Charlie Swanton: What is cancer?

An introduction to the disease...
28 January 2025

Interview with 

Charlie Swanton, Francis Crick Institute

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Cancer cells

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Charlie Swanton was born in Poole in Dorset on the 24th of February 1972. He attended St Paul's School before he continued his studies at University College London and it was there that his interest in oncology, the study of cancer, began. He's a world-leading lung cancer expert and he studies the management of metastatic cancer and also drug resistance and incurable cancers. He's won dozens of prestigious awards for his work. He's currently the Deputy Clinical Director at the Francis Crick Institute in London, and the clinical lead in Cancer Research UK. He gave an extended interview to Chris Smith...

Charlie - Cancer refers to essentially an uncontrolled proliferation in the human body that can breach the normal tissue barriers and in many cases can spread beyond those tissue barriers to other organs through either the blood or the lymph or direct invasion and result in what we call space occupying lesions or metastases in other organs. The reason why patients die of this disease is due to subtle metabolic and immune consequences that prevent the immune system from working effectively or drive abnormalities in the way in which we metabolise products from what we eat or how we digest those products, through to just the consequences of the volume of disease on that underlying organ which could be the liver, the lung, the brain, the kidney etc. that ultimately lead to organ failure.

Chris - So if cells are disobeying the normal genetic instructions and they're just growing where they shouldn't, when they shouldn't, does that mean they can also disobey biochemical rules as well? They can basically make any of the things any other cell in the body can make and just start doing that whenever they want so it's a sort of biochemical disease as much as a physical growth disease.

Charlie - I think that's exactly right yes and indeed there was the effect that you've probably heard of called the Warburg effect and cancer cells in general are much more dependent on glucose metabolism, glycolysis, the biochemical breakdown of glucose. One of the sort of hallmarks of this disease is the uptake of glucose very rigorously by cancer cells and we image that in the clinic using something called FDG PET, which is essentially a radiolabeled glucose tracer that's taken up by cancer cells more than surrounding cells and so that helps us image where the cancer is in a patient's body, that is an example of the sort of biochemical consequences of a cancer cell.

Chris - But certain bits of my body, the healthy bits, are talking to other bits, chemically, they're sending signals through nerves in some cases but through the blood for example with hormones, so do cancers also have recourse to that? Can a cancer influence another organ via hormonal signaling for example?

Charlie - Well that is a great question and it's a question that we are thinking very deeply about actually at Cancer Research UK in our Cancer Grand Challenge scheme which is an international grant programme and here we're doing exactly that which is trying to understand the sort of systems level changes that occur in patients with cancer and we're setting questions to address some of those problems. I'll give you one example which is cancer cachexia which refers to weight loss either of fat or of muscle in patients with cancers like pancreas cancer or cancers of the upper gastrointestinal tract, so gastric cancer for example, esophageal cancer and even lung cancer actually, cachexia is quite common and patients lose weight and it's unclear why or how this happens and we've got increasing insights into this metabolic process and as you say this likely comes about through mediators, potentially hormonal mediators that either are released from the tumour or surrounding tissue in response to the burden of disease that suppresses appetite or makes a patient feel sick or nauseous and ultimately reduces their calorific intake and probably also potentially increases their metabolic rate as it were to degrade muscle and fat to presumably liberate the building blocks that are required for the cancer to grow and divide.

Chris - So the cancer is effectively turning itself into the primary thing and using the body almost parasitically. It's growing off the body?

Charlie - Yeah that's the way I see it in some cases and I think it's quite a scary proposition, it's very important to say right from the outset there's no reason behind any of this, this is purely a reflection of genetic diversity in the evolving cancer mass, that is the number of cells and the differences between them genetically. We call this genome instability that comes about because of the inability of cancer cells to repair their DNA effectively or the fact that they have ways of replicating DNA that's less faithful than normal cells so you get more mutations and it's that genetic diversity between cancer cells that acts as a sort of a substrate upon which so-called natural selection acts and so everything we see in cancers is a reflection of that genetic diversity and natural selection playing out.

Chris - What fraction of the population, if we just pick the human race, what fraction of us are destined to have this happen to us?

Charlie - Well I think in western worlds we'd estimate that somewhere between one in three and one in two of us will suffer from or die from cancer now. We've made great inroads into the management and prevention of cardiovascular events and cardiovascular disease. Our progress in cancer and neurodegenerative disease has been slower. I see cancer as sort of the next big challenge that we're tackling after what I would state is a sort of revolution in our understanding and management of cardiovascular disease and the community is doing an extraordinarily good job but we still have a long way to go to develop new therapies, new means of early detection and most importantly prevention, new ways of preventing cancer.

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