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Sunday, 15 July 2012

Another Tiny Piece in the Cancer Jigsaw

Most cancers kill by spreading to other organs. Breast cancer, for instance, if it stayed at the original site, would cause a nasty ulcer, but this would not cause death. Surgery could cure every case. The problem comes when it seeds secondaries in places like the lungs or liver, co-opts the blood supply and eventually prevents an essential organ from doing its job. Result - another cancer death. Not surprising then that one branch of cancer research is trying to find out how this process takes place. How do those marauding cells break away and travel to far-flung parts of the body?
Surgery, radiotherapy and chemotherapy are a bit like tackling an overgrown garden - you can slash the weeds down, burn them off or spray them with weedkiller. Trouble is that you might also destroy attractive plants and helpful creatures in the process. These combined methods have saved many lives, including mine, but we all know that they are far from ideal and can cause a fair bit of collateral damage to healthy tissues.
So research these days delves into the most detailed, molecular level. Until you know the exact molecular interactions, you can't devise a treatment that could halt the progress of cancer in a focussed way, with limited side effects.  
A team in Germany has just made progress in this area. They have discovered that some cancer cells use an immune system chemical to break through artery walls and gain access to the body's high-speed transport system - the blood.
There are many of these immune chemicals, known as chemokines or cytokines. Together they form a complex communication system that allows our millions of immune cells to communicate with the other cells in the body. When the immune system sets up an area of inflammation, some of these chemicals act on the walls of blood vessels, opening up gaps and allowing immune cells to move out of the blood and attack bacteria in the surrounding tissues. Normally blood vessels will allow simple molecules to pass through them, but not relatively huge objects like cells. During inflammation however, some of the body's largest cells can travel out of the blood system and into the tissues.
It seems that some cancer cells use this mechanism in reverse, using a specific immune chemical, opening up holes in nearby blood vessels and creating a route into the blood.
Painstaking research like this opens up the possibility of blocking the action of such chemicals and so outwitting more and more cancers.
Wolf et al. Endothelial CCR2 Signaling Induced by Colon Carcinoma Cells Enables Extravasation via the JAK2-Stat5 and p38MAPK Pathway. Cancer Cell, 2012; 22 (1): 

Sunday, 8 July 2012

Could flu be stopped in its tracks?

During a 'flu epidemic vaccination helps. It reduces the pool of susceptible individuals and reduces infection rates in groups most likely to need hospital treatment. The big limitation is that it does not work very quickly. It takes the adaptive division of the immune system a week or two to respond to the vaccine and by that time someone could have contracted flu and become seriously ill. So it would be very handy if there were some means of protecting those who have been exposed to the disease - family members, carers, patients in hospital wards and residents in residential settings spring to mind. Not to mention people with weakened immune systems who may be vulnerable to both 'flu and secondary infections.
The other limitation is that flu vaccines are currently strain-specific. When swine flu started to spread in 2009 it took months before an effective vaccine was in full production. Too late to nip the pandemic in the bud. Too late to prevent some quarter of a million deaths, worldwide. These numbers are far higher than original estimates according to a recent analysis published in The Lancet Infectious Diseases last month
Exciting then, that an American research team have identified a protein that, when administered to mice that had just been deliberately infected with 'flu virus, seems to have a significantly protective effect. It works by stimulating the innate division of the immune system into action - something that is slow to happen in normal 'flu infection. Furthermore this protein is already approved for use in humans, as an immune-stimulating adjuvant in vaccines. This means that translating the research into human trials will be easier than if it was an untried substance. One of the benefits might be that it is generic, rather than strain-specific, which could be a real life saver next time a new pandemic strain emerges.
This would be an unusual treatment - something that truly "boosts" part of the immune system - as opposed to a wide range of ineffective vitamins, potions and herbs.
Sam D. Sanderson, Marilyn L. Thoman, Kornelia Kis, Elizabeth L. Virts, Edgar B. Herrera, Stephanie Widmann, Homero Sepulveda, Joy A. Phillips. Innate Immune Induction and Influenza Protection Elicited by a Response-Selective Agonist of Human C5a. PLoS ONE, 2012; 7 (7):