What happens when we cure cancer?


We’re all getting older. I’m getting older.  You’re getting older. Brad Friedel is definitely getting older.

We can run and row and eat raw fish but we age every hour, every day. Every Facebook click. Every keyboard peck. Every tock. Every turn of the clock.

However much Oil of Olay you knead into your craggy face, those lines will harden and your tears will drain in new and different ways.

But I also mean this – we’re all getting older. Owing to better diet and better medicine we are all living longer into our 70s, 80s and 90s. The British public is now an older collection of people than ever before.

I work for a medical research charity whose stated aim is to rid the world of breast cancer. We’re doing pretty well too, to the extent that we can (admittedly somewhat ambitiously) claim to help make the disease a chronic, non-lethal condition within a couple of generations. Our efforts – and the efforts of those like us – will further contribute to an aged population.

We should be mindful of hubris of course. In 1971 an ailing and Vietnam-vexed Richard Nixon declared war on cancer and promised a cure for the disease within 10 years. His intention was to generate public positivity around a highly ambitious project, in much the same way that JFK had used his moonshot announcement in 1961.

Since the 60s, men have flown to space and returned with moon-dusted boots but more than 40 years after Nixon took up arms, millions still die from cancer every year.

A recent Time article neatly compared these presidential bluffs, highlighting Nixon’s naivety:

In 1961, when JFK announced that the U.S. was going to the moon, the idea was no longer science fiction. The physics were understood. What remained was a giant engineering project: apply enough money and aerospace engineers and you eventually get to Neil Armstrong’s giant leap for mankind. When President Richard Nixon announced the war on cancer in 1971, victory wasn’t remotely possible. It was as if someone had announced a moon shot in 1820.

But that was the 60s and half a century is a long time in science. Billions of dollars of investment and years of hard work have allowed us to understand a huge amount about how the machine of cancer works – in the same Time article’s words, ‘the physics of cancer’.

We know what fuel cancer uses and, for the most part, which genes and proteins drive its engine.  This knowledge has helped us understand where we can wedge our spanners in the cancer machine to slow it down, if not quite break it completely. Such progress has seen cancer death rates steadily decline since the mid-1990s.

Though much remains to be done – lung and pancreatic cancers are two examples where survival rates remain particularly low – the punchy rhetoric used by CRUK and others has substance; research will beat cancer.

We should absolutely be proud of these achievements as pure human triumphs. But when we finally elude a disease that has plagued us for as long as we have been on Earth, I think it’s prudent to ask…what happens next? What happens to the masses of ageing cancer-free pre-corpses trundling to bingo in Bognor on free buses? What happens when the average Briton lives to a 100?

Well for one thing, rates of Alzheimer’s Disease will skyrocket.

Currently, one in three people over the age of 65 develop dementia, with Alzheimer’s accounting for the majority of cases. As the over-65 bracket of the UK population swells, the numbers of people living with dementia will grow from 800,000 today to 1.7m by 2050.

Alzheimer’s is an isolating, terrifying and utterly draining condition for carers, relatives and sufferers. The disease stalks around the brain destroying first what makes us human – memory, judgment, and personality – and then what keeps us alive.*  Available drugs can alleviate the symptoms but give no recourse to the neuronal decay that underpins the disease.

The gradual mental and physical deterioration takes an average of 8-10 years from diagnosis to death, with attendant healthcare requirements costing the UK £23bn a year.  Clearly, this figure will spiral as the disease grows more prevalent.

Indeed, so bleak is the current and future picture that when I came across the Guardian headline, ‘Alzheimer’s treatment: landmark study gives hope for simple pill’ I rolled my eyes.  Newspapers regularly inflate health claims to sell themselves, ignoring important caveats to sex up scientific studies.

But this felt different. For one thing, the traditionally staid and conservative research community described the recorded results as ‘very dramatic’, ‘highly encouraging’ and a ‘turning point in the search for medicines to control and prevent Alzheimer’s disease’.  It takes something extraordinary for the men and women in white coats to ditch their comfort blanket of vernacular uncertainty.

This was also a completely new way of approaching the disease. Alzheimer’s is characterized by a build up of mis-shapen proteins that stick together in clumps in the brain.  As these clumps accumulate, nerve cells respond by shutting down their own protein production lines.  If this shutdown** continues for too long, the brain’s nerve cells waste away and die, resulting in loss of mental faculties.

Enormous sums of money have been wasted in attempting to stop neurodegeneration by limiting the initial accumulation of mis-shapen protein clumps.  A series of high profile clinical failures has seen several high profile big pharma companies cut their losses on Alzheimer’s research, viewing the clumps as an insoluble problem***.

In the new approach Professor Giovanna Mallucci and her team ignored the clumps, focusing instead on preventing the shutdown of protein production in nerve cells.  Guided by this theory, Professor Mallucci’s team tested a drug developed by GlaxoSmithKline on mice with prion disease, a neurodegenerative condition that shares many parallels with Alzheimer’s.

Five weeks after treatment, the mice remained free of symptoms such as memory loss, impaired reflexes or limb dragging. They also lived longer than untreated animals with the same disease.  This was big news and I shared the researchers’ excitement.

Of course, huge questions remain, not least how to modify the drug so that it is safe and effective in humans.  False dawns are common in research science and optimism is usually met with suspicion.

But by understanding how to prevent cell death in Alzheimer’s disease, we may just be beginning to understand the physics of the condition.  All that’s left is for us to shoot for the moon.

*Swallowing becomes difficult, meaning that food and drink can enter the lungs and cause infection, leading to pneumonia and death.

**So nearly topical

***Couldn’t resist


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