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Podcast "Caring & Sharing"

In this paper, not only a short history of cancer and cancer research is delineated but more so the possibilities that come with observational and comparative biology. Do you know how many copies of the (in)famous tumor suppressor protein TP53 an elephant has (the answer is in the paper)? What can we learn from dog oncology for transplantation medicine (the answer is in the podcast)? 

Tune in to learn more.:  




Transcript of the interview:

Unveiling Nature's Clues: Animal Cancers as a Gateway to Understanding Human Biology

(this transcript was edited slightly for legibility)

USS: Welcome to Caring and Sharing – the Advanced Oncology podcast. I am here with the extraordinary professor Mike-Andrew Westhoff of the Department of Pediatrics of our university. Andrew is a lecturer in the Advanced Oncology study program. You are teaching our students about cell death. First, a warm welcome.

MAW: Pleasure to be here.

USS: When choosing a topic, we decided that the best topic is the one that you covered in your 2021 article in the journal Theranostics. It's called “What Animal Cancers Teachers About Human Biology”. Why do you like that paper so much?

MAW: I like it because it's not obvious. And everything which is not obvious, in my mind, is at least interesting. And interesting even if I don't agree with stuff, is always better than boring.

And when we did research, when we got started, and it was extraordinary how little is known about this. I mean, if you think about cancer and cancer research, and if you think about animals and you always go with, well, we have our mouse system. We have knockout mice and we have inbred mice for generations, and we always use them. And we always assume for some bizarre reason that they're a good model. And then, if they don't work the way they should work, we always go, well, you know, these are mice and they're actually a crappy model. But if you go back further to the – sort of – very beginning of cancer research, we actually used animals, not in a particular modeling system, but in a more interesting system. And it makes sense. And I started very long ago when the world was black and white, and doing research on focal adhesion kinase (FAK) and SRC. And SRC is, of course, called SRC because it's sarcoma, and it was found in chicken. That was Peyton Rous in 1910.

Back then, there was a very aggressive sarcoma in chicken. And he went “I wonder why this sarcoma is spreading through a chick population”. And once you had it in your population, it spread and you couldn't use the chicken for meat anymore. So, he went and looked into it, and he basically found the Rous sarcoma virus, fortunately named. And he found out that it was

  • one of the first retroviruses
  • it contained the first oncogene
  • it contained one of the first tyrosine kinases.

And it was only possible because he used chicken. And a couple of years before that, there was a German scientist called Sticker who did exactly the same experiment. So what Rous did, he cut out the sarcoma and sifted. This way, he created a cell free lysate and applied that cell free lysate to a healthy chicken. And that healthy chicken developed cancer as well. And the German scientist, who did basically the same experiment in dogs, where there's also a very aggressive tumor which passes on, and got the opposite result. His cell free lysate didn't cause cancer. And many years later, it turns out that Sticker tumor, which it is now called, is actually a disease where tumor cells are passed on from one dog to another. So, it's not a virus which is passed on, it's actually the tumor. They looked into this and that tumor is at least 5000 years old. It's the oldest known cell line we have. And was basically the starting point where we went, oh, maybe, just maybe if we actually concentrate on animals more and not use them just as a tool – basically – we can learn a lot.

And it really confused me because cancer cells passed on from one dog to another shouldn't be infectious. I mean, dogs have an immune system. The immune system from the major histocompatibility complexes are very similar to human immune systems.

  • So why do dogs get infected with cancers?
  • And are dogs the only one or other animals?
  • And if there are other animals, what do these animals have in common?
  • And why do some animals can get infected?
  • Why can't others get infected?
  • What will that teach us about the immune system?
  • What will that teach us about transplant biology?
  • And what will that teach us about ourselves?

And that's basically the starting point of that paper.

USS: How can you justify doing research on animals which everyone will be teary-eyed of if you do experiments on animals other than white mice with red eyes? Even if it comes to mice, I think animal protection is quite harsh and in Germany even more difficult.

So how do you want to get there?

MAW: That's a loaded question. I am not proposing to work on animals. I am not proposing to use animals as a tool. I am proposing to understand more about animals and I am proposing to understand more about animal cancer and about animal physiology and biology and compare and contrast that to human cancers. So, the very important point is we were not talking about using tools. We are actually accepting the cancer you get in animals as the entity of interest and compare that to human cancer. And that of course the interesting bit is what is the difference? If you've got two sets and we've got one let's say infectious cancer in dogs and if you find out why that's infectious, that will teach us quite a few things. It will teach us about the differences. And I very much suspect it will end up being the immune system. So, it will teach us more about how the immune system protects us humans. And it will also teach us about how to avoid that protection. Not – I honestly should not be needing to make this point but it should be obvious – it's not to then go on to infect humans with cancer going “yes, we know why they're resistant to cancers, now finally we can break this”.

But if you think about transplant biology, if we want to transplant organs to save lives, if we understand how cancer cells can infect you, we can actually prevent the donor organ from being rejected by the recipient. We can stop making that patient dependent on immunosuppressants for the rest of his or her life. So, by using the cancers as an entity of interest on their own right, we can learn more about humans and we can help humans.

We can also try to understand different types of cancer. I mean pediatric cancer, which is obvious – I’m in the pediatric department – so I should be talking about pediatrics, is very distinct from adult cancer. And a couple of years ago we did a paper which actually gets quoted. So, people seem to at least accept or really be annoyed by the idea that pediatric cancer should be considered a completely different disease entity to adult cancer because there's a different kinetic going on and there's a different causative agent, apparently. Because you don't accumulate mutations, you have those huge deletions, at least in neuroblastoma, where they did lots of studies. So, it's not an accumulation of mutation over time. Now if you have shorter lived animals who also developed cancer, they will need to also have the same procedures going on as pediatric tumors. So instead of taking our cues from adult tumors and try to treat pediatric tumors and then marvel at why it doesn't work because it's a different disease - nobody would try to treat a flu virus based on HIV research - so if we can then sort of find a common cause of cancers in animals who are shorter lived and in pediatric tumor, we might actually again get new ideas of treatment. If we find common ground in different entities that will teach us about the causative effects of those entities.

USS: I think you made your point very well. Thank you for joining us today and I hope that you will get the funding that you are seeking for. Thanks a lot for joining us.

MAW: Pleasure being here. Thank you.



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