This approach is what I normally do for any concern I or others I know might get. It takes some time (a number of hours), but the results can be inexpensive to implement and make huge differences in outcomes.
Do note I am not a doctor and I strongly encourage you to pass this by your doctors. What I am providing is just what I would do, absent a doctor's involvement. It is just meant as an illustration of the thinking and is a walkthrough of what I would want my wife and anyone else to do, absent me being able to do it (even for myself, if incapacitated). In fact, I am providing my wife with this as my most recent example to go by.
My first step was to find out the signaling pathways that start and propagate this cancer.
From “Molecular pathways in periampullary cancer: An overview” (costs $27.95 to purchase for 48 hours) [I did not purchase this, but used the abstract and snippets offered at the link as much as possible].
“Epidermal growth factor receptor (EGFR) signaling pathway
EGFR is a signaling pathway that regulates growth, survival, proliferation, apoptosis, and differentiation in mammalian cells.
WNT Pathway
The Wnt pathway has a role in cell proliferation and differentiation and is important for both normal physiological and pathological activities. This pathological growth can process into malignant tumors.
TGF-β pathway
Transforming growth factor (TGF-β) signaling pathway is involved in regulating several physiological functions including cell growth, differentiation, apoptosis, and migration. Its deregulation has been linked to cancer initiation and progression.
mTOR/AKT pathway
The Phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway (PI3K–AKT–mTOR) is an important pathway that is involved in the regulation of cellular processes as survival, growth, proliferation, motility, metabolism, energy balance, stress response, and angiogenesis [78,88]). It consists of two parts: Phosphatidylinositol 3-kinase (PI3K) and its downstream molecule serine/threonine protein kinase B (PKB/ AKT) [89]. Hyperactivation of mTOR signaling has been observed…
HGF/c-MET signaling pathway
MET (c-Met), also known as hepatocyte growth factor (HGF) receptor, is a tyrosine kinase receptor (RTK) with multiple downstream effects including regulation of cell survival and migration of epithelial and myogenic precursor cells
Chromatin remodelling pathway
Switch/Sucrose nonfermentable chromatin-remodelling complexes are pleomorphic multi-subunit cellular machines that utilize the energy of ATP hydrolysis to modulate chromatin structure [106]. It is involved in regulatory cellular processes, DNA damage repair and cell cycle regulation [10] Recent genome sequencing studies have reported 20% high mutation frequency in SWI/SNF subunit genes, in all human cancers.”
https://www.sciencedirect.com/science/article/abs/pii/S0898656822002236
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I then dig into each pathway to see what can affect it from diet, exercise, and supplementation. I note the medicines along the way, but those generally are out of bounds for what we can do at home. We explore those with doctors and by giving them our original studies or authoritative web site pages.
EGFR Pathway - Other Sources
Epidermal Growth Factor Receptor Signaling Pathway is Frequently Altered in Ampullary Carcinoma at Protein and Genetic Levels
“EGFR was more commonly expressed in pancreatobiliary-than in intestinal-type tumors (p=0.002)…Similar to EGFR expression, the activation of EGFR was more common in pancreatobiliary-than in intestinal-type tumors.”
https://pmc.ncbi.nlm.nih.gov/articles/PMC4007414/
My take: I am assuming you have the pancreatobilary form/location, as older people normally get that one. EGFR confirmation helps direct how to possibly approach addressing it with diet and such.
Abstract 129: The Microbiome Product Urolithin a Abrogates the Tgf-β Egfr Pai-1 Pathway by Inhibiting Egfr Activation and Expression
https://www.ahajournals.org/doi/10.1161/hyp.74.suppl_1.129
My take: The title directly states Urolithin A blocks this pathway. My wife and I take MitoPure Urolithin A bought off Amazon on a sale occasion, but you can buy a year's worth for less directly from the manufacturer's storefront. This is the only tested form of Urolithin A.
Targeting EGFR in Combination with Nutritional Supplements on Antitumor Efficacy in a Lung Cancer Mouse Model
“Selenium (Se) and fish oil (FO) exert anti-epidermal growth factor receptor (EGFR) action on tumors…Mice receiving the combination treatment with Se/FO and gefitinib or erlotinib had a lower tumor volume and weight and fewer metastases than did those treated with gefitinib or erlotinib alone.”
https://pmc.ncbi.nlm.nih.gov/articles/PMC9783964/
My take: These are both normal things to get from diet or supplements—and we take these in our supplements.
This pathway appears straight-forward for the condition, but the purchase of the original study above for $27.95 would elucidate this.
WNT Pathway - Other Sources
Small Molecule Wnt Pathway Modulators from Natural Sources: History, State of the Art and Perspectives
https://pmc.ncbi.nlm.nih.gov/articles/PMC7140537/
Various foods / supplements in places. It wasn't conducive to copy / paste the separate instances. Table 1 has a large list of activators and inhibitors.
My take: A number of supplements increase this pathway, including berberine, ginkgo, and seemingly, marijuana. Resveratrol, EGCG (green tea extract), quercetin, and curcumin seem to only turn it off.
I did not find a study that elaborated on a specific increase in Wnt as an enabler of this specific cancer. It looks like the “Molecular pathways” main study might tell us, if we bought it. It would be worth buying for this clarification.
TGF-β Pathway - Other Sources
Transforming Growth Factor-Beta (TGF-β) Signaling in Cancer-A Betrayal Within
“Besides induces[ing] tumor suppressive role by activation of programmed cell death, TGF-β promotes tumor suppressive role by regulating immune cell function in favour of tumor cell death (Schrantz et al., 2001). Taken together, TGF-β at the initial stage of tumorigenesis promotes tumor suppression activity, by arresting cell cycle, induces DNA damage and apoptosis is malignant cells… In the later stages of cancer, TGF-β can paradoxically result in tumor progression and metastasis (Katz et al., 2013).”
https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2022.791272/full
My take: This is a warning, as a potentially fine line could reverse the expected outcome, based on if it is a “later stage.” Note this study does not talk to our original cancer. It looks again like the “Molecular pathways” study might tell us, if we bought it. It would be worth buying for this.
What is TGF Beta? + Factors that May Inhibit/Increase It
https://health.selfdecode.com/blog/tgf/
My take: What stage are you? This matters if you smoke or have stress (both increase TGF Beta) or take supplements or foods like resveratrol, zinc, extra virgin olive oil and others (these decrease TGF Beta). It seems strange that, if an advanced enough cancer is affected by this pathway, people are now in a place to smoke or stress out, to better control it (based on the immediately prior study), because this control for the pathway swaps, then.
mTOR Pathway - Other Sources
Selfhacked: “All About mTOR + Natural mTOR Inhibitors & Activators”
https://selfhacked.com/blog/mtor-natural-mtor-inhibitors/
My take: There are things you can eat or take directly that curb mTOR. Diet and supplements both address its activation. You will note a couple items from the PDF above that started this whole cancer thread on this site are listed in the “Inhibitors of mTOR” subheading of the SelfHacked site, about halfway down the page, along with a number of other food or supplement options.
Because the original study at the beginning of my response specifically states “Hyperactivation of mTOR signaling has been observed…,” it seems most likely the mTOR pathway should be attacked, in my opinion, but the study should be bought for better assurance.
HGF/c-MET Pathway - Other Sources
Clinical value of plasma hepatocyte growth factor measurement for the diagnosis of periampullary cancer and prognosis after pancreaticoduodenectomy
https://onlinelibrary.wiley.com/doi/10.1002/jso.21676
My take: There is very little elsewhere on this pathway, This study is behind a paywall and appears to only look at your Whipple surgery effect on HGF. It's highly elevated for ten days, which might be from the extensive surgery, it says within. Not a help. This pathway doesn't seem to offer help, from what is publicly available. Maybe the $27.95 study better explains.
Chromatin remodelling pathway - Other Sources
Chromatin-remodeling links metabolic signaling to gene expression
“—Chromatin modifications facilitate responsive, rapid, and reversible gene expression.
—Metabolic signaling pathways, such as the TOR pathway, cooperate with chromatin-remodeling.
In addition, in ccRCC, where PBRM1 is commonly mutated, mTOR activation was found as a critical contributor to malignant transformation [28].”
https://www.sciencedirect.com/science/article/pii/S2212877820300466
I had to dig to get something helpful. This study is about this pathway and cancers, in general.
My take: Nothing else seemed to speak to pancreatobilary cancer with this pathway, in my opinion, but getting mTOR better may help this Chromatin-remodeling pathway stay sane for renal cancer (ccRCC).
Summary: I would talk with your doctor about these various study “bites” after buying and saving / printing out the “Molecular pathways in periampullary cancer: An overview” report / study.
With clarification from that purchase, the direction you could take on any pathways will be made clear. The ways to leverage the pathways are above, if the Molecular pathways report does not also state how to best utilize the pathways.
I hope this helps and I hope you are one of the ones who beats this cancer, Myrddin.
I found few for your cancer, but the following one showed a new therapy approach that showed this success (overall survival (OS)):
Different outcomes for positive, negative pancreatic cancer patients receiving chemoradiation and systemic therapy
“The primary endpoint for the trial was OS, which was only improved for patients with node-negative disease (5-year OS 48.1% for patients on the Chemo+CRT arm versus 28.6% on the Chemo arm).”
https://medicalxpress.com/news/2024-06-outcomes-positive-negative-pancreatic-cancer.html
It sounded like you may be considered node negative right now. If so, consider this option, which greatly increases overall survival at five years.
As this condition is rare and has less on it, my final review becomes the most manual review, which is a search of the studies off search terms from the NIH PubMed site:
Why do I limit my use of AI? Because the output is beset by political correctness around what are the most professionally-agreed upon answers, which hides the one-off studies of something novel. Why do I like “novel?” Because it can be harmless to try out, yet, not have a Cochrane Review-level of “authority.” I have had great success with these “hidden”opportunities. “Novel” does not mean “scientifically implausible,” however.
General website searches can also bring up these actionable study references, but often, study outcomes are just included in a paragraph with no named study to go back and reference. I do find search engines have the same bias (“weighting”) that can prevent less known research from sparking an idea path to then follow with a deeper dive. The NIH site seems largely free from bias, compared with most search engines.