New cancer treatment disguises drugs in fat

30 July 2019

Interview with 

Nathan Gianneschi, Northwestern University

CANCER-HEADLINE

Headline about cancer

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Every two minutes someone in the UK is diagnosed with cancer. And there are a range of options when it comes to treatment. Frequently, though, chemotherapy drugs, designed to hit fast-growing cells like cancers are used. But not all rapidly-growing cells are cancerous, so there are inevitably side effects. Now, scientists at Northwestern University have found that dressing up chemotherapy drugs as fat molecules makes it much easier to concentrate their actions on cancer cells alone. Izzie Clarke heard how it works from Nathan Gianneschi.

Nathan - We're hoping to disguise cancer medicine as fat molecules, as nutrients. There are proteins, for example, that circulate within your blood that will transport long chain fatty acids around the blood, and then there are receptors on cells of all types that are hungry to consume these proteins and the fat that they carry. Tumour cells are very very interested in this as a nutrient source. They're dividing and they're growing and they're wanting to consume fat and energy and so we connect drugs to one half of this modified fat and then allow the other half of the fat to engage the body's transport systems, so you sort of hitchhike on the tumour's systems for acquiring and consuming energy.

Izzie - This really is a Trojan Horse cancer treatment?

Nathan - Right. And it really is one of the goals; how you can get to the point where normal tissues are, let’s say, less damaged. The idea is to make the patient less sick by getting more of the drug to the tumour.

Izzie - And what is this drug that you're using and how does it get into that fatty molecule?

Nathan - The drug, what we would call the warhead, the active part that goes and kills the cell is called Paclitaxel. In the clinic today it's used in two main formulations. We took that same drug and the carrier, the rocket for that warhead is this fat chain; 18 carbons in a chain with what we call a carboxylic acid at the end. And so it's a chemical bond between the drug and that fat chain and the preservation of that carboxylate is what tricks the body.

Izzie - And how well did it work in tests?

Nathan - It works very very well. We used animal models for bone, colon, and pancreatic cancer. These are animal models of human tumours and the human tumours will grow in the mouse. We're able to treat with our drug versus the clinically approved drugs and show that we increase the survival of the animals as well as decreasing the size of the tumours. But just because you did that in the mouse, of course, doesn't mean that it's going to work in a person. If it does work then you have an advantage over current medicines and you can get approval and help people.

Izzie - Why is this better than current methods?

Nathan - In the study, we did a head-to-head or, in other words, a direct comparison with two of the FDA approved formulations for these types of drugs, and the fact is that we have much higher doses so we can go to higher doses because we can target better than the currently approved drugs. And so by being able to target to the tumour better that means you can inject much more drug and that means you can more quickly kill the tumour. At the maximum doses, what we call maximum tolerated doses, we had better efficacy than the clinically approved drugs because of that targeting ability. The next step is to see if we can actually translate that to a human outcome of course.

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