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10 thoughts on “D17 – Moran”
Do you think there is a similar strain close to mytomycin that could potentially have the same effects?
Yes! Our group actually had planned on using the compound, capecitabine, for our research, but Dr. Pamela Harvey had already extensively researched it. In her research, several other candidates were identified in the same compound screen as capecitabine which included mitomycin, gemcitabine, and azacitabine. These last two compounds would still need to be tested before we could determine that they have similar effects (which, from my understanding another group had tested gemcitabine if you want to check it out). Great question!
You mentioned this process isn’t incredibly indicative of how this would work in the body, how would you adjust future experiments to include considerations for what conditions within the body are like?
Great question! Our research did take many steps in order to replicate conditions of the human body as closely as we could. An example of this was incubating our dilution plates for 24 hours at 37 degrees Celsius (as that is the average normal body temperature of the human body). In the future, it would be important to test mitomycin for its effectiveness in macrophages such as in cardiac cell, liver cells, or neurons to figure out the toxicity and then eventual progress to testing in animals.
How did you decide on mitomycin as the drug to study?
Mitomycin was identified in a compound library from the National Institute of Cancer Research. In a compound screen of capecitabine, mitomycin was another compound identified that also exhibited cytotoxic properties as both are chemotherapeutics. One disadvantage to testing chemotherapeutics is that they have the possibility of being bactericidal at certain dilutions, which may have the possibility of producing a high toxicity – killing other healthy cells. Therefore, that would be our next step in our experiment: determining the toxicity of mitomycin.
Do you know the mechanism of action of mitomycin as it operates as a chemotherapy? Why would this mechanism kill bacteria as well as cancer cells?
Great question, Delwin! Although we did not determine the mechanism of action in our research, mitomycin was identified from a compound screen of another chemotherapeutic called capecitabine. Capecitabine has been extensively researched as a successful antibiotic and is known to interfere with the production of function of DNA. We can hypothesize that DNA synthesis in mitomycin was inhibited by a pyrimidine nucleoside analogue which likely inhibited DNA polymerase, although further research on mitomycin would be necessary to confirm this. Because both bacterial and cancer cells contain DNA polymerase as a source of replication, inhibiting it would kill either type of cell.
Great presentation! In your figure in the results section, does a “hit” mean that it could be used to be tested, or you’re sure that it would be effective?
Really good presentation! Could you explain why you incubated for 24 hours at 37 degrees? Also, are there any recommendations that you have for future researchers to make the conditions more similar to the human body and you said that was one of the limitations of your experiment?