Case Report Stage IV Pancreatic Cancer: Good News from Jess

During this summer, on August 10, 2018, Jess was informing us (here) regarding the fact that her dad, dealing with Pancreatic Cancer Stage IV, will start a similar treatment approach as that successfully used by Marcos, and shortly discussed on this website (here).

Jess and I have exchanged a large amount of e-mails this year and consequently also became friends. She is extremely clever, and everything she does is carefully and extensively addressed leading to high quality work. Not only that her quality approach to what she is doing is impressive, but also her care for others is outstanding. Jess dose so much for helping her dad but she doesn’t stop there. And so recently, she did something very impressive: One of our good friends and visitors of this website needed some specific help for her dad, and Jess decided to fly to another continent for a day just to help our friend that she never met before. How impressive is that?

Status before the treatment, before August 2018:
– Jess’s dad was diagnosed with Stage IV pancreatic adenocarcinoma on Oct 3, 2017, with a primary tumor in the tail of the pancreas and several liver lesions. His CA 19-9 marker was 47.000 at diagnosis
– performed FOLFIRINOX until April 17th, 2018, and his CA 19-9 was 3.440
– removed oxaliplatin due to toxicity and continued with FOLFIRI but markers started to go fast up during the summer of 2018 (see graph below)
– during August 2018 decided to start low-dose Gemcitabine supported by many treatment approaches discussed on this website, and latter also introduced Abraxane

Results reported on October 2018:
CA 19-9 dropped by almost 95% over 2 months of treatment. Not only was the CA 19-9 response to this combined therapy much more rapid than the response to his first-line chemotherapy, in fact the CA 19-9 fell more rapidly than it rose during the two month “rest” period. Finally, a PET scan from Oct 10th, compared to one from July 25, showed decrease in intensity of the primary tumor and most importantly, “significant decrease in FDG uptake [from 8.1 to 4] within the large liver tumor, with mainly large photopenic region in the center of the lesion and a moderately FDG avid rim.” This result is consistent with necrosis in the body of the tumor.

The treatment:
Next to the chemotherapy, the treatment schedule included a few other substances expected to exert a strong pressure on the cancer cells including glycolisis inhibitors such as 2DG intravenous, Salinomycin, 3BP, Photo Dynamic Therapy (PDT), thyroid protocol but also diet approaches such as fasting, and various supplements and drugs.

As it can be seen from the graph kindly provided by Jess, the initial (low-dose) Gemcitabine dose could only slightly reduce the markers. Only after the introduction of the supportive therapies, the markers started to strongly decline. These impressive results clearly indicate the importance of the supportive therapies when dealing with advanced cancers.

In order to share her experience and help others, Jess started up a website. Please visit Jess’s website in order to get more details regarding the treatment schedule employed in treating her dad, as well as the related dose of chemotherapy and the supportive therapies used. In addition to that, Jess will continue to share on her website information regarding new treatment approaches she is researching and considering, so it would be a good idea to check her website from time to time for new content.


This site is not designed to and does not provide medical advice, professional diagnosis, opinion, treatment or services to you or to any other individual. Through this site and linkages to other sites, I provide general information for educational purposes only. The information provided in this site, or through linkages to other sites, is not a substitute for medical or professional care, and you should not use the information in place of a visit, call consultation or the advice of your physician or other healthcare provider. I am not liable or responsible for any advice, course of treatment, diagnosis or any other information, services or product you obtain through this site. This is just my own personal opinion regarding what we have learned on this road.

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27 thoughts on “Case Report Stage IV Pancreatic Cancer: Good News from Jess

  1. Great news!!!

    This demonstrates once again the efficacy of the adjuvant metabolic approach to chemotherapeutic treatments.

    We use a similar protocol perhaps more aggressive in number of drugs fighting a glioblastoma.

      Best wishes

  2. Great news!

    D, I am seeing a pattern here! It is amazing! This has almost emerged out of nowhere. All of sudden everything seems to be clicking. There is this emergent property where you have a lot of energy and a set of variables and people can work through the combinations and before you know everything falls into place. Extremely exciting.

    I will be anxious to hear of any updates that you might post.

    D, Jess is doing a fantastic job!
    I know in the past you have suggested that people stick with success, I agree, though having something on the backshelf
    also seems to be a good idea to me.

    Thus, nanoMG if possible might be a good choice.
    Easy synth, selectively toxic to cancer cell OXPHOS subunit 1.
    nanoMG is much more cancer specific than MG, enhanced with combo with vitamin C.

    Best Wishes D, for a job well done!

  3. Speaking from my experience of FOLFIRINOX and Gemcitabine + Abraxane combinations used for a loved one for a Pancreatic Adenocarcinoma diagnosis.

    Both these chemo regimen are first line/second line treatment for Pancreatic Adenocarcinoma and shows excellent results (in terms of activity on the tumours and reduction in CA 19-9 markers) on people who respond to these drugs till the resistance kicks in. So in this case the drastic fall in the CA 19-9 markers after introducing Abraxane with Gemcitabine is typically seen in a lot of people who respond to Chemo drugs and addition of Abraxane is very likely the key here.

    One other thing is for people responding to these drugs FOLFIRINOX and Gemcitabine + Abraxane can be used in sequence i.e. when one of these regimen fails; the other combination can be started; like it has been used here.

    1. Thanks. As an abstract level, fair comment. I would think the same but the “details” make the difference:

      1. we could make it sound very easy but the reality is the opposite – let’s not forget this is one of the most aggressive cancers – little number of patients can influence so nicely the tumor and this is why the overall survival is extremely short when following the conventional treatments only; increasing the chance to be one of the responding patients is extremely valuable
      2. here the patient was using lower dose chemo, and lower frequency:
      – typically Gem+Abraxane is given at Gem 1000mg/m2 and Abraxane at 125mg/m2 every week (Ref.)
      – the patient here used only Gem first at 800mg/m2 and when Abraxane was introduced at 80mg/m2, Gem has been further lowered to 500mg/m2
      – as it can be seen in the graph above, when Gem (800mg/m2) is introduced first there was not a major response – as the 2DG metronomic dose has been increased and PDT & 3BP introduced the marker started to decline faster while Abraxane was not yet added. Next, Gem dose has been further reduced to half while adding lower than normal dose Abraxane and latter Salinomycin. The markers continued declining.
      3. indeed, the doctor following the patient stated that the response is faster and better vs. what she has seen in patients before
      4. most treatments that have been used here have strong scientific base (not B17 or similar) and are indeed expected to do what we see here
      5. this is not a single case – it is part of a larger number of patients with different cancers using similar approaches and experiencing response to conventional therapies while all are in a difficult stage IV

      Therefore, what we have here is a patient using low dose chemo and responding nicely to that in one of the most difficult to treat cancers.

      1. thanks Daniel for the details and clarifying it. It makes perfect sense to me now.

        If you can upload the other graph (from 8/12/2018 onwards) which zooms-in to the specific area of the drastic fall of the CA 19-9 markers to this blog post itself; it will be great and i think it will keep the complete context in one place for future too.

        About your point #4; I have NO doubt on the detailed analysis (of scientific nature) that goes into each treatment option mentioned here. This website is the ONLY of its kind and is really making a difference in the lives of patients especially stage-IV who are left with limited or no options from conventional therapies and you and (others helping out) cannot be thanked enough for making this happen; so thanks again for all the efforts that you are putting in here.

        About FOLFIRINOX; Jess mentioned that the oncologist removed oxaliplatin (and continued with FOLFIRI) out of concern for “potential” future nerve damage. I could not make out from her description if the neuropathy was actually there or not when the decision was made; because the drug-resistance kicked in immediately after dropping oxaliplatin. Basically from the options available currently in the conventional therapy for Stage IV Pancreatic Adenocarcinoma the only instances of long term remissions that i have read about (a couple of them only though) are with FOLFIRINOX only where people continued (who could tolerate) on maintenance FOLFIRINOX for really long. So if someone is responding to FOLFIRINOX and tolerating fine; then I think they can try to talk to their oncologist to go ahead with a full combination of this regimen as long as it responding.

        And I sincerely hope that the other supportive therapies being administered are able to remove drug-resistance of the tumour for FOLFIRINOX here and they can revisit this regimen at a later point in time if required and if the fitness levels allow.


  4. D, finally we seem to have turned the corner.
    It is almost 4 years since I entered the conversation and we have lost dear friends and you your soul mate.

    It has been so tough moving through this abyss with no idea when we would finally arrive at the journey’s end.
    Yet, here we are and we are starting to see some very startling responses.
    These responses are happening right now!
    Typically published research is YEARS distant from patient outcomes even when it is freshly published.

    One speculation that I will put forward is that if the metabolic response is truly happening for these patients so far,
    then we would likely see the response continue. With metabolics there are very few escape routes, cancer cells have
    to produce energy somehow and 2-DG is entering via a glucose pathway. I would find it difficult to believe that a cancer
    cell could find an effective means of avoiding glucose uptake. With glycolysis under stress it might switch to OXPHOS,
    though MG would be there to block out that escape route as well.

    D, if more evidence for this accumulates there could be a wave of patients reaching out to you on your site. I think the basic protocol might be tightened up somewhat, though the core idea of metronomic metabolic dosing seems very solid.

    Best Wishes, J

    1. HI J,

      Thank u for your nice comment. It becomes clear to me that metabolic treatments alone are not enough since we will never be able to fully shut down cancer cells using that approach without shutting down the normal cells as well. However, metabolic treatments represent amazing tools to put cancer cells under pressure while being attacked by conventional therapies.
      There is more evidence accumulating that suggests that.
      But that means that in order to have effective treatment strategy, you need not only an effective metabolic tool (such as 2DG metronomic) but also an effective conventional tool. If the conventional tool (such as chemo) is not able to kill cancer cells not even when they are under pressure, the conventional treatment needs to be switched. So far it looks like just adding 2DG metro to chemo is enough to produce effectiveness (implying results from slowing down cancer growth, to stopping growth and even killing totally the tumors).
      But there is more to understand in order to maximize even more the outcome. For example, in some cases, the treatment may not be effective in reducing tumor below a certain size. In that case the remaining type of cells are not responsive to the therapy. When that happens, the reason for that could be either the remaining cells are of oxidative nature (slower and thus not responding to chemo and glyco inhibitors), or have acquired resistance to the specific chemo and that needs to be change to another regime. Another option could also be e.g. the physical barriers for the treatment to reach the tumor. However, I think the first (oxidative slower cancer cells) is the most relevant. Therefore we need to think of solutions against oxidative cancer cells for cases when resistance may be reached. One approach could be a more intensive use of mito inhibitors and/or fibroblast inhibitors (feeding the oxidative cells) and/or ion dynamics modulators. Actually I now realize that angiogenesis inhibitors should also work very well for these type of cells. Any idea is very welcome. We need to innovate together 🙂

      Kind regards,

  5. I have to improve the therapy ….. glioblastoma seems much more resistant. It has advanced much slower than expected but has advanced.
    I need to incorporate other iv in addition to 2 dg metronomic, vitamin c and salinomycin.
    Jcancon MG is methylglyoxal? Methylglyoxal crosses the BBB? If so, I can try to find a nano or chitosan formulation ….
    I need a game changer for gbm

    Dear Daniel I am waiting for your answer when you are less busy

    Best whises for everyone

    1. Manuone, I am so excited by this recent development!
      It has been years and years and it looks like we have finally found something!
      Before, we might see a short term response, yet then there would be progression.
      Ongoing responses now appear to be occurring!
      We should not over-assume, though this looks very promising.

      This could be our first major step forward.

      My understanding is that this is related to the metronomic metabolic approach (specifically 2-DG).
      When you look at the list of the treatments that are being used the one notable difference is the metronomic dosing.
      All the other treatments are mostly well recognized by those on the forum.

      It should not be assumed that step 2 will be any easier to achieve than step 1, though we can start to think about what we
      could modify next. I will let D show leadership on this, yet for me the obvious next amp up would be to go combo metronomic metabolic. From what I see only 2-DG is dosed metronomically now. Trying combo 2-DG and MG metronomically could be a very
      powerful combo. Instead of shutting down glycolysis over time you would be shutting down both glycolysis and OXPHOS over time.

      I have been suggesting NanoMG for some time now, though posters of the thread have not been able to do this synth. The url below shows how very powerful this nanoformulation could be. The synth presented appears very straightforward. It was only recently that I discovered that MG is a quite selective OXPHOS inhibitor (it is suggested thought that creatine be given to protect against cardiac toxicity). The suggestion was to use low doses of vitamin C in combination when using the non-nano form of MG.
      I am currently wondering how effective combo metronomic NanoMG and vitamin C would be. On paper it should be quite a powerful combo. Some might even start with the easier to obtain though less effective approach of simply metronomic iv MG and iv vitamin C. There is a great deal of excitement and I am looking forward to how D feels about the various options available.

      It surprises me how many cancers now appear to be metabolically vulnerable, including GBM.
      “Glioblastoma (GBM) is the most common brain tumor; however, no effective treatment for it is available yet. Monocarboxylate transporters, which are highly expressed in GBM, play a role in transporting antitumor agents, such as 3-bromopyruvate (3-BrPA).”

      On a first run through, yes chitosan does appear to be bbb penetrable.

      Another idea that I picked up from a url given by lullabyman on the metronomic 2-DG blog page was the idea of chaotic cancer treatment. An oncologist proposed that creating a treatment model in which cancer is constantly exposed to unexpected stresses
      could give a treatment boost. As real world evidence of this effect he showed successful cancer regimens that did have to some extent a chaotic treatment schedule. How would this chaotic treatment approach work with metronomic 2-DG? One could cycle through different metronomic treatment combinations such as vitamin C, MG, 2-DG, DCA and others (though I would tend to steer clear of dosing 3-BP metronomically). The strategy would be to destabilize the ability of cancer to effectively respond to the stresses involved. Simply giving the same treatment with the same dose over the same time interval gives cancer the advantage of
      being able to create a possible counter-strategy. A chaotic might counter the counter-strategy.

      I realize that this must be a very difficult time for you.
      I wish that the efforts of those on the forum will be able to help you.

      Best Wishes, Jcancom

    2. I’d start hitting the damned thing with a different chemo, and a combo of supplements:
      Vitamin D3
      Liposomal Curcumin + Berberine
      Honokiol + Magnolol
      Betulinic acid + Delphinidin
      Citric acid
      Sodium selenite
      Resolvins(EPA, DHA and DPA)
      Royal Jelly(has Phenylbutyrate) + Melatonin

      Drugs: phenylbutyrate, Tamoxifen

      Take care

    1. J, I was away these days – this is why a little delay in my response.

      For metronomic 2DG, I think its best to take a different approach compared to other treatments discussed here. The approach could be one of the following two options:

      1. the patient finds a doctor willing to help him/her with implementation -> the patient contacts Lampidis Foundation or myself -> receives the e-mail address and his medical doctor requests the treatment protocol from the academic team -> the medical doctors receives treatment protocol as a document & continuous support in discussions during the implementation
      The medical doctors sends feedback back to the academic team regarding treatment results.
      2. if the patient really cannot find a medical doctor but wants to consider 2DG, which is not the recommended route, I (as a blogger) can have an informal discussion (via private communications) with the patient where I can share what I know.

      However the best route is the first one, because there is a doctor assistance, there is an assistance from the US academic team, and the protocol (including the dose, time & additional drugs used) may be adapted on the way as a result of the learning following the consolidation of information we receive from various medical doctors using 2DG. Potential side effects can also be addressed much better on the first route. All this will not be available to the patient if patients chose to do the treatments by own means.

      I agree to share information with the patient even if he doesn’t find a medical doctor, as the purpose is to help people. But I do that via private communications in order to keep the process clean and coherent. Only through clean and coherent processes we can learn and be able to use that to help even more people, as opposed to the more chaotic implementation of e.g. 3BP. The goal is to keep things clean while accessible to anyone.
      If u like to discuss dose of 2DG etc., we can have a Skype call and discuss about this. It would be a pleasure anyway to finally talk to the man known as “Jcancom” 🙂

      If u have ideas about improving the process described above, please let me know and will be glad to consider improving our current approach on this treatment route.

      Kind regards,

  6. Hi guys,
    I am considering applying vitamin c iv metronomically. Similar to 2dg metronomical:
    -I have vitamin c vials of 50g in 100ml
    -I have elastomeric pumps from 100ml to 2ml / h

    An option of 10 gr per day would be to use 20ml of the 100ml vial, this would be 10gr administered in 2ml / h would be equivalent to 10 hours of metronomic infusion / day.
    Any ideas? suggestion?….
    It is difficult to measure interactions with the rest of the cocktail: temozolamide low dose, sodium phenylbutyrate 3 gr, tamoxifen 40mg, metformin 1700mg, naproxen 550mg, quetiapine 20mg, simvastatin, ecetrol, tetrandine liposomal ….

    Best whises

    1. Hi Manuel,

      lullabyman seems to have good knowledge on metronomic Vit C. Maybe a god idea is to write your questions related to this as a reply to one of his comments, so he can receive e-mail notification on this. Regarding the interactions, I do not see any major issues but this is difficult to estimate as there is no literature on that.

      Kind regards,

      1. Thanks Daniel!

        I will ask lullabyman for the metronomic administration of vitamin c ….. jcancom seemed interested in this administration of vitamin c
        What did you think of my treatment plan?

        kind regards

    2. Hi Manuona

      Have you looked at Berberine?

      – enhances anti-tumoir activity of tomoxifen (PMID: 27432642)
      – potent anti-tumor effect against glioblastoma (PMID: 25504754, PMID: 27557493)
      – Berberine protects against metformin-associated lactic acidosis PMID: 28656086

  7. Dear Manuone, yes I am very interested in this approach. What I find so compelling is that there is a range of metronomic options that could be applied (perhaps even in combination). The combo potential of metronomic vitamin C and metronomic methyglyoxal (metronomic 2-DG) seems especially powerful.

    There are many ideas that could be tried. With these metronomic approaches you have a wide range of combos that are open to you and you could continue to change the dosing rates and days of treatment etc. in order to attempt to capture the chaotic effect that is mentioned by an oncologist in a link supplied by lullabyman. I will wait anxiously for his response. He has a very good understanding of the vitamin C protocols and how to boost up their effectiveness.

    D and I talked about myxoma virus on this forum previously. The same company that is developing this oncolytic myxoma virus is also developing an oncolytic virus for GBM (Tasadenoturev). I wish that these viruses can finally be approved so that they could help patients like you!

    Best Wishes, J

    1. Hi Jcancom,
      Thanks for your words.
      I’m not going to stop looking for all the options ….. you do not doubt this!
      It has caused me sadness about Dnx unfortunately the reality is not like that.
      My mother was not chosen for dnx 2440 … they considered that their karnofsky index was not appropriate to participate … they decide continuously for the lives of others as if they were gods.

      kind regards

  8. Hi Manuone,
    That’s an impressive cocktail, I truly hope it’ll knock out the gbm.

    Have you looked at Berberine?
    It could enhance tamoxifen (PMID: 27432642)
    Potent anti-tumor effect against GBM (PMID: 25504754, PMID: 27557493)
    Berberine/Metformin synergy (PMID: 28656086)


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