A swap results in the fusion of genes BCR and ABL (hence the hybrid gene BCR-ABL) which codes for a protein that functions like an ‘on' switch which cannot be turned 'off'. In other words, your cells don't respond to the body's signal to stop growing and this leads to a vast increase in your number of white blood cells. Not only are there far too many white blood cells, but these white blood cells are immature and are thus incapable of doing their jobs. This increases your risk of infection, means you are not getting enough oxygen around your body and you cannot stop bleeding properly, potentially making it a very serious disease to have to battle. Your spleen is also likely to become very large, contributing to the symptoms.
CML typically progresses slowly.
Over time the cells grow more uncontrollably and the disease can pass through distinct phases. When it's not progressing very fast, we call it chronic phase when there may be minimal or no signs and symptoms of illness. It can eventually lead to accelerated phase where symptoms progress faster, and finally to blast crisis which is an equivalent of an extremely advanced leukemia.
Thankfully, modern medicine has seen the most amazing advances with regards to CML therapy. This is all thanks to the development of drugs known as tyrosine kinase inhibitors (TKIs) which are able to switch off the harmful BCR-ABL protein by blocking the 'on' switch and enabling those suffering with CML to live a full and rewarding life.
To put it in simple terms, CML highlights how a relatively minor genetic defect can lead to an uncontrolled cellular malfunction, but also proves how our understanding of disease at a molecular level has allowed for the development of powerful therapies that make an enormous difference to the lives of those who have the condition.
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