1. First Theory - Dr. Goodman stated, "Ovarian cancer is interesting in that the cells in a person's tumor are not all the same." This statement maybe the major reason for a very high recurrence rate. When we approached our Onc about additional drugs to fight the disease, I asked: "We have a cytotoxic drug (Gemzar), a biologic drug (Avastin), why not add a hormonal drug? After all Ovarian Cancer is still hormone-driven. Our Onc said yes to Femara.
2. Second Theory - Since Ovarian Cancer has so many different kinds of vessels or receptors that feeds the tumors, there is a need for a varied kind or combination of drugs. There are just so many to lists: VEGFR (vascular endothelial growth factors receptor), PDGF (platelet derived), EGFR (epidermal), estrogen and progesterone receptors, and the list go on and on. No wonder, Carbo/Taxol may put many to sleep, but majority wakes up again and many times it just resist them in a short period.
Here's a statement from the clinical trial/study of Femara:
"Some types of ovarian cancer cells are thought to be stimulated to grow through the presence of estrogen and/or progesterone, two female hormones. These types of ovarian cancer cells have receptors, called estrogen receptors and progesterone receptors, and laboratory tests can determine their presence. Researchers have speculated that estrogen receptor- positive (ER-positive) and/or progesterone receptor-positive (PR-positive) ovarian cancers may respond well to treatment with hormonal therapy, which works by blocking the effects of the hormones on the cells or reduces the hormone levels in the body."
3. Third Theory - It's a must that we increase the chances of drugs to work. Since we don't have a 100% cure yet, why not increase the probabilty of the drugs we are using to be as close to 100%?
So for example if we are offered Topotecan or Doxil or Gemzar alone and assign a probability of 30% to work (positive response), then why not ask another drug say Avastin and assign another 30% or 40% to add to that drug? So far we have now 70%. Then why not ask Femara or Tamoxifen or Arimidex and add from 10% to 20%? Then we have a maximum of 90%. This is the reason why people go on clinical trial.
When we had our 2nd opinion at UCLA, two doctors agreed that the addition of Femara was an excellent idea. In fact one said, that the addition of 10% was huge in this kind of cancer and Femara won't interfere with the mechanism of the drugs we are using.
4. Conclusion: Since it takes some 30 days or more for Femara to work, it is worth starting now since they are taken daily in pill form.
Here's the result of that study of Femara,
"Researchers from England recently conducted a clinical trial to evaluate the effectiveness of Femara