Posted 6 May 2016
Today it is six months since my cancer diagnosis. I am grateful to still be here!
The chemo and radiation have enabled me to keep going a little longer, fighting back the cancer briefly until the treatment stops working (the original chemo) or the treatment can’t safely be continued (radiation).
Sadly, this is the usual state of affairs for pancreatic cancer. For the cancer I most likely have, duodenal adenocarcinoma, there’s very little data because of its rarity, but the prognosis isn’t much different from what I’ve been told.
It is impossible to say for certain, but the consensus of the doctors seems to be that there’s a good chance I wouldn’t be alive today without these treatments. The treatments and their side effects haven’t been pleasant, to be sure, but I have no regrets about this path.
Starting Chemo Again
Now I am approaching a restart of my treatment, with the metastases in my liver being the biggest concern. I have decided to go ahead with the new chemo regimen, starting at the end of the month.
It will take some time for the doctors to get insurance pre-approvals, so I can’t start immediately. We’re going to take our one-week Portland trip, starting on the 20th, for our anniversary. As soon as we return from that trip, I’ll start the new chemo.
The new chemo regimen, Gemzar and Abraxane, is one used primarily for pancreatic cancer. It’s considered less toxic, but also generally less effective, than the FOLFIRINOX regimen I was on earlier. The results vary from one person to another, of course.
In any case, having tried FOLFIRINOX, the new chemo regimen is the second-line treatment. Because the drugs are completely different, the hope is that the cancer will not have yet found a way around them, as it did with the earlier ones. Whether they are effective on my tumors at all, however, remains to be seen.
No one expects that this chemo is going to cure me; as with all of the treatments I’ve had, it is palliative, intended to buy a little time.
My New Friends, Gemzar and Abraxane
Here’s a brief rundown on the two drugs. Skip to the next headline if you aren’t interested in pharmacology!
Gemzar (gemcitabine) is classified as an antimetabolite (more specifically, a Pyrimidine antagonist). Gemzar has been used in combination with other chemotherapy drugs to treat ovarian, breast, and lung cancer. It was also used as a single-agent therapy for pancreatic cancer, with very modest results.
Here’s the mechanism of action, in case you have the background to make sense of this:
Gemcitabine kills cells undergoing DNA synthesis and blocks the progression of cells through the G1/S-phase boundary. Gemcitabine is metabolized by nucleoside kinases to diphosphate (dFdCDP) and triphosphate (dFdCTP) nucleosides. Gemcitabine diphosphate inhibits ribonucleotide reductase, an enzyme responsible for catalyzing the reactions that generate deoxynucleoside triphosphates for DNA synthesis, resulting in reductions in deoxynucleotide concentrations, including dCTP. Gemcitabine triphosphate competes with dCTP for incorporation into DNA. The reduction in the intracellular concentration of dCTP by the action of the diphosphate enhances the incorporation of gemcitabine triphosphate into DNA (self-potentiation). After the gemcitabine nucleotide is incorporated into DNA, only one additional nucleotide is added to the growing DNA strands, which eventually results in the initiation of apoptotic cell death.
In 2013, trials showed that combining Gemzar with Abraxane (nab-paclitaxel) improved results for pancreatic cancer patients. The increased life expectancy, compared with Gemzar alone, was 1.8 months. In the world of pancreatic cancer, that’s a meaningful improvement, but it isn’t much.
Abraxane is made from the bark of the Pacific Yew tree. The “nab” part of the name refers to the binding of paclitaxel to albumin, which reduces its toxicity.
Here’s the mechanism of action:
Paclitaxel is one of several cytoskeletal drugs that target tubulin. Paclitaxel-treated cells have defects in mitotic spindle assembly, chromosome segregation, and cell division. Unlike other tubulin-targeting drugs such as colchicine that inhibit microtubule assembly, paclitaxel stabilizes the microtubule polymer and protects it from disassembly. Chromosomes are thus unable to achieve a metaphase spindle configuration. This blocks the progression of mitosis and prolonged activation of the mitotic checkpoint triggers apoptosis or reversion to the G-phase of the cell cycle without cell division.
I think I’m going to pass on trying to understand that myself.
As things have worked out, May is going to be my treatment-free month, and in June I’m back on the treatment treadmill.
The past few days have been emotionally tough, but I feel like I am on the way back up. Staying present-centered has become more difficult, but more important, than ever before.