You posited that if the astragalus extract were combined with immunotherapy, the ‘patients’ would have a strengthened immune system and would therefore would be able to withstand a higher drug dose. Does this mean that astragalus extract is ‘poisonous’ to the ‘patients’?
Any amount of drug can be poisonous to ‘patients’ or models. This experiment through the dosing series wanted to show what a lethal does would be, but we were unsuccessful. The 100mg/mL that we initially used, as stated in the presentation, was the highest concentration that could be used in the blood of humans. Immunotherapy would allow us to start with an even higher initial concentration and then do the dilutions to figure out the effects of the compound.
So our experiment was tested as a potential chemotherapy. The things is chemotherapy is not 1 drug, but many. Chemo treatments that are used are old and have not been updated and here we are trying to find one that could be more effective. This is why the positive control is the known chemotherapy Colchicine. So, with this background info I cannot say how many new chemotherapies they are and since this lab tested chemotherapies it is outside the scope of my project to have a say on alternate therapies to chemotherapy.
If astagalus extract is not effective as a chemotherapy in this study, what types of cancers do you hypothesize will be more suscetible to this treatment then?
Well there was an study done, that we used for reference (Mechanism of astragalus
membranaceus in the treatment of laryngeal cancer based on gene co-expression network
and molecular docking), The study we conducted on fruit flies was done to model treatments that work on neck and throat cancer. The study we reference showed how the extract can work on mice when treating laryngeal cancer. Other cancers that this extract had been seen to work is also in non-small cell lung cancer and breast cancer. The papers that we saw discussing this are “Anticancer activity of astragalus polysaccharide in human non-small cell lung cancer cells” and “Anti-tumor potential of astragalus polysaccharides on breast cancer cell line mediated by macrophage activation”.
In our future plans section there is a really small part that does show that using mice or a human cancer cell line model would be better. The problem with fruit flies is that they are very tough and have a strong DNA repair network so they can be pretty hardy when it comes to chemotherapies. The reason mice might be the best model is that the studies we referenced for this project were done on mice and saw success.
If the drug was put into the flies food how can you accurately determine how much food (drug) each fly consumed and if it was an equal dosage to each fly?
To determine the concentration of the drug it was always mixed in with 5mL of the food. So none of the flies got the exact concentration we used, but because it was always the same food and same amount the impacts of the concentration of the drug in the food could still be quantified. A simpler way to think of it is the M1V1-M2V2 equation to determine concentration. If we wanted 1mL of the compound to be present in 5mL of the food with a 100mL/mg initial concentration we can figure this out from this, which is how everythting was calculated.
The results we expected were that of this being a hit. This means that a hit would need to have a percent survival below 16%, we did not get close with any of our tests.
In our presentation I have mentioned in future directions that a better biological model would be mice. This is because our references tested this compound in mice and found success with it against cancer.
You posited that if the astragalus extract were combined with immunotherapy, the ‘patients’ would have a strengthened immune system and would therefore would be able to withstand a higher drug dose. Does this mean that astragalus extract is ‘poisonous’ to the ‘patients’?
Any amount of drug can be poisonous to ‘patients’ or models. This experiment through the dosing series wanted to show what a lethal does would be, but we were unsuccessful. The 100mg/mL that we initially used, as stated in the presentation, was the highest concentration that could be used in the blood of humans. Immunotherapy would allow us to start with an even higher initial concentration and then do the dilutions to figure out the effects of the compound.
How many cases of the alternate therapy to chemotherapy have been done and successful? Why aren’t they more well known?
So our experiment was tested as a potential chemotherapy. The things is chemotherapy is not 1 drug, but many. Chemo treatments that are used are old and have not been updated and here we are trying to find one that could be more effective. This is why the positive control is the known chemotherapy Colchicine. So, with this background info I cannot say how many new chemotherapies they are and since this lab tested chemotherapies it is outside the scope of my project to have a say on alternate therapies to chemotherapy.
If astagalus extract is not effective as a chemotherapy in this study, what types of cancers do you hypothesize will be more suscetible to this treatment then?
Well there was an study done, that we used for reference (Mechanism of astragalus
membranaceus in the treatment of laryngeal cancer based on gene co-expression network
and molecular docking), The study we conducted on fruit flies was done to model treatments that work on neck and throat cancer. The study we reference showed how the extract can work on mice when treating laryngeal cancer. Other cancers that this extract had been seen to work is also in non-small cell lung cancer and breast cancer. The papers that we saw discussing this are “Anticancer activity of astragalus polysaccharide in human non-small cell lung cancer cells” and “Anti-tumor potential of astragalus polysaccharides on breast cancer cell line mediated by macrophage activation”.
Although this didn’t work with fruit flies, do you think there would be different results for tumors within a human or a different organism?
In our future plans section there is a really small part that does show that using mice or a human cancer cell line model would be better. The problem with fruit flies is that they are very tough and have a strong DNA repair network so they can be pretty hardy when it comes to chemotherapies. The reason mice might be the best model is that the studies we referenced for this project were done on mice and saw success.
If the drug was put into the flies food how can you accurately determine how much food (drug) each fly consumed and if it was an equal dosage to each fly?
To determine the concentration of the drug it was always mixed in with 5mL of the food. So none of the flies got the exact concentration we used, but because it was always the same food and same amount the impacts of the concentration of the drug in the food could still be quantified. A simpler way to think of it is the M1V1-M2V2 equation to determine concentration. If we wanted 1mL of the compound to be present in 5mL of the food with a 100mL/mg initial concentration we can figure this out from this, which is how everythting was calculated.
Great job I love your poster!! how different did your actual results vary from the results you expected?
The results we expected were that of this being a hit. This means that a hit would need to have a percent survival below 16%, we did not get close with any of our tests.
Do you think there could have been a better model organism? And what would have made it better
In our presentation I have mentioned in future directions that a better biological model would be mice. This is because our references tested this compound in mice and found success with it against cancer.