Good Morning AutntBerly,
I hope today finds you well. I am going to try and explain a little about GIST. I am going to start at its origin in the body so that you can understand your disease. It is important that you know it from this level so that you can better understand the treatment..so bear with me. In the bodies tissues and organs there are three layers called embryonic germ cell layers. There is the outer layer called the Ectoderm, the Endoderm which is the inside layer, and the Mesoderm which is the middle layer. GIST are of the Mesenchymal (Mesoderm) origin. Molecularly, they express CD34 antibody which is an antibody that is responsible for a number of different functions in the body. The mutation that causes GIST is called c-KIT or just KIT and also sometimes PDGFRa. This is a mutation on the 4th chromosome, long arm between the 11th and 13th band.
Both are called Tyrosine Kinase Receptors. PDGFRa is a platelet derived growth factor receptor alpha class and that is what the letters stand for. These receptors are responsible for sending a signal from inside a molecule to other nearby cells to tell them to start producing proteins and tumor cells so when they mutate, what results is a signal that gets out and is not able to shut off, therefore a mass ensues. Gleevac is a targeted therapy. It's chemical name is Imatinib Mesylate. The last two letters of a targeted therapy usually tells you its function or what it is targeting. Because the receptor is inside the cell on the surface of the nucleus of the cell, it is an Internal Binding targeted therapy. Therefore, ImatinIB. GIST tumors are sensitive to this type of therapy. Gleevac and surgery are usually the first line in treating them. If the tumor becomes resistant to Gleevac, then patients are switched to Sutent which is Sunitinib Malate, same IB ending. Sutent is a multitargeted tyrosine kinase inhibitor that targets more variety of these kinases. Now that you get an idea of how they come about, There are an estimate of 7 cases per million in the US and that is about 1500 cases a year. They can occur anywhere along the GI tract and breakdown like this: Stomach-60%-70% of cases; Small Intestine-20%-25% of cases; Colon 5% and Esophagus is less than 5%. There is no clinical staging for GIST. The prognosis depends on the size of the tumor, its location, and its grade or how differently (differentiation) it looks from other cells at its location. It rarely metastasizes to distant locations. It tends to move to localized areas if it moves. I hope this helps you understand and you know where to reach me if you have further questions. I know this stuff is rather dry, but it will help you understand the treatment better. If you know the enemy you are fighting, you have a greater chance of becoming the victor. Best of luck, Carm RN.
This link shows you the function of a tyrosine Kinase receptor:
http://faculty.plattsburgh.edu/donald.slish/tyrosinekinase/tk1.html