Why is cancer so hard to cure?

October 1, 2024

Cancer is a leading cause of death worldwide, despite big breakthroughs in treatments. What makes it so very tough to treat?

Published in Sydney Morning Herald on 16 July 2023 as Why is cancer so hard to cure?

Excerpt:

Despite decades of research and hundreds of billions of dollars dedicated to the search for cures, cancer is still the world’s biggest killer, responsible for the deaths of hundreds of thousands of people every year, 50,000 of them in Australia.

What is it about cancer that makes it so hard to “cure”? And where are we up to with treating it?

What is cancer?

Asked why we haven’t cured cancer, Professor Glen Boyle doesn’t hesitate: “Because it’s bloody hard!”

Rather than one disease, cancer is a constellation of more than 200. It’s been linked to mutations in between 500 and 1000 genes (of the 20,000 or so in each person). “We are literally trying to tackle hundreds of different diseases and none are easy,” says Boyle at the QIMR Berghofer Medical Research Institute in Brisbane. “Every cancer is different – so there’s our first problem. In breast cancer alone, there are 20 to 30 different cancers [differentiated by their genetic mutations]. Almost every patient has a different kind of disease that behaves differently in their individual body.”

This is where the refrain about the moon breaks down. “We know what the moon is,” says Saunders, “we know where it is, we know how far it is, what it’s made of – so it’s a fixed target. Cancer is very different in that we still don’t completely understand what it is and how it works. In terms of that metaphor, it would be like trying to fly to thousands of different moons in thousands of different places … and halfway to a moon, it might change shape or direction, or move into a different part of the sky.”

For a long time, cancers have been categorised by the organ in which they first appear (even cancer of unknown primary, which gives no clues about where in the body it started, is its own category). Today, cancer subtypes are increasingly being described by their genetic or molecular markers. In breast cancer, for example, we might talk about the mutations in the BRCA1 or BRCA2 genes. Or we might talk about HER2-positive cancer, which tests positive for a protein called human epidermal growth factors receptor 2 and tends to be more aggressive than other types of breast cancer. These markers “allow us to better define the thing we’re working against,” says Saunders, now the deputy chief scientist and engineer for NSW.

Scientists can now examine a tumour’s “fingerprint”, says Boyle, who heads the cancer drug mechanisms group at QIMR Berghofer. “We can see up to six different sorts of melanoma cells in one tumour, and they are all doing different things, mutating and growing at different rates and potentially responding differently to potential treatments.” When he started working on melanoma, the consensus was that one person’s melanoma was the same as another’s. “But when we looked at the genome, we realised, well actually, no, it’s not the case at all.”

Still, cancers do have something in common: they’re cells that have lost the normal control of their growth.

The trillions of cells in our bodies have specific functions – liver cells to break down fats and produce energy, blood cells to carry oxygen – and follow a predictable cycle of growth, division and death. “We have all of these complex control mechanisms that make our cells copy themselves only when they need to,” Saunders says.

But with cancer, one of these cells ignores the body’s inbuilt controls and multiplies uncontrollably. These haywire cells can travel through the blood or lymphatic systems, burrowing into tissue and flourishing there. “They become really nasty and can invade and spread into other parts of the body,” says Saunders, “and that is when you have very serious and often untreatable versions of the disease.”

When cancer spreads, it is called metastatic. Medicos call the original tumour “primary” and the secondary tumours “mets”, short for metastases. Pathologists speak of grades of cancer (how aggressive it is) and stages of its development (how much there is and how far it has spread). Although it is different in each case, generally a small tumour that has not spread is described as stage one, while cancer that has spread to at least one other body organ is stage four.

The deadly thing about some of the most common cancers found in parts of the body not essential for survival (say, mammary glands in the breast) is that they can infiltrate vital organs such as the lungs. “Let’s say you have a massive ball of cancerous cells growing in your lungs,” Saunders says. “That part of your lung is no longer going to be working as a lung should because those cells have lost their ability to do their jobs.”

Cancer can spread to the liver, stopping it from keeping toxins out of our system. It can cause blood to become “stickier”, heightening the risks of blood clots, including in the brain, where a stroke can occur, or in the heart. Tumours can push on parts of the brain, eventually causing a person to lose alertness and then consciousness. Infections such as pneumonia and other co-morbidities can contribute to someone’s death.

If cancer in one of his patients is yet to spread, Associate Professor Tom John will use the word “cure” when speaking with them “from the get-go because the whole intent of treatment is curative”. But for patients with metastatic cancer, John, who is deputy director of oncology at the Peter MacCallum Cancer Centre, is more circumspect, explaining to them “we’re aiming to control this, but we can’t cure it”. However, some new treatments are leading to people recovering from metastatic cancer (more on this later). If, over a long period of time, scans are continuing to show no signs of cancer, John will say: “We don’t use the c-word very often but, in this case, you may well be cured of the cancer. We don’t know this for sure. But, at this point in time, it certainly looks that way.”

Read the full article to learn more, including:

  • Why can’t we just stop cancer cells spreading?
  • Is it possible to target the root cause of cancers?
  • Why are some cancers easier to treat than others?
  • What are the promising new treatments?

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