Good job on the presentation!! One question I have is why did you specifically choose to study the RFC-1 gene over other genes? What is unique about this gene that might lead to cancer if there is something wrong with it?
We chose the Rfc-1 gene because it has a similar expression profile to Rad51 during T therm replication. We do not know the Rfc-1 genes full function, it is presumed to be a component in the replication factor C
We determined that the Rfc-1 gene had no change in regulation. We are unable to determine what role, if Rfc-1 has one, the gene product plays during DNA damage repair.
The limitations are just the knowledge around the DNA damage repair pathway and the time it takes to research the genes possibly involved in said pathway. It has not have direct patient applications.
Good job on the presentation! One question I have is what specifically did you do to induce damage in the DNA? Are there other mechanisms of inducing damage that you could further experiment with?
Great presentation! I appreciated the introduction and orientation to the poster. Regarding your approach, why did you start with a qualitative RT PCR vs. quantitative RT PCR? In retrospect, would you have approached the experiment differently?
We just didn’t have time to use qrtPCR, we were only able to run the rtPCR for qualitative analysis. I would have liked to run a qrtPCR to determine the exact expression changes, if any, to the rfc-1 gene.
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I liked the use the laser pointer, it was helpful to follow what you were saying. Why did you choose that gene, Rfc1, specifically to study?
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We chose the RFC-1 gene because it had a similar expression profile to the Rad51 gene during T therm replication.
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Good job on the presentation!! One question I have is why did you specifically choose to study the RFC-1 gene over other genes? What is unique about this gene that might lead to cancer if there is something wrong with it?
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We chose the Rfc-1 gene because it has a similar expression profile to Rad51 during T therm replication. We do not know the Rfc-1 genes full function, it is presumed to be a component in the replication factor C
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What lead you to determine that RFC-1 is up-regulated, and what does that mean when comparing it to Cancer and DNA damage?
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We determined that the Rfc-1 gene had no change in regulation. We are unable to determine what role, if Rfc-1 has one, the gene product plays during DNA damage repair.
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What are the limitations of this research in the medical world when testing it on patients?
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The limitations are just the knowledge around the DNA damage repair pathway and the time it takes to research the genes possibly involved in said pathway. It has not have direct patient applications.
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Good job on the presentation! One question I have is what specifically did you do to induce damage in the DNA? Are there other mechanisms of inducing damage that you could further experiment with?
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We introduced Hydroxyurea to the DNA which causes DNA damage by stalling polymerases. We could use UV induced DNA damage as another option.
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Great presentation! I appreciated the introduction and orientation to the poster. Regarding your approach, why did you start with a qualitative RT PCR vs. quantitative RT PCR? In retrospect, would you have approached the experiment differently?
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We just didn’t have time to use qrtPCR, we were only able to run the rtPCR for qualitative analysis. I would have liked to run a qrtPCR to determine the exact expression changes, if any, to the rfc-1 gene.
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What if any is a concern when thinking about using this in patients?
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The research we did does not yet have applications to humans. The research was more for understanding the DNA damage pathway
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What if any are limitation when considering this for administration on patients
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The research that we are doing does not yet have an application for patients, more of a project about understanding the DNA damage pathway better.
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