There were dramatic headlines in the papers this week claiming a “Breast cancer breakthrough”, with “Scientists ‘close to breast cancer cure’” or even “Two years from developing ‘potential cure’ for breast cancer”.
It almost seems too good to be true – and it is. The headlines have come from a scientific paper describing laboratory-based research that is still a long way from the clinic, published in the journal Proceedings of the National Academy of Sciences.
There’s no doubt that the findings in the paper are interesting and potentially important, but we feel that headlines touting that “millions of lives could be saved” by an imminent “cure for breast cancer” are excessive and give false hope to patients and their families.
This research isn’t about clinical trials of new drugs, or even about the development and testing of a new drug – it looks at fundamental cancer biology – the sort of foundations that such future developments are eventually built on.
In their paper, the researchers studied tiny molecules called microRNAs (miRNAs – for more background see this previous post), which help to control the activity levels of genes within cells. They discovered that particular miRNAs can, under certain conditions, switch off the oestrogen receptor, a key player in the development of breast cancer. And, in turn, shutting down the oestrogen receptor also shuts down production of the miRNAs themselves – the sort of feedback loop that’s quite common in biological systems.
This research helps us to understand more about the complex molecular circuitry inside our cells, and about some of the molecules we could try to target in order to develop new treatments.
But it’s not yet a treatment for breast cancer – as we’ll see.
MicroRNAs – small but powerful
We’ve blogged before about one of cancer research’s hottest topics, miRNAs – tiny molecules that help to ‘fine tune’ gene activity.
In recent years, scientists have begun to understand that miRNAs are made from much smaller fragments of longer RNA ‘precursor’molecules. Dr Justin Stebbing at Imperial College, London, has been studying how miRNAs are made from these precursors, and how this process is affected in cancer.
The oestrogen receptor and breast cancer
In some women, the female sex hormone oestrogen fuels the growth of their breast cancer – explaining why hormone-blocking drugs like tamoxifen and anastrozole are often effective at treating the disease. Oestrogen works by attaching to a molecule within cells called the oestrogen receptor. Together, the hormone and its receptor travel into the cell’s nucleus switching on various genes, telling cells to multiply.
The researchers discovered that the oestrogen receptor switches on the production of certain miRNAs – tiny stretches of a molecule called RNA (see our previous post for more info). In turn, these miRNAs can switch off production of the oestrogen receptor.
In healthy cells, this helps to ensure that cells don’t over-respond to oestrogen – once the message has got through, the receptor is switched off – a bit like hanging up the phone at the end of a phone call. But in cancer cells, the receiver doesn’t get hung up, the message keeps getting repeated, and the cells multiply out of control in response to the hormone.
The scientists investigated this in more detail, and found that although the oestrogen receptor was switching on production of precursor miRNAs in breast cancer cells, for some reason, they weren’t being properly processed into functional miRNAs – so they couldn’t ’hang up the receiver’ and stop the cells from dividing. A very interesting finding, but it’s not close to being a treatment for patients yet.
What does it mean?
Dr Stebbing’s results help to unravel the complex communications circuits within cells that controls the activity of our genes, and helps to explain how this goes wrong in cancer. Now we know more about this, we can start to look for potential treatments.
One speculative idea might be to add extra processed miRNAs to breast cancer cells, to switch off the oestrogen receptor so the cells stop growing – but this needs to be explored in further experiments.
Will it lead to a “cure for cancer”?
These results come from experiments on cells grown in the lab, and on samples from breast tumours. Although there are a few miRNA-based treatments in early clinical trials, this research is nowhere near being a widely-available treatment, and to suggest otherwise is to raise false hopes.
Some of the news reports suggest that drugs based on the discovery “should be available within a couple of years” (hence the dramatic headlines). Given the pace of scientific research, this is over-optimistic. And predicting when discoveries will be made – and when treatments will become generally available – is like trying to guess the length of a ball of very tangled string.
If all goes well, there could perhaps be an experimental treatment based on this research in pre-clinical development within a few years, before going into early-stage, small-scale clinical trials. Further large-scale trials would take even longer.
As an example, the discovery of the prostate cancer drug abiraterone was first made in 1995, yet despite the success of smaller studies we are still waiting for the results of large-scale trials.
Ensuring that cancer treatments are safe and effective is not something that can be rushed, because the stakes are too high. And the results of early, exploratory laboratory research should be communicated with care and context, lest we raise expectations too far in today’s patients and their families.
- The NHS Choices blog has covered the science behind this story in more detail.
- The drug abiraterone, mentioned in this post, was made available across the UK on the NHS for men with advanced prostate cancer in 2012.
Castellano, L. et al (2009). The estrogen receptor- -induced microRNA signature regulates itself and its transcriptional response Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0906947106
Bobby Blackwell June 8, 2011
I hope this is true, if it is not, then I wish those who are making out these stories will stop raising the hopes of those who wants to achieve this through false promises.