|
Hello Nedra,
I am definitely NOT the best person to answer this but I found some information but it's from 1999 when I was first diagnosed and many of these things were bad for me also. In 1999 I wasn't given Herceptin so that's how much things have changed for the better and I'd asked the oncologist about it since I was so HER2+++ So a lot has changed since then but I do agree in knowing as much as possible so that you can ask what can I do about this and that. When you read the stories about people on this site you realize that inner strength is a powerful treatment. I hope this posting doesn't freak some people out as I said many were bad for me and it's 7 years later. I think the HER2 and ER status is the most important and they have treatments for them. here's what I found:
Epidermal growth‑factor receptor (EGFr) All cells have receptors that are 11 switched on" by growth factors telling the cell to multiply. altered cells, the receptors cause the cells to multiply uncontrollably. About half of breast‑cancer cases have altered receptors.
Ki‑67 In simple terms, this measures the speed of cell growth and division.
S-phase The S-phase test how quickly slowly divides also cks DNA - diploid(better) versus aneuploid (bad)
cathepsin D Patients with low levels of the enzyme cathepsin D and positive axillary nodes invariably outlive those with high levels of cathepsin D and negative nodes.
p53 This is a gene mutation that is known to be present in about half of all breast cancers. An abnormality of p53 gives an increased risk of ovarian and bowel cancer as well as breast cancer. When the gene is normal it restricts cell growth;
|
Threaded Mode