Lung cancer is the world’s biggest cancer killer and one of the poorly-understood
of cancers.
Luckily, researchers at
UCL and University College London Hospital NHS Foundation Trust are now unlocking the secrets of lung cancer, tracking in real time how lung tumours
develop and evolve as patients receive treatment.
This is one of the largest
ever studies of lung cancer patients globally and over nine years it will
examine exactly how lung cancers mutate, adapt and become resistant to
treatments. The study, called TRACERx (Tracking Cancer Evolution through
Therapy), recruited 850 lung
cancer patients from across the UK and took samples of their tumour before and
following surgery and subsequently if the disease recurs.
Professor Charles
Swanton, lead researcher at the UCL Cancer Institute, said: “Success in
treating lung cancer has been difficult to achieve but we’re hoping to change
that. The first step to improving cancer diagnosis and treatment is to
understand more about the disease and how it changes over time."
The study collected a series of tumours from patients with early stage
lung cancer who had had surgery aimed at curing them and then analysed and
compared DNA from several different regions of each tumour.
It was found that tobacco causes specific types of damage to DNA.
The tumour showed all the characteristic diversity and chaos as seen in
other cancer types – on average, about 70 per cent of a tumour’s DNA errors
were found throughout the whole tumour. The rest being unique to one region or
another. This implied that the tumour’s early life was relatively homogenous,
with a late explosion of diversity. And they saw the tell-tale faults known as
‘C-to-A’ changes, caused by tobacco carcinogens. The C-to-A changes were much
more likely to be early, common errors than to be unique faults confined to
specific regions of each tumour. These late-occurring mutations seemed to be
caused by DNA-editing proteins called APOBEC proteins. APOBEC proteins turn out
to be one of the most important DNA damaging forces in a range of cancers.
It looked like the cancer-fuelling ‘driver’ mutations in genes tended to occur early in a lung cancer’s
development.
This contrasts with kidney cancer, where similar mutations tended to
occur relatively late on. This is good news, as it suggests that the so-called
targeted therapies might be more effective in lung cancer, particularly if used
in combination.
Moreover, it is more evidence that lung
cancers take a very long time to develop – maybe more than twenty years.
And so it might be possible to detect early signs of the disease in the blood
long before symptoms develop – something that could make an enormous difference
to patient outcomes, as Professor Jacqui Shaw of Leicester University, who
studies circulating tumour DNA in breast cancer, explains:
“A growing tumour can shed its DNA into a patient’s blood as its cells
die,” she says.
“At the moment, we don’t know enough about whether early lung tumours shed
DNA into the bloodstream, but it is certainly an idea that’s got a huge amount
of potential, and one we’re eager to explore.”
A reliable method of detecting lung cancer early could prevent countless
thousands of premature deaths. Now, only 14 in every hundred patients diagnosed
with late-stage lung cancer survive for five or more years. For early-stage
disease, that goes up to 71 in a hundred.
Currently, around 42,000
people are diagnosed with lung cancer in the UK every year, with around 35,000
deaths from the disease.
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