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CEA and CA19-9 Results as Predictors of Treatment Outcome
I had a distal pancreatectomy and splenectomy on May 17 following a diagnosis of pT2N2 ductal adenocarcinoma. Surgery was done utilizing laproscopic/robotic method at MGH Boston. A 2.2 cm tumor was removed. Pathology indicated that the margins were clear, there was small and large vessel invasion and 6 positive lymph nodes out of 24 were examined. I have just completed my 3rd of 8 cycles of oxplatinin(sp?), irinotican(sp?) and 5FU. Prior to surgery my CA19-9 was 53. Post surgery 15. Post 2nd chemo cycle 7. CEA was 1.3, 1.0, 1.6 respectively. While these numbers look encouraging I'm wondering if anyone has any experience or knowledge that would indicate whether this could be predictive of a postive outcome. Care givers indicate that it's good but don't like to sound overly optomistic especially at such an early stage. I have my first CT scan scheduled for next week.
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Very helpful and may things all go in a positive direction for you.
My husband also had a terrible time with diarrhea
I start Imodium at 2 AM the night before chemo, and every six hours I give him two Imodium until he tells me he don’t need it, which is usually a week.
He still will have some diarrhea, but this is helped a lot
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1 ReactionFor our example, these numbers are useless as predictors. My spouse had a high of 80 CA-19-9 for a few months before his Whipple— they were in the 30s at time of diagnosis. Pathology report from surgery showed the course of neoadjuvent Folfirinox was ineffective and 4/31 nodes were cancerous, margins clear.
Once inflammation calmed, CA-19-9 plummeted, then rose to normal levels (from single digits to teens to twenties—considered normal—over the course of nine months).
CEA levels were normal too. Post surgery Gem/Abx levels were in low normal range—like yours. Even on the day a CT scan showed reoccurrence, nine months after surgery.
The two extensive blood Labs taken for clinical trials so far for a targeted inhibitor did not include either test. I did not ask why.
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1 ReactionThank you for all your advice. Will discuss these ideas with Oncologist later this month when it is decided how to proceed after breaking from treatment for a month. Hoping things continue to move forward in a positive direction for you and your loved ones.
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2 ReactionsSo hard to know what signs to look for. My husbands CA-19 in March before starting Chemo (post Whipple) was 40. In July new CT-scan came back clear, but CA-19 was 53. CEA was in the normal range. Every visit and test is so scary. Wishing you only positive results.
I have found MarkyMark’s link to Dr Matthew Katz at MDAnderson Houston helpful. Top cancer centers are still using decades old treatments with a few tweaks as Standard of Care in return for a few positive results. After we sacrifice our loved ones for data, hopefully targeted screening and therapies will become the new norm before a tumor manifests.
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3 ReactionsPlease post your physician’s recommendation regarding maintenance therapy. After pronounced NED I asked for it and was advised there may not be anything. Now I understand there is. Xeloda I believe (can anyone confirm?)
Standards of Care-
We need the physicians that are willing to think out of the box for otherwise healthy patients!
Look for oncologists that actually have “pancreatic cancer” on their business card..
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2 ReactionsI don't remember which med(s) he has been taking, but @stageivsurvivor is a living testament to continuing systemic treatment despite NED status.
The "NE" stands for "No Evidence," and one of my favorite quotes is, "Absence of Evidence is not Evidence of Absence!"
The Minimal/Microscopic Residual Disease can always come back to get you. In my case, the recurrence was below the threshold of detection on four circulating tumor DNA tests, until it wasn't.
A quick search turned up two interesting factoids quoted here:
1. "Median survival was 7.4 months among patients treated with Xeloda plus gemcitabine, compared to 6 months among patients treated with gemcitabine alone." -- This implies the presence of disease, but shows some effectiveness.
2. "Capecitabine (Xeloda ®) is currently the most biologically active oral fluoropyrimidine drug, and is widely used in adjuvant therapy for pancreatic cancer." https://classic.clinicaltrials.gov/ct2/show/NCT03959150 -- This trial was on post-op, post-adjuvant therapy, NED patients, and was supposed to wrap up in June 2023. I haven't seen results or FDA approval decisions.
For "stable disease," there has been some research and discussion about maintenance therapies. Docs are considering a switch from my chemo (GemAbraxCis) to avoid worsening neuropathy, but I've been holding on as I'd rather avoid worsening cancer.
Dr. Eileen O'Reilly (MSKCC) has done some research in this, and found that patients with BRCA mutations who have been stable for ~16 weeks on a platinum-based therapy reach a "sweet spot" where it may be preferable to switch to (or add?) a PARP inhibitor like Olaparib (Lynparza), and noted better outcomes from switching before disease progression. Apparently, after the disease becomes resistant to platinum, it also becomes resistant to PARP inhibitors.
There's a short, 3-year old video of her discussing it here: https://www.onclive.com/view/dr-oreilly-on-the-utility-of-parp-inhibitors-in-pancreatic-cancer
By now, she may have newer data related to other DNA Damage Repair mutations like PALB and ATM, as well as other PARP inhibitors.
Ours were from top GI cancer centers with oncologists with lots of pancreatic cancer experience. However, thinking out of the box means recognizing that this cancer originated from cellular replication mutations common to other cancers. Standard of care must incorporate this information rather than simply identifying the tumor and treating this gross manifestation of the cancer. In my husband’s case, the errors in his BRAF mutation are also found in melanomas and gliomas. For many others, the same mutations are more commonly manifest in colon or breast cancers. Therefore we need to target the initial breaks and mismatch repairs and attack those as well as cutting out or killing the visible tumor.