenty of data from patients, we can check the role of gene and who it affects to our body by checking KEGG pathway. By using this information, we can block the main cause by synthesizing certain drugs which works for the main cause in certain organ. Also, it can give a guidance to choose patient-specific drug. It&rsquo;s because as testing, doctors can know what kind of mutation or oncogene patients have. However, this kinds of drugs have side effects and not suit for every cases. Also, to develop new drugs, it needs a lot of time and funding. Moreover, new kinds of cancer cells which has different mutation emerge, so we could not find the eventual solution.</p>
<p style="margin-left: 40px">&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Second method is Gene-editing. It is much more direct way to cure the cancer. Also, it is quite essential solution because it fix the main problem, by editing the specific site. For example, in case of CRISPR-Cas9 system, it used CAs9 enzyme to cut specific region of DNA and edit the sequence by guiding RNA. However, it does not guarantee that the target gene is removed in all cells. Also, as it cut the DNA, non-homologous end joining occur and it can lead to other mutations. </p>
<p style="margin-left: 40px">&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Third methods are the new idea that I made. What about stopping cancer by aging? Actually, cancer cells keep proliferating and hardly ever stop. Although aging is also not good factor for us, cancer is fetal, so it can be a solution to suppress the cancer growth. First way is to block the activity of the telomerase. In case of adult stage, most of cells in humans does not activate telomerase. However, in case of cancer cell, it can keep replicating because they activate the telomerase to lengthen the telomere length. Second way is merging the gene of Progeroid syndromes with cancer. People who have this Progeroid syndromes age faster than normal people. Also, it caused by genetic mutation before they are born and also it is not inherited by their parents. Therefore, there exist the genes which occur Progeroid syndromes. So, if we inject the DNA which contains that gene directly to the cancer cells, we can suppress the cell cycle of cancer cell and finally it die because of rapid aging.</p>
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<p>Telomerase in the human organism, Kathleen Collins and James R Mitchella, [[http://www.nature.com/onc/journal/v21/n4/full/1205083a.html]]</p>
<p>[[https://ghr.nlm.nih.gov/condition/hutchinson-gilford-progeria-syndrome]]</p>
<p>[[http://www.cancerresearchuk.org/health-professional/cancer-statistics/mortality/age#heading-Two]]</p>
<p>CRISPR: gene editing is just the beginning_The real power of the biological tool lies in exploring how genomes work, Heidi Ledford</p>
<p>[[http://www.nature.com/news/crispr-gene-editing-is-just-the-beginning-1.19510]]</p>
<p>[[https://www.jax.org/news-and-insights/jax-blog/2014/march/pros-and-cons-of-znfs-talens-and-crispr-cas]]</p>
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