Can we put the brakes on cancers’ ability to metastasize? In episode 33, John Lewis from the University of Alberta talks with us about his research into inhibiting cancer cell movement and metastasis through genomic targets. His article “Quantitative in vivo whole genome motility screen reveals novel therapeutic targets to block cancer metastasis” was published with multiple co-authors in the June 14, 2018 issue of the open-access journal Nature Communications.

Halting Cancers' Spread - John Lewis
Halting Cancers' Spread - John Lewis
Halting Cancers' Spread - John Lewis Halting Cancers' Spread - John Lewis
@rwatkins says:
Lastly, Ryan and I were interested in hearing John's thoughts on the promise of developing genetic therapies that could halt the progression of cancers, whether it's through the use of CRISPR for gene editing or some other method.
@rwatkins says:
Given the potential of the methods that John and his team identified, we were eager to learn how long it might be until we can expect human trials to take place ... as well as what that process will entail.
@rwatkins says:
Before the break, John was about to describe the "eureka" moment when he realized that the methods he and his team developed could block over 99% of metastatic cancer cells.
@rwatkins says:
We followed up by asking John to share the "eureka" moment when he realized that the eleven genes he and his team identified could block over 99% of metastasis among cancer cells. We'll hear from him about this revelation after this short break.
@rwatkins says:
John and his team's methods were over 99% effective in blocking the metastasis of cancers. We were curious to learn what methods he and his team used to quantify this.
@rwatkins says:
Just because the genes worked to halt the spread of cancers in animal models doesn't necessarily mean that they're equally relevant to humans as well. So we asked John how he and his team went about identifying which of the genes that they investigated might be most likely to be associated with cancers in humans.
@rwatkins says:
Doug and I were struck by how extensively cancers can divide and migrate within as little as two day's time. We wondered how it is that they're able do so, as well as how John and his team went about inhibiting a single gene within each embryo in order to test the effect of that gene on metastasis.
@rwatkins says:
After injecting cancers, many cells make their way throughout the embryo then back to the chorioallantoic membrane. We asked John to describe this process in more detail ... as well as how they go about tracking the development of the cancer cells that they injected into the chicken embryos.
@rwatkins says:
Doug and I were interested in learning how John and his team maintain the de-shelled chicken embryos as they mature ... as well as what parts of the chicken embryo they test their anti-metastasis therapies on.
@rwatkins says:
Before testing these therapeutic targets' ability to block cancers in lab mice, John and his team first carried out their experiments on a much faster growing animal model: fertilized chicken eggs whose shells had been removed in order to access the embryo during the three weeks in which they develop. Ryan and I wondered where these eggs came from, as well as how researchers in John's lab learn to de-shell the eggs without disturbing the fragile membranes inside.
@rwatkins says:
John likens this approach of blocking the spread of cancers by increasing their adhesiveness to it being a sort of "tumor glue." He and his team, however, ran into some challenges inhibiting the CD151 gene, as he describes next.
@rwatkins says:
John and his team discovered eleven genes that are widely involved in the metastasis of cancer cells, but which are also not unique to any one type of cancer. So Ryan and I were curious whether this approach built on other previous advances in cancer research.
@rwatkins says:
As John explains, cancer is not one disease, but rather is a collection of diseases that are deeply complex and far from fully understood. We began our conversation by asking him how it is that cancers can develop and, through metastasis, spread.
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Press coverage

Folio | EurekaAlert | MedicalPress | ScienceDaily | eCancer | Med India | TechnologyNetworks | University of Alberta

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Hosts / Producers

Doug Leigh & Ryan Watkins

How to Cite

Leigh, D., Watkins, R., & Lewis, J. D.. (2018, October 2). Parsing Science – Halting Cancer’s Spread. figshare. https://doi.org/10.6084/m9.figshare.7158998

Music

What’s The Angle? by Shane Ivers

Transcript

John Lewis: The premise of the study was that if we really wanted to learn about how to block metastasis, we really had to do it in a living system.

Ryan Watkins: This is parsing science. The unpublished stories behind the world’s most compelling science as told by the researchers themselves. I’m Ryan Watkins…

Doug Leigh: And I’m Doug Leigh. Over 380,000 deaths are predicted to occur this year in the United States and Canada due to cancers. In more than one million Americans as well as over a hundred thousand Canadians are estimated to be diagnosed with some form of cancer in 2018. Today in episode 33 of parsing science, we’re joined by John Lewis from the University of Alberta in Edmonton. He’ll talk with us about his research into the application of molecular tools to almost completely block the spread of any form of cancer in living cells. Here’s John Lewis.

Lewis: Hi there! My name is John Lewis. I am an associate professor at the University of Alberta in the department of oncology, and I hold the chair, Frank and Carla Sojonki chair, in prostate cancer research supported by the Alberta Cancer Foundation. So, I grew up in a small town called Owen Sound, about 20,000 people, and actually I thought I might become an engineer, so very very interested in new technologies and tools, and became very interested early on in computer programming and things like that. So, I started my education at the University of Western Ontario in London Ontario Canada and studied genetics. But, at the time, I wasn’t sure what career I wanted to enter in. So, I actually took a job, believe it or not, as an income tax consultant and worked for four years doing income tax and corporate income tax and audits and all that. So, I learned a lot about business and I think that’s informed me a lot and sort of what I’m doing now, but realized that I didn’t want a career in bookkeeping. So, I moved out west and started my PhD in the Department of Biochemistry microbiology at the University of Victoria. And the whole time I was doing my PhD, I was sort of searching for how I was gonna use this amazing knowledge. Rather unfortunately, my fiance at the time her father came down with kidney cancer have metastasized to his liver, and so it was, you know, it was at a fairly late stage, and you know, while I was doing these amazing techniques in the laboratory, you know, we had sort of state-of-the-art computers and these amazing analytical techniques, you know, the clinical trials that were offered to him at this sort of late stage were pretty shocking to me. So, at the time there was a clinical trial for, believe it or not, the thalidomide and of course it didn’t have much activity. The other one there was a clinical trial in interleukin-2 which can create some really really horrible side effects, and also didn’t have any effect in his cancer. So, at the time, I was motivated and sort of by the low technology of the clinic to try to apply some of the stuff I learned in my PhD toward cancer. And so, pretty much ever since then I’ve been working on cancer.

Watkins: As John explains, cancer is not one disease but rather a collection of diseases that are deeply complex and far from fully understood. We began our conversation by asking him how it is that cancers can develop and through metastasis spread.
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