Thank you again, let me see what I can add:

My oncologist said he didn’t want to start with abraxane too, and I didn’t press him on it. I have to say that “just” gemcitabine and cisplatin has not only apparently been very effective, it has been very easy to tolerate. I’ll ask if that was his consideration, but I did want to share that treatment has been easier on me than I expected.

There was a two month delay between discovering I had stage IV PDAC and getting treated, and that was far harder on me.

The plan is to switch to maintenance with a PARP inhibitor soon. Thank you for raising the possibility that I shouldn’t dawdle because resistance to the one might be related to resistnce to the other, I’ll ask when I meet my oncologist again in a week. That raises the whole question of why people are so excited about PARPi, which I hadn’t started thinking about yet. Is it because it is easier to tolerate, less likely to develop resistance, or something else I hadn’t thought of?

I guess there are non-obvious issues around getting a biopsy, so I’ll share that I had to press to get one. It still doesn’t make sense to me, but my first oncologist seems to have more or less felt it was obvious what I had and too late to do much about it. I assumed that genetic testing of the tumor was the whole point, but they apparently never planned to do that, and hadn’t mentioned that biopsy by fine needle aspiration might not provide enough material for it. “Pancan.org” did get a sample from them and was able to run their panel for me, confirming in my case that BRCA2 was the only “actionable” mutation.

I am apparently very lucky to have this version of PDAC, since it is responding very well to a relatively recently developed protocol.

Be well everyone!