9 thoughts on “D83 – Cardella

  1. You did so good Caleb! What do you think was the most challenging thing you came across when conducting your experiments?

    1. Hi Zahra, the first thing that comes to mind when I think about what was most challenging was quantifying the second round. It was difficult and somewhat time consuming to wipe the marker off from the first quantification! Thank you for the compliment and for your question, for teaching me how to work in the lab, and for answering all of my questions throughout the semester.

  2. Do you think that the third instar larval stage is the best time to treat Drosophilia with clofazimine? Or do you think that another life stage may be more representative of cancer cell growth?

    1. Hey Rachel, the third instar stage is the longest larval stage at 2.5-3 days. Each other pre-pupal stage is about 1 day long. The third instar stage is also when the larvae climb up the walls of vials in order to begin metamorphosis into pupae and adult flies. This makes our quantification of survival much easier because in the other larval stages they would still be at the bottom of the vials eating. To my understanding, Drosophila are model organisms as a whole and no life stage is more ideal than another. For the purposes of our experiment, due to the length of time spent in this stage and the way they climb up the vial walls, the third instar stage was the best time to initiate Clofazimine treatment. Thank you for your question!

  3. What aspects of the chemical structure would you change to increase the hits? How does the chemical structure impact the hits?

    1. Hello Alexis, a study came out last year about enhancing the safety of Clofazimine by testing the toxicity of analogues. I would just take this research further and look at safety as well as its ability to suppress the Wnt pathway which is excessive in the triple negative breast cancer subtype. Clofazimine has also been shown to cause an increase in caspase-3 activity, which is worth examining. Caspase-3 has been called the “executioner protein” due to its roles in apoptosis (including catalyzing the cleavage of key proteins, fragmenting DNA, degrading cytoskeletal structures).

  4. Great work, Caleb. I like that you considered in vitro studies as a future direction. Do you know why clofazimine works well in treating cancer, even though it was originally used for leprosy? How would you want to modify it if you could?

    1. Hi Abhi, Clofazimine has been shown to suppress growth on various cancer types and a possible cause is that it increases capsase-3 activity. Capsase-3 is activated in different apoptotic pathways. Modifications should emphasize this feature as well as reduce toxicities when possible. Thank you for your question!

  5. Might be a duplicate comment lol. Good work Caleb. I like that you considered in vitro studies as a future direction. What exactly would you want to do? Working with HeLa cells maybe? Why does clofazimine work as an anti-cancer drug even though it was originally approved for leprosy?

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