19.5!
Last Wednesday’s bloodwork revealed my newest PSA number — the key number to OS (overall survival) for people experiencing mCRPC (metastatic castration-resistant prostate cancer) — had increased yet again, this time to 19.5. My last two levels yield a PSA doubling rate of 1.9 months which is the most direct connection between OS and PSA (there are doubling rates of “greater than 10 years”). At the moment I’m not investigating just what that doubling rate means about my own OS because I’m confident my PSA will stop rising and it will become a “what might have been?” question. As soon as I saw the new number I started looking for one of those business graphs where the arrow slams through the top of the graph.
I’ve been getting so much help from my friends, and I’m using some of it to make things happen in the real world. Rick Kline and Neil Alexander both(!), via different histories, suggested seeing Dr. Daniel Petrylak at the Yale Cancer Center; he responded immediately to my request for an appointment — I’m setting that up as we speak — and I’ve become adept at emailing all my medical records. Both the Klines (Robin and Rick) suggested I see one of oncologists working as part of Columbia’s prostate cancer team, and I’m very relieved to be able to say we’ll be going to Columbia to see Dr. Mark Stein tomorrow. From his biography: “Dr. Stein has a particular interest in the development of novel immune therapies for the treatment of prostate cancer.”
There’s a clinical trial going on at Columbia involving a treatment called Chimeric Antigen Receptor T-Cell Therapy, something that sounds incredibly cool that Rick Kline suggested I look into.
Here’s how CAR-T works: T-cells (the killer cells of the immune system) are removed from my body, re-engineered to give them the ability to recognize specific tumor cell antigens, then returned to my body. They reproduce and go in search of cancer cells, and when they find them, they kill them. Sounds good, right? Here’s an encouraging word, “CAR-T cells are engineered to express two antigen receptors at the same time, reducing the likelihood that the T cells will attack non-tumor cells. Treatments with these cells have less intense side effects. A study in mice showed that dual-receptor CAR-T cells effectively eradicated prostate cancer and achieved complete long-term survival.” Another of the unbelievably amazing tools in the cancer killing armamentarium. I’m thinking, “Sign me up for that!” You can bet I’ll be asking Dr. Stein about that therapy.
My friend Kevin G. O’Neill just so happens to have gone to high school with Dr. Jay (Jay Lalezari) who is running clinical trials of an experimental drug called Leronlimab. There have been very encouraging human trials for breast cancer (breast cancer being, it turns out, a cancerous kissing cousin to prostate cancer). They’re not running prostate cancer trials at the moment, but I they will be at some point. Keeping our fingers crossed on that one.
For many men, the (incredibly expensive) drug enzalutamide (the bizarrely named & scandalously expensive (that’s another story — stay tuned) Xtandi) can reduce PSA levels to between 1 and 0, or even “non-detectable.” In the month I’ve been on it my PSA went from 12.9 to 19.5. The PSA change in the first 30 days of enzalutamide are the most significant survival-wise. Good news would be a reduction of 30% or even 50% — my increase of 150% is not good news. On Friday my current oncologist was surprised to see note the increase — and suggested giving Xtandi another month, just to make sure it’s not going to start working.
One interpretation of my PSA numbers is that not only did enzalutamide have no effect on the vigor and aggression of my cancer cells, but neither did chemotherapy — that the only effective treatment has been ADT (Androgen Deprivation Therapy — that’s what reduces my testosterone nearly to zero), and that back around April 28th its effectiveness was thwarted by clever mutations of my cancer cells. Which would mean that my cancer has become (here’s a charming phrase) castrate resistant. This is a significant milestone in the progression of prostate cancer.
I’ve lost confidence that anything we’ve been doing, except the ADT, is going to tame my cancer. And I’ve lost faith that my oncologist is likely to come up with a different treatment more likely to work, and definitely not in the next month. He’s following a very vanilla, by the book protocol and seems at a loss when confronted by my cancer’s stubborn refusal to take much notice. My confidence remains undimmed that there are people out there who are ready to suggest treatments that, if they won’t kill my cancer, will at least domesticate it. The journey continues.
