BRAF BRAF BRAF

So just found out I’m BRAF positive from my clinical nurse specialist this morning. This is very exciting news as the medication I started on my birthday should be working. I am very grateful all the presents I received that day I think you’ll all agree the NHS gave me both the best and the worst (liver biopsy) presents that day. About two minutes after that I was phoned by this media (more on this,if it comes to fruition) so weirdly the first person I told the news was someone I’d never met, she was delighted by the way. I then rang all my family and here we are, the fastest event to blog post yet. 

What does this all mean? Well roughly half of all melanomas have BRAF genes, so first hurdle jumped. The drug I’m taking dabrafenib is a BRAF inhibitor which causes tumours to shrink in about half of the people who have this gene change, and in the other half it suppresses growth. Therefore for me it should firstly prolong my life, secondly reduce my opiate requirement (read reduce the pain) as the liver capsule should become less stretched, reduce the fevers I was having (it appears to have already done this) and settle my cough. The spleen doesn’t really have symptoms associated with it! (See YouTube video what does the spleen do). Tentatively it seems to be doing all this without any side effects, it’s typically s very well tolerated drug despite the long side effects list.

So what is BRAF? It’s a gene that makes a protein called B-Raf which is involved in directing cell growth. Mutations in BRAF can disrupt cell growth and cause cancer by causing uncontrolled replication of cells.

A lot has happened in the 12 years since I was first diagnosed. Vemurafenib (Dabrafenibs older brother) was only FDA approved in 2011 . The treatment prior to this was dacarbazine which only about 10percent of patients responded to treatment and not for very long with a lot more side effects. Unfortunately the melanoma will eventually evolve to overcome the BRAF inhibition after about 12 to 18 months. This has vitally given me time to try the potentially curative (and very often life extending) treatment ipilimumab, a monoclonal antibody, which works by modifying the immune system so it can fight against the melanoma* this was only approved in 2012. The lastly the third line therapy Pembrolizumab another monoclonal antibody works in a similar way to ipi but targets programmed cell death 1 receptor and has been FDA approved in 2014 which again is showing huge promise this is under NICE review. 

I was doing my best to try and keep it simple but to be fair even as a doctor these things aren’t easy to understand. I’ve got no idea what other patients do. As you can see the 12 years between primary and secondaries has given me treatment options, in 2010 I would have had nothing at all let alone NICE approved tried and tested therapies. This goes to show how incredibly vital further cancer research is, the breakthrough in treatments against melanoma, which was such a hard nut to crack, shows the fight against cancer can be won.

*for the scientists this down regulates  CTLA-4 in the melanoma which inhibits cytotoxic T cells from attacking it. Therefore inhibits this inhibition therefore allowing the cytotoxic T lymphocytes to again recognise melanoma cells and destroy them. 

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