I wasn’t eligible for the trial. It was a Phase II trial with Taxol and AMG 386, an experimental drug meant to stop the formation of blood supply vessels to the tumors. I wasn’t too upset about being ineligible — I’d already decided I didn’t want to do it. I’ve been on Taxol for awhile, and while I know the dosing is different on the trial and there could still be therapeutic benefit from it, blah blah blah, I don’t put a lot of faith in a drug I’ve been on while the cancer still grows. And because it’s a Phase II trial, there was a chance I might not get the AMG 386, but rather a placebo.
My oncologist moved on to my other choices. There’s Caelyx, she said, and that would be our first choice. But we don’t have a steady supply of it. There is a clinical trial you would be eligible for that’s coming up, but unfortunately that’s still a few months away. I sighed inwardly. It always comes back to the Caelyx and the fact that we can’t get it. It’s only available for research purposes right now. In fact the reason why the upcoming clinical trial is happening, my oncologist explained, was so they could secure a supply of the drug for the patients who need it, which is why I’ll be eligible for it despite having three lines of chemo so far.
The year is 2012 and the only way to obtain a very effective drug for the treatment of ovarian cancer is to create a research trial. The maker of the drug cites manufacturing problems. The actual reason for the drug shortage is far more complicated. This isn’t just a Canadian problem. Access to older, cheaper, generic drugs becomes more and more difficult, regardless of effectiveness. Mull that one over for awhile.
My oncologist put forward a few options for me — do nothing, go on Gemzar (once a week for three weeks, one week off), Topetocan (every day for five days once a month), or go on a Phase I trial.
The whole idea of Phase I vs Phase II is likely confusing to most of you, but that’s what Google is for.
One of the Phase I clinical fellows came down to meet with me during my oncology appointment. I was meeting with her team later that afternoon, but my doctor wanted her to briefly explain the Phase I option they were looking at for me. It wasn’t chemotherapy (so it woudn’t shrink the tumor), instead it was a protein inhibitor (which, if I had the right protein expressions, etc., could mean slowing or halting the growth of the cancer). My tumor would have to be sent off again (for the third time) to be analyzed before I would even know if I was eligible for the trial.
This is the most terrifically boring post I have ever written.
Anyway, I met with the Phase I research team later in the afternoon. My appointment was over an hour late and I was getting cranky and hungry and tired and annoyed, but I forgot all about that after I met with the doctors.
The reason they were so late bringing me in is that they had an AMG 386 trial — remember that from the beginning of the post? — that they were pretty sure didn’t mention anything about previous bowel perforation as an exclusionary factor. So they sat down and read through all 160 exclusionary factors to ensure that, indeed, it was not listed and in fact nothing in my history was listed as exclusionary, and thus I was eligible for this trial.
I don’t know why this AMG 386 trial doesn’t list previous bowel perforation as an exclusion. Neither do the trial doctors (and none of them are terribly concerned that I’m at high risk for another perf, touch wood, please). It may have been an oversight on the part of the drug company and this is kind of another loophole, but whatever.
This trial combines AMG with a protein inhibitor called temsirolimus. There’s all kinds of crazy side effects that could come about, though my biggest worry is edema because I’m terribly vain and I don’t want to walk around with legs like an elephant.
I haven’t signed anything yet and I’m not entirely positive that I’ll do it, but at this rate it’s either this or a drug that has a 15% response rate. These clinical trial drugs are too new to know what kind of success (if any) they’ll have, but the head trial doctor — a woman who said excitedly, Whoa, you’re young! when she saw me and who kept her eyes closed more than half the time she spoke, with an expression you might wear if you were biting into a really decadent piece of cheesecake, and to whom talking about cancer and protein pathways and angiopeteins seemed to give some kind of religious ecstasy — said that some of her patients have even had regression on this trial. Considering I have a disease in which the most common mantra is stable is good, I’ll accept regression in ‘some’ of less than 100 people as better-than-bad odds.