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Tumor can’t be removed: What are chances of survival now?
Pancreatic Cancer | Last Active: Dec 28, 2023 | Replies (38)Comment receiving replies
My case is somewhat similar to yours. I'll be getting the "less effective" chemo this week for my reoccurrence though my metastasized very quickly to the liver , as it appears that my 5FU (what an appropriate name!) chemo after distal surgery didn't really work for me, or maybe should have been continued beyond the typical protocol of 12 sessions. Have you done any research about the effectiveness of oral chemo following systemic chemo?
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@mnewland99 , Sorry to say I have not done any research into that. In fact, I started digging into it after your question, and now know less than I did when I started. (Or more accurately, I now realize how much I didn't know and how many of my assumptions were wrong.)
Head-to-head searches for terms like "capecitabine vs iv 5fu" and "capecitabine vs gemcitabine" and targeted searches like "capecitabine mechanism of action" return some useful hits, but with no real biochem education to my name, it takes me forever to read and understand them. Not to mention, those searches return papers addressing many types of cancer, and if there's enough variety, they need to be narrowed down as appropriate to pancreatic cancer.
The results make capecitabine sound (to me) like a somewhat attractive and viable alternative to intravenous 5FU, more convenient than infusions, but when I asked my oncologist about it last month as an oral-only maintenance alternative to gemcitabine infusions, she said their mechanisms of action were different enough that it might be risky to switch me since I'm doing so well on the current regimen, whereas capecitabine would be an unknown.
What I gather though, from the head-to-head papers of oral capecitabine vs intravenous 5FU is that they have a similar mechanism in the end:
1) https://pubmed.ncbi.nlm.nih.gov/15763604/
Capecitabine was developed as a prodrug of FU, with the goal of improving tolerability and intratumor drug concentrations through tumor-specific conversion to the active drug.
2) https://www.accessdata.fda.gov/drugsatfda_docs/label/2000/20896lbl.pdf
"[capecitabine] ... is ... an orally administered systemic prodrug of 5’-deoxy-5-fluorouridine (5’-DFUR) which is converted to 5-fluorouracil."
My question for an oncologist would be whether it's the end product (5FU) that is not (or no longer) effective, or whether it's the current delivery method of getting the drug to the tumor that's not effective. In the latter case, switching to oral capecitabine sounds sensible (to me), but in the former, maybe a completely different drug is called for. I (non-medically trained) have no idea, but that's a question today's research would lead me to ask.
Best of luck, and please let us know what else you learn!
--mm