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group_2_presentation_3_-_cancer [2020/03/26 13:50]
gandhr11 [CRISPR-Cas9]
group_2_presentation_3_-_cancer [2020/03/26 22:36] (current)
gandhr11 [What did the study do?]
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 ==== What is cancer? ==== ==== What is cancer? ====
  
-{{youtube>​5fVLacverEY?medium | center}}+{{youtube>​fQwar_-QdiQ?medium | center}} ​
  
 Cancer is the generic term that is used to describe a large group of diseases that can affect any part of the body (“Cancer”,​ 2018). A defining feature of cancer is the rapid production of abnormal cells that grow beyond their normal boundaries (“Cancer”,​ 2018). While a normal cell would mature into specialized cells with specific functions, cancer cells do not; they are less specialized than normal cells (Nall, 2020). One reason cancer cells can divide without stopping is due to its ability to ignore signals that indicate they should stop dividing or begin a process known as programmed cell death - apoptosis, to get rid of unneeded cells (Nall, 2020). Under normal circumstances,​ human cells grow and proliferate new cells as the body needs them; when the cells grow old or become damaged, they die and new cells take their place. However, in cancerous cells, the process is broken down and cells become increasingly abnormal as old or damaged cells survive when they should have gone through apoptosis (Nall, 2020). In addition, new cells continue to form when they are not needed. These extra cells will continue to divide without stopping, which may become tumors. ​ Cancer is the generic term that is used to describe a large group of diseases that can affect any part of the body (“Cancer”,​ 2018). A defining feature of cancer is the rapid production of abnormal cells that grow beyond their normal boundaries (“Cancer”,​ 2018). While a normal cell would mature into specialized cells with specific functions, cancer cells do not; they are less specialized than normal cells (Nall, 2020). One reason cancer cells can divide without stopping is due to its ability to ignore signals that indicate they should stop dividing or begin a process known as programmed cell death - apoptosis, to get rid of unneeded cells (Nall, 2020). Under normal circumstances,​ human cells grow and proliferate new cells as the body needs them; when the cells grow old or become damaged, they die and new cells take their place. However, in cancerous cells, the process is broken down and cells become increasingly abnormal as old or damaged cells survive when they should have gone through apoptosis (Nall, 2020). In addition, new cells continue to form when they are not needed. These extra cells will continue to divide without stopping, which may become tumors. ​
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 +==== What did the study do? ====
 +
 +The researchers began by collecting the patients T-cells from their blood. Following that, they used the CRISPR-Cas9 system to edit three genes (TRAC, TRBC, PD-1). TRAC and TRBC are the T-cell'​s natural receptors and they were removed and reprogrammed to express a synthetic T-cell receptor which would seek out and destroy tumors. The research article mentions that the transgenic TCR ( T-cell) Receptor has been shown to mis pair and/or compete for expression with the a and b chains of the endogenous/​original TCR. Mispairing of the therapeutic TCR a and b chains with endogenous a and b chains reduces therapeutic TCR cell surface expression and potentially generates self-reactive TCRs. The third edit removed PD-1, a natural checkpoint that sometimes blocks T cells from doing their job. Once the three genes are knocked out, a fourth genetic modification was accomplished using a lentivirus to insert the cancer-specific synthetic T cell receptor, which tells the edited T cells to target an antigen called NY-ESO-1. Previously published data show these cells typically survive for less than a week, but this new analysis shows the edited cells used in this study persisted, with the longest follow up at nine months.
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 +<WRAP center round box 50%> ​
 +{{ :​cancerstudy.png?​direct |}}
 +**Figure 4: Retrieved from the study referenced at the start of the section**
 +</​WRAP>​
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 ====== Conclusion ====== ====== Conclusion ======
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