Every single person with cancer has an individual experience and a story to tell but, statistically speaking, one is not enough. In order to study the impact of cancer, and measure improvements in treatment and survival, researchers need to collect information from as many people as possible.
Conventional wisdom says that if you put a good kid in a bad school full of troublemakers, the chances are they’ll make mischief. Put a bad kid in a school of little angels, and they’ll be more likely to toe the line and behave. Before you start thinking that this has become a child psychology blog, rest assured that it’s actually a metaphor for cancer.
For years, researchers have been investigating the ‘tumour microenvironment’ – the cells, signals and biological cues that immediately surround cancer cells. These can have a powerful impact on tumours, either encouraging them to grow aggressively – the good kid gone bad – or keeping them under control, like the reformed ruffian.
This is particularly important for metastasis – the process by which cancer spreads. Cells break away from the original (primary) tumour and travel through the bloodstream, setting up home elsewhere in the body to form secondary cancers. It’s usually these secondary cancers that actually end up being a major problem, and often lead to death as they are difficult to treat effectively.
To continue the analogy, if the travelling cells settle in a ‘good school’, they might never grow into tumours. But if they end up in a bad microenvironment, then trouble can start.
Now Robert Weinberg and his team at MIT have made a discovery that adds an extra twist to this situation – primary cancers can send signals around the body, ‘activating’ the growth of secondary tumours at a distance. Their results are published in this week’s edition of the journal Cell.
While oestrogen is best known as a female sex hormone, men produce it too – albeit in lower amounts. And there’s emerging evidence that oestrogen might be involved in the growth of prostate cancer – particularly fast-growing, aggressive prostate cancers.
As we wrote in February, there are some pretty big gaps in our knowledge about this disease – particularly what causes it, who’s most likely to get it, and, importantly, why some prostate cancers grow much faster than others.
A lot of previous research has focused on ‘androgens’ – male sex hormones like testosterone. And these certainly fuel prostate cancer growth. So prostate cancer is often treated by blocking their action, although tumours frequently become resistant to this treatment.
But there’s a growing stack of circumstantial evidence that oestrogen is also involved.
Just a quick one. We’ve written before about the links between inflammation and cancer, and couched a lot of what we’ve written in all sorts of caveats like ‘may’ and ‘might’.
Well, last week, a few more of those caveats fell away, and the picture became just a little bit clearer.
In the June podcast we find out how one of our scientists switched sides, becoming a ‘human guinea pig’ on a clinical trial for prostate cancer. We investigate the online support available for people affected by cancer, and pound the park to hear the stories of the women running Race for Life.
Simply visit the podcast homepage and click on the player to hear the show. Or click on the player below: