Podcast: Red tape, HPV testing, and the latest brain tumour research

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In this month’s podcast we discuss a new prostate cancer drug that has been licensed in the UK and investigate how red tape is hindering European cancer trials.

New research shows that HPV testing could save thousands of women from having unnecessary cancer tests, and we take a look at a new study investigating whether beta-blockers could prevent cancer spread. Plus, should fair-skinned people take vitamin D supplements?

Finally, we say goodbye to Harry Moseley – an amazing 11 year-old who recently lost his fight against brain cancer – and take a look at some of the latest research into brain tumours.

Listen now through the player below:

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Also, the podcast is available on iTunes to subscribe and download for free.

Alternatively, go to the main podcast page on our website, where you can hear the show directly through our own Flash player. And there’s also a full transcript of the podcast available here.

We hope you enjoy it – please do let us know what you think of the podcast in the comments below, or email us at podcast@cancer.org.uk.

Kat

Expert Opinion: Dr Des Powe

Pills
Dr Des Powe wants to find out whether beta blockers could be used to treat cancer.

Can you teach an old drug new tricks? Thanks to a project grant from our Population Research Committee, Dr Des Powe hopes to find out.

Cancer cells have a tendency to spread (or metastasise) to other sites in the body, forming secondary tumours. Once this has happened, the disease can be difficult to treat. In the next in our series of Expert Opinion interviews, Dr Powe discusses his plans to find out whether a common drug could stop cancer in its tracks.

Cancer Research UK: Why are you so interested in breast cancer spread?

Des Powe: Around a third of breast cancer patients develop metastasis but those patients account for 90 per cent of breast cancer-associated deaths. So, if you can stop the cancer spreading in the first place, you could save the majority of those patients from dying and improve their quality of life in the process. And really that’s what my study is about.
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Childish cells with legs provide clues to skin cancer

A picture of malignant melanocytes

Melanoma cells can invade surrounding tissue

As we said in a press release last night, our scientists at the Beatson Institute in Scotland have made an interesting discovery about how skin develops – a discovery that also helps us understand melanoma a bit better too.

The researchers were looking at how immature skin pigment cells, called melanoblasts, move around and find their correct location in the developing skin in mice, before maturing into melanocytes – pigment cells that can develop into melanoma when damaged (for example by UV light).

Melanoblasts, scientists had previosuly discovered, move around by extending long ‘legs’ into the surrounding tissue and literally hauling themselves into the correct position.

The Glasgow team, led by Professor Laura Machesky, found that a gene known as Rac1 was a key player in this process. They also discovered that interfering with Rac1 stopped the melanoblasts from moving around, and prevented mice’s skin from becoming properly pigmented. They’ve published their findings in the journal Developmental Cell.

But how is this relevant to cancer? We’ve tried to sum things up in a handy graphic, which you can see below:

Diagram showing how Rac1 is involved in the spread of melanoblasts

Click to enlarge

Although every cell in our body contains the full complement of 30,000 genes, only a subset are switched on in a given cell at a given point in its life-cycle. Consequently, Rac1 is only switched on at certain times – in this case during melanoblasts’ development.

But cancer cells, with their highly disordered and damaged DNA, seem to switch many of these developmental genes back on. In fact, cancer cells seem to regress back to their ‘childhood’ and start misbehaving.

And there’s a fair amount of evidence that Rac1 is indeed switched on in melanoma cells.

Given that researchers now know that Rac1 is a key player in how early pigment cells move around in the developing skin in mice, this suggests that the gene could be doing a similar job in melanoma cells in humans. More work is needed to find out if this holds true, but if it does then interfering with Rac1 – or other proteins it works with – in cancer cells could be a way to stop melanoma spreading (provided, of course, that this doesn’t  interfere with the body’s day-to-day functioning).

It’s a small step, but science is a series of small steps that often take us in surprising new directions. We’ll be following the Beatson team’s future work with interest.

Henry

Image via Wikimedia Commons


Reference:

  • Li et al: Rac1 drives melanoblast organization during mouse development by orchestrating pseudopod-driven motility and cell cycle progression. Developmental Cell (2011)

Annual Review 2010/11 – Understanding why cancer spreads and why it can come back

Doctors discussing patient results

Around nine out of ten cancer deaths are caused by the disease spreading

In our second highlight from our Annual Review, we talk about our progress towards understanding cancer spread and developing treatments that could stop cancer returning, allowing more people to get the ‘all clear’ once and for all.

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Following up on LOX

Breast cancer cell

LOX can help cancer cells spread

Around two years ago we wrote about research from scientists at The Institute of Cancer Research, partly funded by Cancer Research UK, who discovered that a molecule called LOX (lysyl oxidase) plays an important role in the spread of breast cancer around the body.

Now the same team, led by Dr Janine Erler, has shown that LOX also helps bowel cancer cells to grow and spread. As we covered in our news feed last week, their experiments reveal that LOX exerts its effects by switching on another molecule called Src.

Importantly, a drug already exists that can stop Src in its tracks – dasatinib, which is already used to treat people with leukaemia. These new results suggest that dasatinib could benefit people with advanced bowel cancer whose tumours have high levels of LOX – an idea that would need testing in clinical trials.

It may sometimes seem that stories about advances in cancer research hit the headlines then vanish without trace. In reality, every big discovery is preceded and followed by a huge amount of painstaking research, which gets lost in the media scramble. The latest results from Erler and her team tell another chapter in the story of LOX, and are another small step on the road to beating cancer.

Kat

Further reading:

Reference:
Baker AM et al (2011). The Role of Lysyl Oxidase in SRC-Dependent Proliferation and Metastasis of Colorectal Cancer. Journal of the National Cancer Institute PMID: 21282564

Image courtesy of the Cancer Research UK London Research Institute Electron Microscopy Unit

“Cure for most cancers” story is overplayed and misleading

A man reading a newspaper

Claims of a "cure for most cancers" are over-hyped

Anyone looking at the Daily Express front page yesterday could be forgiven for thinking that a “cure for most cancers” was around the corner, according to the headline. In fact, the story is about very early laboratory research, which shows promise but is a long way from yielding anything that could be given to patients.

The NHS Choices blog has already done a great job of dissecting the scientific truth of the tale from the dramatic headlines, explaining that the story is actually about the discovery of a gene involved in a complex molecular pathway leading to cancer spread.

Over recent decades researchers all over the world have discovered genes that drive the growth and spread of cancer, and this research adds one more to this ever-growing list. But, while these new results aid our understanding of the complexities of cancer and could point towards potential leads for future anti-cancer drugs, the work is still at the laboratory stage.

As we’ve said several times before in response to hyped-up cancer stories in the media, misleading reporting of early-days lab research raises false hopes for patients and their families. Ultimately this leads to a loss of confidence in the genuine progress our researchers – and others around the world – are making.

And according to the head of our Cancer Information Nurses, when stories like this hit the headlines, our nurses have to field calls from distressed cancer patients or their carers asking when they’ll be able to get hold of the ‘wonder drug’ du jour.

Because of the unpredictable and experimental nature of research, it’s almost impossible to guess when (or even if) a lab discovery will translate into a beneficial treatment for patients – especially as scientists all around the world are discovering new cancer-related genes every month.

Paul Nurse and Tim Hunt made their Nobel prize-winning discoveries about cell division back in the early 1980s. We’re only now starting to see drugs based on their findings coming through into early clinical trials.

Unfortunately, “Scientific discovery increases our knowledge of cancer – we hope it might be beneficial in the future in some way” doesn’t make such a great headline.

Kat

Related posts:

Bridging the gap between nerve repair and cancer spread

Schwann cells and nerve cells

Schwann cells play a vital role in repairing damaged nerves - but they also give us clues to how some cancers spread

Imagine you’re in an army convoy, carrying vital information and heading along the road towards a bridge across a deep gorge. But the bridge has been blown out by enemy fire.  So the engineers are called in. They get to work, clearing the debris and slinging ropes across the gorge to act as a ‘guide track’, eventually building a new structure for you to drive across.

You may wonder what this military imagery is doing on a cancer blog, but it’s actually a good metaphor for what happens when the nerves that supply our limbs and organs get damaged, whether by injury or surgery.

Cut nerves can regrow across short distances – like the damaged bridge being rebuilt across the gorge – but this process only seems to happen after specialist ‘engineer’ cells, called Schwann cells, lay down molecular ‘guide tracks’.

Professor Alison Lloyd and her team at University College London recently uncovered the molecular signals that guide this repair process. And their findings could have implications for our understanding of how some tumours  - such as neurofibroma – may spread through the nervous system.

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