Great presentation! You explained why the organism you used was a good model, but if more research were to be conducted with this for cancer treatment, would there be a better organism to test on?
The next steps for testing the effects of Clofazamine and radiation would be to begin testing in vitro in cultured human cancer cells. As a result of Drosophila melanogaster rapid life cycle, and therefore rapid cell division, they mimic cancerous human cells very well. Additionally, Drosophila share many common proteins and biological processes with humans, making them the most reliable model organism for this project.
A likely cause of our negative control results being slightly off is our lack of replicates. The composite negative control was data compiled from hundreds of replicates, whereas as a result of limited time, we were only able to complete one replicate. I suspect had we done more replicates, our data would be more accurate, and thus more similar to the composite data.
The next step in researching the effects of Clofazamine on human cancer cells would be to begin testing in vitro, or in a lab in cultured human cancer cells. If that goes successfully, we would move to in vivo testing in animals such as mice.
The different dosages were placed in the food of the Drosophila in their vials. The third instar larvae were placed in these vials after irradiation and would eat the stock solution, thereby intaking Clofazimine, as well as the negative and positive controls.
The lower dose protocol would effectively “zoom in” to the one we have now. Because there was irregular data around 0.5mM of Clofazimine, a dose response protocol starting at 0.5mM with a serial 1.5:1 dilution to test more similar doses.
Clofazamine inhibits cell proliferation by binding to the guanine bases of DNA thus inhibiting DNA replication and organism growth and development. We knew irradiation would cause DNA damage in the Drosophila melanogaster. If we were to combine the DNA damage caused by irradiation with the inability to replicate DNA from Clofazimine, the organism would likely be unable to survive.
Great presentation! You explained why the organism you used was a good model, but if more research were to be conducted with this for cancer treatment, would there be a better organism to test on?
The next steps for testing the effects of Clofazamine and radiation would be to begin testing in vitro in cultured human cancer cells. As a result of Drosophila melanogaster rapid life cycle, and therefore rapid cell division, they mimic cancerous human cells very well. Additionally, Drosophila share many common proteins and biological processes with humans, making them the most reliable model organism for this project.
What are some reasons you speculate your negative control establish a larger hit than the composite negative control?
A likely cause of our negative control results being slightly off is our lack of replicates. The composite negative control was data compiled from hundreds of replicates, whereas as a result of limited time, we were only able to complete one replicate. I suspect had we done more replicates, our data would be more accurate, and thus more similar to the composite data.
Good job! How could be possibly being to apply these results to humans? Would mice or another mammal be used next?
The next step in researching the effects of Clofazamine on human cancer cells would be to begin testing in vitro, or in a lab in cultured human cancer cells. If that goes successfully, we would move to in vivo testing in animals such as mice.
Hiya, well presented 🙂 I wanted to ask, how exactly were the Drosophila dosed with your chemical and controls?
The different dosages were placed in the food of the Drosophila in their vials. The third instar larvae were placed in these vials after irradiation and would eat the stock solution, thereby intaking Clofazimine, as well as the negative and positive controls.
What concentration could the lower dose protocol be?
The lower dose protocol would effectively “zoom in” to the one we have now. Because there was irregular data around 0.5mM of Clofazimine, a dose response protocol starting at 0.5mM with a serial 1.5:1 dilution to test more similar doses.
What led you to believe that Clofazimine, a leprosy drug, would be a good chemotherapeutic?
Clofazamine inhibits cell proliferation by binding to the guanine bases of DNA thus inhibiting DNA replication and organism growth and development. We knew irradiation would cause DNA damage in the Drosophila melanogaster. If we were to combine the DNA damage caused by irradiation with the inability to replicate DNA from Clofazimine, the organism would likely be unable to survive.