Maraviroc: An anti-HIV Drug that Reactivates the Immune System to Fight Cancer

Introduction:

Recently, with the help of a reader of this website (Thank you, Jose!), I came across a very relevant article, Immunotherapy in metastatic colorectal cancer for the first time utilizes the innate immune system, published on the website of the German Cancer Consortium (DKTK).

macrophageThis article describes the results of a recent clinical trial running in Heidelberg, Germany using an anti HIV drug. (As a side note, we may remember that the first application of Salinomycin on humans was also done in Heidelberg.)

This phase I clinical study was conducted in 14 patients and was using the drug Maraviroc, an anti HIV drug known as a potent blocker of CCR5. While due to their mechanism CCR5 blockers are relevant to many cancer including that of blood, prostate, gastric, colon, breast, ovarian, etc. (Ref.), in this study the treatment was first applied on colorectal cancer patients with liver metastasis. Although I do not have yet the details of the study, the outcome of this study seems to be great as the scientists reported that following Maraviroc administration, the tumors in some of the patients disappeared. An example of a PET scan indicating the liver metastasis disappearance is included in this article (Ref.).

The scientific article where the results were published can be found here: http://www.cell.com/cancer-cell/pdf/S1535-6108(16)30087-3.pdf

What is also great about these results is that are based on Maraviroc, a drug that has already received FDA approval for treatment of HIV and has shown little side effects and toxicities even on long term treatment in humans.  https://clinicaltrials.gov/ct2/show/NCT01736813

So what we have here is a drug that alone can lead to reactivation of the immune system in some of the cancer patients and as a result tumor eradication. Until now, the idea that CCR5 blockers can reactivate the immune system and kill cancer in humans was a theory only. But with the results from Hidelberg, this is now a fact. Maraviroc is FDA approved and the side effects are limited. The drug is administrated orally. As further discussed bellow, it can be bought at online pharmacies. The only drawback is that the cost is relatively high (2000 euro /month) but if used with other drugs such as Ketoconazole, the required dose will be half (Ref.) so the cost may be around 1000 euro/month.

Note that, genetic evidence exists that links CCL5 (and thus CCR5 ) with numerous human diseases, such as liver fibrosis, coronary artery disease, multiple sclerosis, rheumatoid arthritis, asthma and atopy, atopic eczema/dermatitis syndrome, atopic dermatitis, hepatitis C virus infection, heart graft rejection and systemic lupus erythematosus (Ref.).

Mechanism:

Maraviroc blocks a microscopic doorway – the CCR5 receptor – which HIV uses to enter and infect human cells. This is why Maraviroc is highly relevant as an anti HIV drug.

In cancer, the relevant of CCR5 receptors is different:

The tumor microenvironment is composed of stromal and inflammatory cells that are recruited and/or locally induced to proliferate or differentiate by tumor cells or by normal cells “educated” by tumor cells. They communicate directly through cell-cell contact but also indirectly through paracrine signals predominantly constituted by cytokines and chemokines. (Ref.) Thus, chemokines, have a fundamental role not only in inflammation and immune surveillance but also in cancer progression.

CCL5, the chemokine that binds CCR5  is one of the very relevant chemokine in cancer progression, and is often detected in neoplastic tissues. Large amounts of CCL5 (that bind to CCR5 receptors) are produced by T cells present in the vicinity of tumors and it is known to be strongly associated with the tumor progression (Ref.). CCL5 plays an active role in recruiting a variety of leukocytes into inflammatory sites including T cells, macrophages, eosinophils and basophils.

CCL5/CCR5 interactions may favor tumor development in multiple ways: acting as growth factors, stimulating angiogenesis, modulating the extracellular matrix, inducing the recruitment of additional stromal and inflammatory cells, and taking part in immune evasion mechanisms. This is done via e.g. activation of IKKalpha/beta, NF-κB, Jak-STAT, MAPK/ERK signaling pathway, inducing the mTOR pathway (Ref.)

Another relevant mechanism related to CCL5/CCR5 interaction is specifically connected to the Macrophages:

Macrophages derived from monocyte precursors undergo specific differentiation depending on the local tissue environment. They respond to environmental cues within tissues such as damaged cells, activated lymphocytes, or microbial products, to differentiate into distinct functional phenotypes. The M1 macrophage phenotype is characterized by the production of high levels of pro-inflammatory cytokines, an ability to mediate resistance to pathogens, strong microbicidal properties, high production of reactive nitrogen and oxygen intermediates, and promotion of Th1 responses. In contrast, M2 macrophages are characterized by their involvement in parasite control, tissue remodeling, immune regulation, tumor promotion and efficient phagocytic activity. (Ref.)

CCL5 is bound by the chemokine receptor CCR5, which is expressed on the surface of macrophages. Antagonist of CCL5 receptors is strongly associated with a shift of  macrophage subsets to a pro-inflammatory phenotype, i.e. a shift from M2 to M1 (Ref.). Therefore, blockage of CCR5 by maraviroc is expected to lead to the reprogramming of tumor-associated macrophages, which then destroy the cancer cells, rather than promoting tumor growth.

Indeed, this is what has been observed in the recent clinical trial from Heidleberg (Ref.).

The results suggest that monocyte/macrophage subsets differentially contribute to progression and resolution of tumors and that this balance can be successfully modulated by chemokine antagonists.

Note: another drug that may be used to modulate macrophages by inhibiting M2 is Plerixafor and has been discussed earlier on this website https://www.cancertreatmentsresearch.com/?p=265

Synergies:

Statins: CCR5 receptors, are located on cholesterol-rich ‘lipid rafts’ within cell membranes. Statins may reduce lipid raft numbers, potentially altering CCR5 availability and efficacy. http://hivclinic.ca/main/drugs_interact_files/CCR5-int.pdf

Administration and Dose:

The drug administrated in the clinical trial was Maraviroc at 300mg 2x/day https://clinicaltrials.gov/ct2/show/NCT01736813

However, with Ketokonazole it has to be taken at 150mg, 2x/day https://aidsinfo.nih.gov/drugs/408/maraviroc/0/professional

Source:

Maraviroc, 60 Tabs 300mg $2147.74 http://www.buy-pharma.co/Celsentri-p-2560.html

Safety and Side Effects:

According to the clinical trials before becoming an anti HIV drug, the most common side effects reported with twice-daily treatment were cough, pyrexia, upper respiratory tract infections, rash, and dizziness. The most common side effects reported with once-daily dosing were diarrhea, edema, influenza, esophageal candidiasis, sleep disorders, rhinitis, parasomnias, and urinary abnormalities. Nausea, diarrhea, fatigue, and headache were common in Phase 2b/3 trials. (Ref.) Maraviroc may also cause severe liver symptoms.

More about side effects can also be found here http://www.rxlist.com/selzentry-side-effects-drug-center.htm

In contrast to this long list of potential side effects, the Heidelberg trial did not encounter any major issue as suggested by this statement: “The data show that the HIV medication is very well-tolerated” (Ref.)

References:

Tumoral Immune Cell Exploitation in Colorectal Cancer Metastases Can Be Targeted Effectively by Anti-CCR5 Therapy in Cancer Patients http://www.cell.com/cancer-cell/pdf/S1535-6108(16)30087-3.pdf

The immune response influences the clinical course of colorectal cancer (CRC). Analyzing the invasive margin of human CRC liver metastases, we identified a mechanism of immune cell exploitation by tumor cells. While two distinct subsets of myeloid cells induce an influx of T cells into the invasive margin via CXCL9/CXCL10, CCL5 is produced by these T cells and stimulates pro-tumoral effects via CCR5. CCR5 blockade in patient-derived functional in vitro organotypic culture models showed a macrophage repolarization with anti-tumoral effects. These anti-tumoral effects were then confirmed in a phase I trial with a CCR5 antagonist in patients with liver metastases of advanced refractory CRC. Mitigation of tumor-promoting inflammation within the tumor tissue and objective tumor responses in CRC were observed.

Anibamine, a Natural Product CCR5 Antagonist, as a Novel Lead for the Development of Anti Prostate Cancer Agents http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2914538/

Accumulating evidence indicates that the chemokine receptor CCR5 and the chemokine CCL5 may be involved in the proliferation and metastasis of prostate cancer. Consequently, chemokine receptor CCR5 antagonists could potentially act as anti prostate cancer agents. As the first natural product CCR5 antagonist, anibamine provides a novel chemical structural skeleton compared with other known antagonists identified through high-throughput screening. Our studies demonstrate that anibamine produces significant inhibition of prostate cancer cell proliferation at micromolar to submicromolar concentrations as well as suppressing adhesion and invasion of the highly metastatic M12 prostate cancer cell line. Preliminary in vivo studies indicate that anibamine also inhibits prostate tumor growth in mice. These findings indicate that anibamine may prove to be a novel lead compound for the development of prostate cancer therapeutic agents.

The Inflammatory Chemokine CCL5 and Cancer Progression http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3910068/

Until recently, inflammatory chemokines were viewed mainly as indispensable “gate keepers” of immunity and inflammation. However, updated research indicates that cancer cells subvert the normal chemokine system and these molecules and their receptors become important constituents of the tumor microenvironment with very different ways to exert tumor-promoting roles. The CCR5 and the CCL5 ligand have been detected in some hematological malignancies, lymphomas, and a great number of solid tumors, but extensive studies on the role of the CCL5/CCR axis were performed only in a limited number of cancers. This review summarizes updated information on the role of CCL5 and its receptor CCR5 in cancer cell proliferation, metastasis, and the formation of an immunosuppressive microenvironment and highlights the development of newer therapeutic strategies aimed to inhibit the binding of CCL5 to CCR5, to inhibit CCL5 secretion, or to inhibit the interactions among tumor cells and the microenvironment leading to CCL5 secretion.

CCR5 Antagonist Blocks Metastasis of Basal Breast Cancer Cells http://cancerres.aacrjournals.org/content/72/15/3839

The roles of the chemokine CCL5 and its receptor CCR5 in breast cancer progression remain unclear. Here, we conducted microarray analysis on 2,254 human breast cancer specimens and found increased expression of CCL5 and its receptor CCR5, but not CCR3, in the basal and HER-2 genetic subtypes. The subpopulation of human breast cancer cell lines found to express CCR5 displayed a functional response to CCL5. In addition, oncogene transformation induced CCR5 expression, and the subpopulation of cells that expressed functional CCR5 also displayed increased invasiveness. The CCR5 antagonists maraviroc or vicriviroc, developed to block CCR5 HIV coreceptor function, reduced in vitro invasion of basal breast cancer cells without affecting cell proliferation or viability, and maraviroc decreased pulmonary metastasis in a preclinical mouse model of breast cancer. Taken together, our findings provide evidence for the key role of CCL5/CCR5 in the invasiveness of basal breast cancer cells and suggest that CCR5 antagonists may be used as an adjuvant therapy to reduce the risk of metastasis in patients with the basal breast cancer subtype.

The significance of macrophage polarization subtypes for animal models of tissue fibrosis and human fibrotic diseases http://clintransmed.springeropen.com/articles/10.1186/s40169-015-0047-4

The systemic and organ-specific human fibrotic disorders collectively represent one of the most serious health problems world-wide causing a large proportion of the total world population mortality. The molecular pathways involved in their pathogenesis are complex and despite intensive investigations have not been fully elucidated. Whereas chronic inflammatory cell infiltration is universally present in fibrotic lesions, the central role of monocytes and macrophages as regulators of inflammation and fibrosis has only recently become apparent. However, the precise mechanisms involved in the contribution of monocytes/macrophages to the initiation, establishment, or progression of the fibrotic process remain largely unknown. Several monocyte and macrophage subpopulations have been identified, with certain phenotypes promoting inflammation whereas others display profibrotic effects. Given the unmet need for effective treatments for fibroproliferative diseases and the crucial regulatory role of monocyte/macrophage subpopulations in fibrogenesis, the development of therapeutic strategies that target specific monocyte/macrophage subpopulations has become increasingly attractive. We will provide here an overview of the current understanding of the role of monocyte/macrophage phenotype subpopulations in animal models of tissue fibrosis and in various systemic and organ-specific human fibrotic diseases. Furthermore, we will discuss recent approaches to the design of effective anti-fibrotic therapeutic interventions by targeting the phenotypic differences identified between the various monocyte and macrophage subpopulations.

Disclaimer:

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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57 Comments on "Maraviroc: An anti-HIV Drug that Reactivates the Immune System to Fight Cancer"

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ovidiu
Member

After searching for info on maraviroc, it seems the tumor and metastasis reduction is due not only to immunostimulation, but more due to suppression of cancer associated fibroblasts.
Blockade of the chemokine receptor, CCR5, reduces the growth of orthotopically injected colon cancer cells via limiting cancer-associated fibroblast accumulation.
http://www.ncbi.nlm.nih.gov/pubmed/27340784

Also found something more interesting – a cytotoxicty of 78% by a combination of temozolomide + ritonavir + aprepitant, against a glioma cell line.
“We conclude that a remarkable synergy exists between aprepitant and ritonavir”, which may apply not only to glioma cells. This was also proposed part of the CUSP9* protocol.
Antitumor action of temozolomide, ritonavir and aprepitant against human glioma cells.
http://www.ncbi.nlm.nih.gov/pubmed/26603162
In combination with the previously tested temozolomide + macitentan (remarkable results), this could become a new standard for glioma treatment.

Emad
Member

Hi Daniel

today results about my mother
the tumor markers climbed to 938 !!!
it was 450 just before 4 weeks !!?
the Scan showed that nearly every thing is stable like before 3 months , but also there is a very very little new spots on the liver

note : there is a big spot on the liver that are still stable for months , the size of it is 2.5cm , this is the biggest spot in the body

—————
our protocol the past 4 weeks was the same as before , except :-
we run out of DCA the past 2 weeks , but we also added Baicalien (Scute) 5g daily , Mebendazol 600mg daily , and increased the dose of artemisia annua to 10g daily …
————-
another thing , my mother can’t stand easily on her legs due to the neuropathy , its not caused by the DCA it self , but also by the chemo
———–
at last , i have a little question about the liver mets : with this size (2.5cm spot + very little spots) , would it considered a problem ? if not : when it will be a problem ?

thank you so much

madama
Member

hi emad,

are you doing dca in iv or orally?

i hope you ll heal your mother asap

thanks

Emad
Member

orally , just for now

im planning to do IVs next days 🙂

Emad
Member

thank you for your hope

my best wishes for you Madama

anna
Member

Good article, very promising, as not so often can we have a good clinical trial outcome for a drug, which exists already.

Question 1 – would it be good to use it together with gcmaf? to make macrophages more potent?
Question 2 – how long treatment should be, I read something about 8 weeks…
Question 3 – toxicity to liver, we are fighting to make liver again functional after complication after Sirt.

Hanh
Guest

Hello Ann, my husband had the same problem after Sirt just like your husband. Did you do anything to help the liver recovers.
I am so worried, my husband has no energy and starts getting jaundice. I gave him milk thistle, quercetin, lemongrass tea. Did you try maraviroc or Koch therapy (MG)? Artemisinin treatments reduces his pain a lot but I’m afraid the lost of energy means the cancer is growing.
I was looking into cancer ablation (image guided). However, I just read about a young woman died when she was undergone that treatment and they operate out of Mexico. Her medical bill went up to 600K. To find something that works for this disease is so hard.
Any one with experience on liver mets please chime in.
Thank you.

anna
Member

Daniel.
Ad 1. We intend to make TACE with prof Vogl next week if parameters are good enough to proceed. But there is just small issue that we would not know if Maraviroc works or not, I mean is result of TACE or not. But ok I understand your point that the most important is that sth works (unfortunately we have to watch expenses ?).

Pouya
Member

Hi Emad, did you start on MG? i thought that was a part of your plan..
also, Dear D, are you aware of the cost of the treatment at Heidelberg? are they still using Salinomycin too?
thanks in advance.

Emad
Member

Hi pouya

no we didn’t receive MG yet , but its a matter of time until we get it , and sure I will always share our results for all of you

and also we will receive Salinomycin , and I will add 3-BP and Diflunisal after that so I will have a more options in case some of them didn’t work

but my hope is that MG will work and do the job 🙂

my best wishes for you

Pouya
Member

thanks D, I’ve contacted prof Ray and i’m probably going for MG first. now i’m trying to develop a plan B in case MG didn’t work well for us.

madama
Member

hi emad

can you tell from where did you get the dca? and do you know the process and dosage for iv dca?

thanks in advance

madama
Member

hi daniel

thank you for your reply.

i ll order the dca this week and try it.

For the same purpose,do you have a method for preparing iv curcumin but without kolliphor?

i ve read that your two methods ,and both are with kolliphor.

thanks again

Emad
Member

Thank you Daniel for your answer 🙂

other sources I know for DCA :-

http://www.puredca.com
http://www.dcacancer.org

madama
Member

hi daniel

thanks for the reply

but if we start from the extract already,how do we do the iv sol?

in the meantime,do you have any provider of the iv solution without kolliphor as the one i have contacted in germany said i have to come there if i want to buy from them (they do not ship)

madama
Member

i have contacted this one:

http://cfb-eigenherstellung.de/

no i m not ,just want the curcumin in iv form for family member

madama
Member

Hi again,

i m trying to find the way to prepare salinomycin iv ,do you have any method as well for this?

specially with sodium salt

thanks daniel

madama
Member

hello,

anyone can help for the curcumin prep and salynomicin sodium salt administration/preparation for iv?

thanks in advance

madama
Member

hi daniel

i m in location where i can t do this in a clinic,

we can have a nurse who can prepare all this if i can get the instructions and process to do it

thanks

madama
Member

Daniel,

i ve just sent you an email ,please advise

thanks

madama
Member

hi daniel

how come?

don t you see the email adress?

i m using the same since 2/3 years and there is nothing to hide beside protecting everyone privacy

Hanh
Guest

Hi Daniel, if we can raise fund, which clinic do you think have the best promising protocol. Before we were thinking Dayspring with 3-bp but that is not an option anymore. My husband developed ascites, no energy and has abdomen pain most of the time but his oncologist keeps insist on using 5-fu and avastin while his tumor marker still going up. We use tagamet, metformin, curcumin, artemisinin & artesunate, I recently added cyproheptadin, quercetin but I think we needed to do more than that. He has terrible abdomen pain when I added mebendazole so I stop. Is this Maraviroc
medication something we can do it ourselves. His liver is in bad shape after SIRT. If I am the patient it would be much easier but since it is my husband’s life I am so scared of making mistake. I would appreciate every one experience.
Thank you.

anna
Member

Hi Hanh, sorry I didn’t see your post.
That is exactly the same situation like we had. After SIRT first everything was ok, then two months after, markers and liver enzymes started to raise. As we already did è ablation at prof Vogl, our oncologist put fault on all these treatments , that my husband liver is full of scars. But for me all the symptoms were relared to radiation hepatitis.
My husband also developed jaundice, bilirubin was 5, not any treatment could be added.
Very important step in recovering ( now bilirubin is 2,5 still to high but now we are under folfiri which is metabolizedd by liver )was adding cortison ( we used Medrol quite high dose of 50 mg) it took oone month of cortison to calm inflammation) Liver cannot regenrate if inflammated. Little by little it started to get better, but very slowly and honestly they were moments were I thought we will not make it. I stopped all the treatments, I gave only milk thistle – 210 mg per day , Essentiale forte and Hepa merz and also Alpha lipoic acid). but I think it was cortison which made it worked. it was idea of prof Vogl to add it and luckily our oncologist agreed to give it to us There was also a blood clot in liver so injection Clexane was added. it is important that they make MRI to see if there is not a blood clot in liver of your husband because it can make liver stop working.
I am sorry for a mess in my message, but I am very tired but I would like to help you. Can you tell me your last liver enzymes, CRP etc. I think you should insist on cortisone this should make bilirubine falling down. Do not think now about ablation or any other hard treatment, let liver first recover. I know it is hard, but looks the best solution.
I contacted prof from Heidelberg and he told us the same, we have to wait liver works beter.
Now we are dealing with withdrawal of cortisone, we were not sure if liver will start to work without cortisone, we are dealing with general inflammation now, but liver seems to improve slowly. Long term cortisone ike we had made our husband very sick, small viruses made big damage to his organism, but as I told it was I think the only way.
I am not sure it is already fixed but it is better than it was.
if you have any question, let me know.

anna
Member

Hi Hanh, sorry I didn’t see your post.
That is exactly the same situation like we had. After SIRT first everything was ok, then two months after, markers and liver enzymes started to raise. As we already did è ablation at prof Vogl, our oncologist put fault on all these treatments , that my husband liver is full of scars. But for me all the symptoms were relared to radiation hepatitis.
My husband also developed jaundice, bilirubin was 5, not any treatment could be added.
Very important step in recovering ( now bilirubin is 2,5 still to high but now we are under folfiri which is metabolizedd by liver )was adding cortison ( we used Medrol quite high dose of 50 mg) it took oone month of cortison to calm inflammation) Liver cannot regenrate if inflammated. Little by little it started to get better, but very slowly and honestly they were moments were I thought we will not make it. I stopped all the treatments, I gave only milk thistle – 210 mg per day , Essentiale forte and Hepa merz and also Alpha lipoic acid). but I think it was cortison which made it worked. it was idea of prof Vogl to add it and luckily our oncologist agreed to give it to us There was also a blood clot in liver so injection Clexane was added. it is important that they make MRI to see if there is not a blood clot in liver of your husband because it can make liver stop working.
I am sorry for a mess in my message, but I am very tired but I would like to help you. Can you tell me your last liver enzymes, CRP etc. I think you should insist on cortisone this should make bilirubine falling down. Do not think now about ablation or any other hard treatment, let liver first recover. I know it is hard, but looks the best solution.
I contacted prof from Heidelberg and he told us the same, we have to wait liver works beter.
Now we are dealing with withdrawal of cortisone, we were not sure if liver will start to work without cortisone, we are dealing with general inflammation now, but liver seems to improve slowly. Long term cortisone ike we had made our husband very sick, small viruses made big damage to his organism, but as I told it was I think the only way.
I am not sure it is already fixed but it is better than it was.
if you have any question, let me know.

anna
Member

One more thing, I saw you were using just like we did metformin. If I were you Iwould also stop it, it is very toxic for liver, specially for the liver damaged byt SIRT. I will again add metformin when liver will fully recuperate ( means all enzymes within normes) but I will carefully check enzymes after adding metformin.

Hanh
Guest

Hi Ann, thank you for your reply. After reading your reply I asked his doctor for dexamethasone and my husband has been taking it for the last 3 days. I can tell he looks less jaundice, his urine is lighter (before it was so dark almost like brownish, sign of liver not functioning), he can eat a little bit better. I feel like there is hope again. Thank you for taking time to let me know how to reduce liver inflammation.
Did you try Gelum drop? My husband wears a mouth guard at night. In the morning I can smell acid from the piece. After using Gelum Drop (thank to Daniel) for the last 3 days I do not smell acid any more. Hopefully, it does reduce acidity around the tumor thus slow or reverse tumor progression or at least help medications get to the tumor.

Hope for good news for all of us.
Hanh

anna
Member

It is good news Hanh.
Have you maybe idea how to get rid of ascites? We are ready to go to Heidelberg, but as long as we have ascites, no biopsy.
For gelum drops, there is one thing which make me thinking of it is so good. It contains iron, and iron is not good to supplement when we have cancer. Does anyone has here opinion?

Hanh Nguyen
Guest

Hi Ann, my husband’s heart rate had been consistently above 100 for the last 10 months. For the last few days his heart rate has been down to 80s and sometimes even 70s. Maybe Gelum drop does what it claims it does, oxygenate and remove acid lactic. I think both are good. For ascites the liver has to work to produce albumin so the leaking fluid will be stop. I just found some home remedy for removing the fluid. One is to take garlic juice 3 times a day, bitter gourd juice, celery juice. I have no way to see the effect on the abdomen fluid but his leg’s fluid retention has been reduced.
What treatment is your husband going to have at Heidelberg and what is the cost involved if you dont mind sharing. Right now my husband’s situation is improved a bit but I don’t know for how long so I would like to explore other plans.
Your husband has good doctors, my husband’s doctors did not address his liver inflammation after Y90 nor check for blood clot. I still don’t know how to ask them to check for that. Every thing they would contribute to disease’s progression and just chemo if we want treatment. What is your husband’s symptom for blood clot in the liver?
Is your husband’s bilirubin still high? I think sun bathing will be good to help break down bilirubin, my husband does it 30 minutes every day.
Take care.

anna
Member

hi Hanh,

There can be so many reasons for ascites that it is difficult to say what is the problem. I ordered gelum drops, we will see, I hope they will have a good effect.
For the treatment in Heidelberg I will know something more in few weeks, when we see profesor. It will be probably some mix of Maraviroc and immunotherpay drugs, but it depends the biopsy of tumor. I would like to have a biopsy with immunoprofiling, but I am not sure if they will take biopsy due to ascites. We will see and I will describe everything here.
We started from bilirubin 5 now it was one week ago 2,5.
The blood clot was visible on CT, I asked for CT because I thought that jaundice is effect os stone blocking duct in liver, but they found a blood clot. All these research was due to jaundice.

Take care, as soon I know sth more I will write it. Thanks

anna
Member

For us probably reason for ascites were tumors in de belly. We have just receive scans results and it is not only now in the liver but also in the belly and it is possible that these tumors produce liquid.
I expected something beter than that. We will switch to Erbitux now, ans Heidelberg has to wait for some time.

anna
Member

A small update on Maraviroc plus Erbitux.
I am afraid I do not have good news. CEA rised from 120 to 280, what can be rather bad sign.
I will know more after scans and I will update.

Ergin
Member

Hi Ann,
Very sorry to hear that.
Did he get flu or stg like that?It causes big rise in markers as i saw from my mother.
I hope that is because of it.

anna
Member

Yes, he had flu. He had crp 170 now it is 15 after week of antibiotic.
I can understand small rise of cea but from 120 to 280?
I am sorry I do not write too much, I have chronic insomnia for the moment, have just not enough power.
Take care guys!

anna
Member

Hi everyone!
So we had scans today.
It wasn’t good, all the tumors grew back.

So I can state that maraviroc plus Erbitux is surely not a good mix.
We stopped maraviroc temporairly, we will be now on erbitux plus irrinotecan alone.
I will report !

For everyone fighting, good luck. I keep my fingers crossed for you !

Ergin
Member

Hi Ann,
Sorry to hear,and thank you for sharing it with us.

anna
Member

Thank you Daniel for your nice words
Yes, we used some of tips- natural like omega 3, honokiol -we have to be carefull due to liver issue. I will come back to read once again ,maybe will get new inspiration.

Yes, maraviroc (celsentri ) from was Heidelberg.
We will be there again to look for some other options.

Ergin
Member

Hi Ann,
Did you search for phlorizin?
If existing protocol doesnt work,you should look at it.May be you have no time and didnt see it.

Ergin
Member

Hi Ann,
How are you ?
2 months past and i really wonder you,i very hope that there isnt stg wrong..

Helga
Member

Hi Daniel,

I knew this name, Mebendazole was familiar from somewhere. Apparently, from the news. After it proved to be effective against cancer, the company that acquired the exclusive rights to it, increased the price for a single dose from a dollar or so to more than 700 dollars! For a drug that has been in use for 40-50 years against worms! Insane. See this: http://www.news4jax.com/consumer/pinworm-prescription-jumps-from-3-to-up-to-600-a-pill This is for Ergin: https://www.mesotheliomahelp.org/2017/02/mesothelioma-patients-may-someday-use-pinworm-drug-treat-asbestos-cancer-30255/

Here is the story about the price increase: http://moneyweek.com/the-pharma-price-gouging-scandal/ They called Martin Shkreli, the man behind this abomination “the most hated man” in America. Thanks God, people can order it in the US from abroad.