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We've tried the organoid approach, but ultimately, you need an animal model to properly model blood flow, immune response, etc. So we developed a pig model of pancreatic cancer: https://journals.plos.org/plosone/article?id=10.1371/journal...

My lab uses an engineering approach to develop new minimally invasive cancer therapies, and some of the new therapies are already being translated into early phase human trials: http://www.edboas.com/lab/

We're hiring biomedical engineers, so please contact me if you're interested.




I'm pretty sure you are well compensated and all that (though probably not as well as your bosses), but also just personally, thank you to you and everyone in your lab.

Cancer killed my grandfather, my best friend, my aunt, and so many other people I know, and what you are working on isn't just making money, it's saving lives.


Are there any plans to study and treat neuroendocrine tumors?


hello,

first thanks for your work, since you're in advanced medical territories, what other labs / people / work do you follow with interest ?


that sounds incredibly interesting actually, great work


You mean you purposefully grew tumors on pigs?


Yes, we induce pancreatic cancer in pigs, and then we try to treat the cancer.

One important question is why so many new cancer treatments are successful in mice and rats, but then fail in human trials. You could point to genetic differences between mice and humans, but I think another important factor is simply the size difference. Just like a scale model of an airplane won't fly the same way, there are also scaling laws in animals. Large animals have a lower metabolic rate (per kg), require lower drug dosing (mg/kg), have more defense mechanisms against cancer, and have differences in blood flow and many other variables. We suspect that cancer treatments that work in pigs will be more likely to also work in humans.


The size of the tumor likely makes a big difference too: a centimeter-sized lump contains 1000x more cells than a millimeter-sized one. It will contain 1000x more drug-resistant cells (given identical mutation rates). For example, a human brain tumor is likely to already contain hundreds of cells carrying a mutation for every amino acid in every protein. Thus for any inhibitor drug you try, hundreds of cells will already be resistant, and they will grow back the tumor in just a few months. That’s much less likely to be the case in a mouse tumor.


You could also say that induced cancers are somehow different from naturally occurring cancers so treatments targeted toward 'artificial' cancers fail to work on real things.


Could be what GP says, could be what you say, but the only way to know for sure is to try and reduce the differences.




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