Tuesday, August 18, 2009
Type 1 and Type 2 Diabetes treatments: Conventional and the Alternative
Immune drug linked to cancer
Saturday, August 15, 2009
James Watson and winning the war on cancer
James Watson and winning the war on cancer
Picture: Edmond Terakopian/PA
To celebrate the 40th anniversary of the Moon landings, The Times last month cast around for a project that would be a worthy contemporary successor to the Apollo programme: a great scientific initiative that might be achievable, given the right support, on a decade-long timescale like the one President Kennedy set out back in 1961.
Our chosen target, set out in a leading article, was cancer. While the challenge of curing the "big C" in all its forms may well be too great, there is a very real prospect that its treatment could be comprehensively transformed within 10 years. As the leader put it:
"We may soon come to see this dread disease largely as a manageable and chronic condition. Within ten years or so, many scientists believe it could become more usual to die with cancer than of it."
The Times is in good company: no less a figure than James Watson, the co-discoverer of the double-helix structure of DNA,has this week also described beating cancer as a "realistic ambition", in an op-ed for the New York Times. The reason Watson cites is the same one highlighted by the Times leader: "at long last, we largely know its true genetic and chemical characteristics," he said.
As the excellent PolITigenomics blog points out, some of Watson's reasoning about the best way forward is a little confused. He seems, for example, to call at once for the US National Cancer Institute to focus more on basic research, and for accelerated patient trials of new drugs. But the timing of his intervention is interesting, for it coincided almost to the day with the publication of just the sort of study that is promising to drive a cancer revolution.
In this new research, published in the New England Journal of Medicine, a team led by Elaine Mardis, of Washington University in St Louis, has sequenced the entire genetic code both of cancerous cells from a patient with acute myeloid leukaemia, and of his healthy tissue. A comparison between the two revealed about 750 genetic mutations that have occurred in the cancerous cells.
Most of these mutations will be passenger mutations, symptoms of the disease rather than causes, if you like. The team, however, picked out 64 mutations that were more likely to be causal because of their position in the genome for further study, and looked for them in 187 samples of cancer cells from other leukaemia patients. One mutation, in a gene named IDH1, showed up in 16 per cent of these samples. It is highly likely to be a "driver mutation" -- one of the genetic errors that can actually cause leukaemia.
A more detailed summary of the paper is available atMassGenomics, a blog written by Daniel Koboldt, a member of the Mardis team. A commentary on the findings by James Downing, of St Jude's Children's Research Hospital in Memphis, Tennessee, also sums up nicely what such research means for medicine.
The results are significant because they represent a step towards the great goal of contemporary cancer genomics: to identify the precise mutations that drive the many different types of tumour, for clues to diagnosis and treatment.
Armed with this knowledge, it should eventually be possible to determine, by sequencing cells from a patient's cancer, how aggressive it is likely to be, and what will be the most effective approach to treatment. Such genomic insights will also identify new targets for medical research, bringing new drugs that are designed with the genomic architecture of particular tumours in mind.
It is studies of this sort that mean the war on cancer might plausibly be won.
POSTED BY MARK HENDE