Whose side are you on?

Writing this blog – intended to be on current cancer-related topics – has been very good for me, if no one else, because it makes me read things I wouldn’t otherwise bother with. So I’m wiser than I would have been – but here’s a shocking admission: I’m becoming increasingly sympathetic to those who wish that scientists would just go away – or at least shut up sometimes. Of course I’m being jolly unfair: it’s not so much fellow boffins I’m miffed with as the ‘media’ – the BBC and the leading newspapers. They’re the ones who bring ‘stuff’ to my attention. Do you think I spend my time reading a journal called Alcohol and Alcoholism?!

Thanks to the medja, in just the last couple of weeks I’ve read that women’s height is linked to ovarian cancer  (BBC), breast cancer screening results in ‘unnecessary treatment’ (Telegraph), and a glass of wine carries a breast cancer warning (The Independent), – oh, and I should take an take an aspirin a day to cut cancer risk (Guardian). Just a month or two ago there was a similar stampede of ‘beef is bad’. This week the University of Gothenburg weighed in by discovering that some people are so ‘addicted’ to Facebook that they open it the moment they switch on their computers! And getting hooked (to Facebook, that is) makes women unhappy. Thank heavens they didn’t get round to emails or prostate cancer in Gothenburg or I might be needing something stronger than aspirin for my depression.

If you’d looked at all these important scientific surveys you’d have spotted that they have one thing in common: they never mention fun. Not one of them. Ever. Not a smile, nary a joyous feeling – and as for anything orgasmic …

Salvation is at hand

The good news is that some relieving guidance has popped up in the midst of all this ‘thou shalt not’, ‘it’s too late’ and ‘now look what you’ve done’. The absolutely astonishing thing is its source – ‘provenance’ as the antiques freaks like to put it. You aren’t going to believe this but it’s to the good old Church of England that we turn in the shape of a vicar from Hove (go on then …). This blessed man has revealed that not only is it a ‘good thing’ but it’s almost a moral duty, perhaps even a religious obligation, to spend Easter Sunday in bed, eating chocolate and having sex – and, by implication, doing anything else that feels as though it should be in the ‘naughty but nice’ statistical bracket. Well – who would have thought you’d read it here – praise be for the C of E!            Photograph by Hemera/Thinkstock

Here comes another of them scientists

Having let the grumpies have their say, shall we do as we preach and have a balanced, non-inflammatory comment on behalf of beleaguered boffins? Oh alright. Should the studies I listed have been done? Yes (apart from the Scandi one, obviously). They’re by excellent groups and they add another brick to the wall, even if it’s only reaffirming what we knew. The ovarian/height link paper makes a good case by pointing out that the evidence so far published on whether height, weight and body mass index (BMI) have any link with the risk of getting ovarian cancer has not given a very clear picture. They were thus prompted to put together 47 of these studies (a meta analysis) – and what emerged was that the risk increases with height and, for women who have never used hormone therapy, with BMI. However, the important point is that although the increases are statistically significant, they are very small. My colleague Paul Pharoah has helpfully estimated that they show that being 5ft 6in rather than 5ft tall raises the lifetime risk of ovarian cancer from about 16 in 1000 to 20 in 1000.

So these reports are good, though not seismic, stuff. And yes, it’s great that the media pick up on what science produces and bring it to the attention of the wider world. It would just be nice if they were less keen on eye-catching, doomy, headlines. How about taking a lead from The Sun, an organ not previously mentioned in this column, that headlined the C of E story with Easter Sinday. What might they do? Aspirin v. Expirin? I came up with a cracker for the ovarian study but a problem with talking and writing about cancer is the ease with which jokes (mine anyway!) teeter into what some would consider to be the realms of bad taste. So a green light for The Sun then!

Final thought for the day: am I now (1) religiously taking aspirin OR (2) opting for Nick the Vic’s life support strategy? I think you know the answer to that one.

References

Collaborative Group on Epidemiological Studies of Ovarian Cancer (2012) Ovarian Cancer and Body Size: Individual Participant Meta-Analysis Including 25,157 Women with Ovarian Cancer from 47 Epidemiological Studies. PLoS Med 9(4): e1001200. doi:10.1371/journal.pmed.1001200

Kalager, M., Adami, H.O., Bretthauer, M. and Tamimi, R.M. (2012). Overdiagnosis of Invasive Breast Cancer Due to 491 Mammography Screening: Results From the Norwegian Screening Program. Annals of Internal Medicine 156, 491-499.

Rothwell, P.M., Wilson, M., Price. J.F., Belch, J.F.F., Meade, T.W. and Mehta, Z. (2012). Effect of daily aspirin on risk of cancer metastasis: a study of incident cancers during randomised controlled trials. The Lancet, Early Online Publication, 21 March 2012 doi:10.1016/S0140-6736(12)60209-8Cite or Link Using DOI

Advertisements

Isn’t Science Wonderful? Obesity Talks to Cancer

A couple of week’s ago we looked at how being obese can give cancer a helping hand. I thought this would be useful as most people know there is a link but perhaps not much more than that. The message had two simple parts: (1) When we make extra fat cells they change the metabolism of our bodies through chemical signals that wander around and, in passing, can also drive cancer growth, and (2) Some of the extra fat cells congregate around tumours and give them direct positive vibes (i.e. other, local chemical signals).

But you may have spotted that I didn’t actually say what these ‘signals’ are – for the very good reason that we know rather little about them. Step forward, right on cue, Ines Barone, Suzanne Fuqua and friends from the University of Calabria and Baylor College of Medicine, Houston with a wonderful paper that’s just been published. Wonderful because it’s got so much data I’m green with envy but also because, like most excellent science papers, the key message is simple: normal cells that have moved into the neighbourhood can indeed talk directly to tumour cells. And the messenger is … leptin!

That’s astonishing. Even those with only a smattering of knowledge about how we work will know that leptin plays a key role in regulating energy balance. It’s a protein – a hormone – that circulates in our blood at levels roughly proportional to body fat. Its job is to signal the ‘full’ state, i.e. to reduce appetite. Somewhat perversely, obesity usually causes abnormally high leptin levels but it doesn’t work very well because the body has become resistant to its signal – much as happens with insulin in type 2 diabetes.

The new results show that leptin, released from nearby cells, can bind to cancer cells and make them do two things: (1) Release a chemical that tells the adjacent cells to send out even more leptin, and (2) Make proteins that help the tumour cells grow and invade.

There are a few wrinkles to these results. The study was on breast cancer cells with a particular mutation (in a receptor for the hormone estrogen) and the ‘groupies’ providing the leptin turned out not to be fat cells but fibroblasts – part of the supportive framework of cells and tissues – so they’re ‘cancer-associated fibroblasts’ (CAFs). And when the CAFs release leptin it floods out and the tumour cells embrace it and make yet more receptors for leptin to bind to on their surface.

But these details matter less than the key point: for at least some types of cancer cell a hormone often made in excessive amounts in obesity can signal directly to tumour cells, telling them to grow and spread. This doesn’t mean that all breast tumours, yet alone all cancers, respond to leptin. What it does show is that a key factor in obesity can talk directly to some types of tumour cell. It’s another example of the painstaking way in which science usually proceeds and, assuming the results are reproducible, we have one more little bit of the jig-saw.

Reference

Barone, I., Catalano, S., Gelsomino, L. et al. (2012). Leptin Mediates Tumor−Stromal Interactions That Promote the Invasive Growth of Breast Cancer Cells. Cancer Research 72, 1416-1427.