What Tumors Eat, And How To Poison Them: Dr. Christal Sohl (Transcript)

Full text of cancer researcher Dr. Christal Sohl’s talk titled ‘What tumors eat, and how to poison them’ at TEDxTulsaCC conference.

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TRANSCRIPT:

Dr. Christal Sohl – Cancer researcher

About the time I first started researching how tumors grow and develop, my aunt Lizzie was diagnosed with breast cancer. I’m sure probably all of you have been in my shoes where a loved one receives a cancer diagnosis, and you want to do everything you possibly can to learn about all of the available treatment strategies.

The breast cancer subtype that my aunt had which was HER2-positive… this actually represents one of the earliest and really most famous examples of a cancer subtype that has a precision medicine associated with it, in this case Herceptin.

And so the difference between precision medicines and traditional chemotherapies which do often work very well is a little bit like spraying a field with a crop duster in order to get rid of weeds, instead of going in and spraying just each individual weed in order to get rid of it.

And so the challenge though in cancer is that we can’t always tell the difference between the weed and the crop or maybe we can tell the difference but we don’t have an effective pesticide yet, or maybe like in the case of my late aunt Lizzie, we can tell the difference between the weed and the crop.

We have an amazing pesticide but ultimately the patient stops responding and relapses.

So in my lab at San Diego State University, we’re interested in understanding how these weeds work, though we call them tumor drivers. And these tumor drivers can happen as a result of any random genetic mishap, a mutation, deletion, amplification.

Imagine, for example, you’re a protein and your job is basically to be stationed right outside the cell, and you are constantly scanning, scanning, scanning looking for clues about the health of the environment whether there’s a lot of resources around. And if you determine that times are good you change your shape in just such a way that you signal to inside the cell that times are great, and that cell now knows that it can grow and divide, and grow and divide.

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But imagine that you pick up a mutation, and so now you’re stuck in that grow shape. So times could be bad, very dark indeed, but you’re still sending that message of grow and divide, grow and divide, grow and divide.

Or imagine you can still make the right shape at the right time, but maybe instead of 10 of you surrounded around the cell, maybe now there’s 10 000 of you lining that cell, and so now you’re screaming that message instead of just saying it.

That’s a little bit like what happens in the case of HER2+ breast cancers.

So we’re starting to think about tumors less in terms of their tissue of origin: breast cancer, lung cancer, prostate cancer, and more in terms of their drivers — EGFR-positive, HER2 positive, p53 mutated. Because these drivers —  it is true that they can represent essentially a superpower for the tumor.

But it’s really important to know that these tumor drivers can also represent an Achilles’ heel because these tumor cells become so reliant on these pathways, so addicted to these pathways, that if you can go in and strategically shut down just that pathway, well you’re going to harm the tumor cell way more than you’re going to hurt any other cell in the patient.

And of course, that’s always what we’re shooting for in precision medicines in cancer.

One of the most interesting examples of Achilles’ heels is tumor metabolism, or how tumors eat. So let’s say for example you look inside a cell and you see a protein that’s catalyzing hundreds and hundreds of reactions in a second which is extraordinary, they can do this.

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