- Hampstead Heath Walk
- Professor Mo Keshtgar speaks at our Patient Support Group
- Study has found a way to stop cancer-causing collisions in cells
Hampstead Heath Walk
Our annual walk takes place on Sunday 8th June and, if you are still to register, we would love you to join us. Participants can chose to walk or run either 5km or 10km and everyone who attends will receive refreshments and a free Cancerkin t-shirt. The walk is always a fun day out – the emphasis is on our patients, supporters and their families walking and having fun together – and so, to abuse a cliché, the more really is the merrier! All the money raised will go directly to Cancerkin to help us to continue to provide free complementary therapies and support services across London.
To take part, simply fill out the form attached to this email and return it to firstname.lastname@example.org or call us on 0207 820 2323. Alternatively, walkers can also register on the day. For more information, please contact me on either the email or telephone number above.
We look forward to seeing you there!
Professor Mo Keshtgar speaks at our Patient Support Group
We were very privileged to be joined by Professor Mo Keshtgar, whose spoke about ‘Cancer Diagnosis and Treatment: Past, Present and the Future’. Prof Keshtgar began with some statistics about the rise in the incidence of breast cancer worldwide in the last 30 years and, thanks to advances in treatment over that period, its low mortality rate relative to other cancers. He then discussed a number of different research projects which he is involved in. They were fascinating in their variety and potential. He placed much emphasis on the importance of patient involvement, especially in research aimed at helping patients understand better the options available to them, as well as the lifestyle implications of breast cancer. This led to a lively question and answer session which itself demonstrated the great hunger there is for information and advice – particularly on lifestyle issues. We are very grateful to Prof Keshtgar for this most interesting and stimulating – and hopeful – discussion, which was accessible to everyone who attended. We are also grateful to him for his continuing support to Cancerkin, especially at our annual fundraising walk.
Study has found a way to stop cancer-causing collisions in cells
A study published in the journal Cell has found a new role for a protein: stopping cancer-causing collisions in cells by preventing DNA from snapping.
Scientists from the Cancer Research UK London Research Institute discovered that if a protein, called RNA polymerase II, stops while travelling along DNA it can lead to catastrophic collisions with another protein, DNA polymerase. When these two proteins collide on a long gene – like a stationary car being hit by an oncoming lorry on a fast road – it can cause catastrophic damage to the DNA by breaking it, which may eventually lead to the cell becoming cancerous.
However, the study shows that a third protein, RECQL5, can attach to RNA polymerase II and act as “a brake” as it travels along DNA, slowing it down so it runs more smoothly and is less likely to stop. The scientists also found that RECQL5 also appears to help RNA polymerase II start moving again when it does stop, although more work needs to be carried out to understand exactly how it does this.
The study has also found that these RNA polymerase II “breakdowns” are take place more often on parts of our chromosomes called common fragile sites – naturally occurring weak points which are more likely to break when exposed to events like the DNA – RNA polymerase II collision. The DNA in all cells have common fragile sites and under normal circumstances they are relatively stable and don’t break often. However, in cancers, common fragile sites are frequently broken or damaged. The researchers therefore now believe that by preventing DNA – RNA polymerase II collisions on these common fragile sites, RECQL5 could play an important role in protecting our cells from becoming cancerous.
Study Author, Dr Jesper Svejstrup, said: “We’ve known for some time that cells that have lost the protein RECQL5 are more likely to become cancerous, but until now, we’ve not been sure why this is.
“Our latest study shows that RECQL5 plays a vital role in moderating RNA polymerase II speed and ensuring stable progress across genes, which appears to reduce the number of collisions it makes with oncoming DNA polymerase proteins on long genes.
“Knowing more about this weakness in some cells could open up exciting new possibilities for targeting cancers with this mistake.”