Prostate cancer cells. Prostate cancer cells
Another day, and another round of headlines this morning from the NCRI Cancer Conference.
— Cancer Research UK (@CR_UK) November 8, 2016
Now on to our highlights from Day 3 of the conference.
Personalising prostate cancer treatment
The way prostate cancer cells look under a microscope, or the molecules they release, often decides which treatment a patient receives. But what if genetics could help too?
Dr Robert Bristow, from the Ontario Cancer Institute in Canada, and his team have read the complete genetic code of tumours from 500 patients with prostate cancer. And they’ve found big differences in the types of genetic faults the tumours have.
Patients with the greatest amount of genetic faults were the ones for whom treatment failed.
“For every 1% increase in genetic instability we calculated a 5-6% increase in treatment failure,” said Bristow.
His team aims to one day use distinct genetic ‘fingerprints’ to predict if a treatment is likely to fail, so that doctors can switch to an alternative, or potentially offer patients a spot on a clinical trial.
Fascinating talk by Rob Bristow establishing genomic instability as a strong indicator of patient prognosis in prostate cancer #NCRI2016
— Matthew Davies (@matthewndavies) November 8, 2016
The ambition to personalise prostate cancer treatment is one that is shared by Professor Johann de Bono, a heavyweight in the field from The Institute of Cancer Research in London.
And one area he has set his sights on is immunotherapy.
Following promising early work in the US on bowel cancer, de Bono and his team are testing whether prostate tumours carrying large amounts of damage in their DNA will respond to the immunotherapy drug pembrolizumab (Keytruda).
So far the team has analysed the genetic details of over 200 prostate cancer samples. And they’ve found that 5-10% of advanced prostate cancers display a hallmark of genetic damage that is linked to cells failing to repair particular faults in their DNA.
These samples also seem to be flooded with immune cells, suggesting that immunotherapy drugs, which release the ‘brakes’ on immune cells, might be a promising approach to treatment.
“This is going to exercise us,” said de Bono as he described the challenge of understanding these data and personalising treatment. And it’s still very early days.
But he said the approach would be a key part of improving the outlook for patients with advanced prostate cancer in the next 10 years.
The journey to a new treatment
How long does it takes to go from a discovery in the lab to treating a patient?
It turns out the average is about 15 years.
And that’s extremely frustrating when researchers have something in their hands that they think could help people, but there are many obstacles in the way. Obstacles like funding, staffing, regulatory approval, and costs.
These are challenges that face all kinds of treatment or technology, whether it’s a new imaging technique or surgical approach, like the iKnife.
Showcased by Cancer Research UK-funded surgeon David Phelps, the iKnife can tell apart cancerous and non-cancerous cells during surgery in a matter of seconds.
This could help surgeons decide what to remove without having to wait for test results to come back from the lab, potentially sparing healthy tissue and making the surgery more accurate.
Understandably, the audience was very excited about this new bit of tech:
A new technology – the iKnife – can tell surgeons whether they're cutting through normal or tumour tissue. Amazing! #NCRI2016
— Emma Saxon (@EmmaBSaxon) November 8, 2016
— Emlyn Samuel (@emlyn_samuel) November 8, 2016
So why isn’t it being used in operating theatres right now?
The issue is that it still has to follow the same kinds of approval hurdles drugs do – clinical trials, licensing, cost-benefit analysis, which all take time.
And they are imposed for a reason – to make sure the new exciting tech is safe, effective and worth NHS funding. How to balance speed and safety is a lingering issue, with no clear answers.
In the same way giraffes have evolved long necks to reach their food, cancers also adapt and change to their environment.
Professor Paul Workman, from The Institute of Cancer Research in London, explained that understanding a tumour’s ‘evolutionary tree’ could help stop it becoming resistance to treatment.
“Historically we’ve just tried to simply kill the cancer cells, and this has helped us double cancer survival,” Workman explained. “But drug resistance remains a challenge and the question is: how do we do better?”
Targeting the genes that help tumours survive may be the answer. And Workman believes scientists “are only scratching the surface of the genes with the most potential”.
Another option could be to target the way that tumours evolve.
Kanu has found that in breast cancers that produce excess amounts of a molecule called HER2, which can become resistant to treatment, there was more APOBEC3 inside the cells.
And Kanu believes that targeting APOBEC3 might one day help delay, or even stop, these tumours becoming resistant to treatment.
This same approach was backed up by another session on how tumours evolve.
“If you’re targeting a cancer’s ability to evolve, you have to know what you’re targeting. You have to know the players,” said Professor Reuben Harris, from the University of Minnesota in the US.
In a thought provoking presentation Professor David Currow, from Flinders University in Australia, discussed how research and cancer care is failing miserably when it comes to controlling symptoms like pain, nausea and delirium in patients with advanced cancer.
And the main reason is a lack evidence around what does and doesn’t work.
Prof Currow: Research not taken into practice. Patient-centred care, meaningful outcomes, intellectual honesty needed #NCRI2016
— Michelle Chen (@mich_chen) November 8, 2016
“At the moment it’s an evidence-free zone when it comes to something that affects our patients on a day-to-day basis,” said Currow. “We need the same level of evidence for managing symptom control as for treatment.”
And when this evidence does emerge, he said, it’s important that it’s taken on board by those in the medical profession. Because according to Currow: “The response we get from doctors is ‘don’t take my medicine away’. But we need to retire old favourites that have had their day if the evidence shows they don’t work.”
David Currow passionately arugues for better uptake of evidence to help palliative symptom control, to avoid failing pts further #NCRI2016
— Richard Berks (@DrRichardBerks) November 8, 2016
He also highlighted that healthcare professionals need to start taking more responsibility for how patients’ symptoms are managed. “We assume someone else will take care of this – a GP, a nurse, the oncologist. But no-one is. We need to rethink symptom control as being the responsibility of everyone who’s involved.”
— Sam H Ahmedzai (@Samhja) November 8, 2016
In his closing remarks, Currow encouraged everyone to do the ‘Grandfather test’. “If your Grandfather had uncontrolled vomiting for 6 weeks before treatment, would that be acceptable to you and your family?”
“The treatments we have today aren’t delivering the symptom control we’d like. This is untenable in a resource rich country in 2016”.
Tackling muscle wasting
One of the final sessions of the day raised a tough topic, both for research and for people experiencing cancer: when your loved one may refuse to eat.
8 in 10 patients with advanced cancer have a condition called cachexia, with 2 in 10 cancer deaths occurring due to its devastating effects.
Science defines the condition as weight loss greater than 5%. But Debbie, who cared for her friend John who died from a soft tissue sarcoma this year, ended Tuesday’s session at the conference with a sobering thought.
“The definition fails to describe the loss of identity, of self, of kinship and dignity. It’s a very lonely place, dying. Cachexia is an announcement that time is running out”.
But data presented at the session also show promise in understanding this condition. And the focus, surprisingly, doesn’t concern fat, but muscle.
Investigating what happens in the muscle of people with cachexia may help scientists solve this problem. For example, making drugs that block myostatin, a molecule that prevents muscle cells forming, was presented as a very promising approach for the future.
— Katie Goates (@KatGoat) November 8, 2016
And finally, Professor David Currow was back on stage stressing the need to change the way doctors think about this condition once treatments become available. “It’s not just about the body but also the psychological impact it has on families,” he said. “It is a constant reminder to people of changes with a very poor outcome.”
Talks this afternoon confirmed cachexia must become a condition that doctors can treat. And it’s reassuring to know that research into cachexia is happening, to improve the quality of life of those with cancer – and their loved ones who care for them.
That’s it for today. Check back tomorrow for our final roundup.
The Cancer Research UK news team