50 replies to this topic

[Logic]

Where's Kim ?

Good Question!

I am supposed to be sending her Mebendazole, but have not got a reply to my PM for around a week!?

[tham]

No reply to mine either.

I noted from her profile that she was online these two days,
but seems to be a bit quiet.

Perhaps she hasn't noticed this thread nor her messages.

[tham]

Arginine fights glioblastoma.


http://clincancerres...17/22/6992.full



" Over-the-Counter Supplement for Brain Cancer ? "

http://www.dailyrx.c...y-target-cancer


http://www.news-medi...ioblastoma.aspx

[Matt]

Fasting Makes Brain Tumors More Vulnerable to Radiation Therapy

http://www.scienceda...20911172308.htm

"Despite the extremely aggressive growth of the type of brain tumor studied, more than twice as many mice that fasted and received radiation therapy survived to the end of the trial period than survived with radiation alone or fasting alone"

[risemystic]

Try mms jim

[tham]

This was Professor's Harn Horng-Jyh's recent reply to my enquiry :

" I am sorry for delay repsonse your mail. About my BP/wafer aganist GBM, it is on Pre-IND
study now. This include PK, tox, dose range finding so on so forth. It is not allowed to
conduct clinic trial on Taiwan or USA except you finish Pre-IND and file IND from FDA and
TFDA. We expect to finish Pre-IND on May, 2012 then apply for clinical trial from FDA.
Hope can hook up patient at the end of 2012. Finally, I am grateful you post Everfront
(EF Biotiech) work on internet. "


Apparently, and unfortunately, Taiwan's FDA has a similar drug procurement protocol
to the US's FDA's silly, cumbersome, time-wasting, long-winded, red-tape tangled
and extremely expensive protocol.

It costs no less the US $450 million and ten years of three phases of trials
to bring out a simple drug to the US market currently.


How could a compound (Bdph) taken from a herb (Angelica), used for
thousands of years, be more toxic than a poorly effective drug (carmustine)
which is actually a crude chemical warfare weapon ?


Carmustine = Nitrogen mustard = World War 1 poison gas.


I think your best chance and option left now is Stanislaw Burzynski's antineoplastons.

Edited by tham, 15 September 2012 - 08:22 PM.

[dblch]

Thanks everyone for the suggestions. I am having a naturopath look into some of the chinese herbs in hopes that they might be a little cheaper through her. Does anyone know the most cost effective to make liposomal CoQ10?

[mikey]

Thanks everyone for the suggestions. I am having a naturopath look into some of the chinese herbs in hopes that they might be a little cheaper through her. Does anyone know the most cost effective to make liposomal CoQ10?

This is the most cost effective way to make liposomal vitamin C that I've seen - http://www.michaelmo...eLiposomalC.pdf.

But vitamin C is water soluble.

Since CoQ10 is oil-soluble, I expect that the process is different.

Maybe one of the chemists here can comment on how to adapt it to make liposomal CoQ10.

[tham]

Frankly, I'm not exactly keen about cimetidine (Tagamet) as an anticancer drug.

1. Its anticancer properties are not particularly impressive.

2. As an antacid, it will reduce your absorption of your supplements and other drugs.

3. It inhibits your liver's P450 enzyme and thus interacts with many drugs.

4. It will give you gynecomastia (enlarged breasts) if taken long term.

[tham]

If there is a drug which you should immediately start on now, it is celecoxib (Celebrex).

Most of the NSAIDS have anticancer action, particularly the newer selective COX-2 ones.


However, celecoxib has unique and potent anticancer pathways way beyond COX-2/PGE2
- and this includes p53 and microRNAs.

This is why Celebrex is the most studied of the NSAIDS against cancer. Search Medline
with "celecoxib" and "cancer" and you will turn out some 1,400 studies. Analogs of celecoxib
have been developed in an attempt to enhance its anticancer action.

http://www.ncbi.nlm....ELECOXIB CANCER



Another potent COX-2 NSAID was the famous rofecoxib (Vioxx).

When they took out rofecoxib (Vioxx) from the market after the big public hoo-hah
about its adverse heart effects which was blown way out of proportin, they effectively
took out a potent anticancer drug.

Continuous low-dose chemotherapy plus inhibition of cyclooxygenase-2 as an
antiangiogenic therapy of glioblastoma multiforme.

http://www.ncbi.nlm....ubmed/15565458/





" We found that celecoxib inhibited the proliferation of various glioblastoma cell lines
in vitro much more potently than traditional NSAIDs. In addition, although several
different selective COX-2 inhibitors potently reduced PGE2 levels in these cells,
none of them exerted anti-proliferative effects that were comparable to celecoxib.
The addition of external PGE2 to celecoxib-treated cells did not restore proliferation,
indicating that growth inhibition by celecoxib was not mediated via the blockage of
PGE2 production. "

http://www.landesbio...bt/article/571/



"..... celecoxib was able to exert pronounced pro-apoptotic effects in vitro and in vivo
in the absence of any apparent involvement of COX-2. In fact, newly synthesized close
structural analogs of the celecoxib molecule revealed that it was possible to separate
COX-2 inhibitory function from the ability to trigger apoptosis; for example, the analog
2,5-dimethyl-celecoxib (DMC) has lost COX-2 inhibitory function, yet exerts increased
cytotoxic potency. "

http://www.ncbi.nlm....pubmed/20879982



The nonsteroidal anti-inflammatory drug celecoxib suppresses the growth
and induces apoptosis of human glioblastoma cells via the NF-κB pathway.

http://www.ncbi.nlm....ubmed/21847707/



MicroRNAs in Human Malignant Gliomas.

Furthermore, miRNAs also regulate specific signaling pathways, including the
critical core pathways in glioblastoma. As a result, miRNAs have the potential to
affect the responses to molecular-targeted therapies. More recent studies have
revealed that miRNAs might be associated with cancer stem cell properties,
affecting tumor maintenance and progression. Recent investigation have revealed
that miRNAs are not only biological markers with diagnostic implications, but also
one of the most promising treatment targets in human glioblastoma.

http://www.ncbi.nlm..../pmid/22848219/



Current Progress on Understanding MicroRNAs in Glioblastoma Multiforme.

http://www.ncbi.nlm....pubmed/22893786



MicroRNA targeting as a therapeutic strategy against glioma.

http://www.ncbi.nlm....pubmed/22934848



microRNA expression pattern and its alteration following celecoxib
intervention in human colorectal cancer.

http://www.ncbi.nlm....cles/PMC3438602


Cancer chemoprevention by targeting the epigenome.

http://www.ncbi.nlm....pubmed/21158707



COX-2 regulates the proliferation of glioma stem like cells.

http://www.ncbi.nlm....pubmed/21763744



Enhanced sensitivity of celecoxib in human glioblastoma cells: Induction
of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy.


" Our findings reveal that p53 increases human glioblastoma sensitivity to celecoxib.
Celecoxib inhibits glioblastoma cell viability by induction of DNA damage, leading to
p53-dependent G1 cell cycle arrest and p53-dependent autophagy, but not apoptosis.

http://www.molecular...m/content/8//66



" Low-dose continuous temozolomide in combination with celecoxib seems
to have activity in recurrent glioblastoma without relevant toxicity. "

Continuous low-dose temozolomide and celecoxib in recurrent glioblastoma.

http://www.ncbi.nlm....pubmed/20446016



Far-distant metastases along the CSF pathway of glioblastoma multiforme
during continuous low-dose chemotherapy with temozolomide and celecoxib.

http://www.ncbi.nlm....pubmed/20306105

Edited by tham, 23 September 2012 - 08:35 PM.

[tham]

Double post.

Edited by tham, 23 September 2012 - 08:33 PM.

[tham]

The celecoxib analog, 2,5-Dimethyl-Celecoxib (DMC).


Antiangiogenic Activities of 2,5-Dimethyl-Celecoxib on the Tumor Vasculature


" We present evidence that celecoxib and DMC are able to down-regulate
the expression of survivin, an anti-apoptotic protein that is highly expressed
in tumor cells and known to confer resistance of such cells to anti-cancer
treatments. Suppression of survivin is specific to these two drugs, as other
coxibs (valdecoxib, rofecoxib) or traditional NSAIDs (flurbiprofen, indomethacin,
sulindac) do not affect survivin expression at similar concentrations. "

" Remarkably, these effects are not restricted to in vitro conditions, but also
take place in tumors from drug-treated animals, where both drugs similarly
repress survivin, induce apoptosis, and inhibit tumor growth in vivo. "


http://mct.aacrjourn...nt/9/3/631.full

[tham]

Show your doctor the above studies and get him to prescrible you Celebrex.

If he will not, this is where I usually order my drugs. They have both originals
and Indian generics. They trade in pounds Sterling.

http://www.unitedpha...507&cat=&page=1

http://www.unitedpha...841&cat=&page=1


They are based in Hongkong.



This was their former "UK" site. Be aware that these guys are likely to be
hounded by the authorities for selling prescription drugs online and would thus
be forced to change their websites every now and then.

http://www.unitedpharmacies-uk.com/




Their "US-based" site, where they trade in US dollars.

http://www.unitedpharmacies.com



This site looks similar and likely belongs to them as well. They don't
have the generic Celebrex, though.

https://secure.pharmacygeoff.co.uk



The standard dosage of celecoxib in cancer is 800 mg daily, single dose.

To reduce the incidence of adverse effects on your heart and kidneys, you
could try 400 mg every other day, single dose.


Start with 100 mg or 200 mg for the first week in case there are allergies or
any kind of drug reaction.

Edited by tham, 23 September 2012 - 09:25 PM.

[Logic]

Very interesting info Tham. Besides potentially helping Kim, (She very quiet??) its good to have it in one place and specific to the condition.

[joelcairo]

FWIW, Celebrex is the one and only drug recommended to me by my oncologist to prevent recurrence. That and vitamin D are the only adjuvant therapies that have managed to break through his skepticism.

In addition to inhibiting COX-2, it also inhibits VEGF, STAT3 activation, IGF-1 receptor signaling, and HIF-1 expression. These are all good things. They are probably interrelated in complex ways.

It also extends mean and maximum lifespan in c. elegans, by about a third.
http://www.ncbi.nlm....les/PMC3094508/

Edited by joelcairo, 24 September 2012 - 05:57 PM.

[Logic]

Does anyone have any contact details for Kim?
I want to get Mebendazole to her so plz PM me if you do.

[tham]

FWIW, Celebrex is the one and only drug recommended to me by my oncologist to prevent recurrence. That and vitamin D are the only adjuvant therapies that have managed to break through his skepticism.

In addition to inhibiting COX-2, it also inhibits VEGF, STAT3 activation, IGF-1 receptor signaling, and HIF-1 expression. These are all good things. They are probably interrelated in complex ways.

It also extends mean and maximum lifespan in c. elegans, by about a third.


http://www.ncbi.nlm....les/PMC3094508/

That is a very groundbreaking study. I didn't know that celecoxib had
life extension properties, albeit in this tiny roundworm so far.

A lack of IGF-1 is also the reason the Laron dwarfs of Ecuador don't get cancer.

http://www.dailymail...d-key-cure.html

http://www.scientifi...ene-in-dwarfism


If so, then IGF-1 would appear to be the key to the ultimate goal of both preventing
cancer and extending lifespan, unlike telomerase which is a double-edged sword.


" The rate of age-associated motor activity decline has been shown to be a
prominent predictor of lifespan as well as a great physiological parameter of
animals’ healthiness (Hsu et al. 2009). "

http://www.ncbi.nlm....les/PMC3094508/



Identification by machine vision of the rate of motor activity decline
as a lifespan predictor in C. elegans.

http://www.ncbi.nlm....les/PMC2747634/



I have several 200 mg capsules of Celebrex in my office drawer.
I think I'll start off with half a capsule (100 mg) twice a week.


Celecoxib is also highly effective for fevers. When I had that prolonged fever of 102 F
last November which hardly went down after numerous paracetamol doses, half a
200 mg Celebrex capsule dropped it quickly to a normal 98.4 F.

[tham]

Kim -

DMC (2,5-dimethyl-celecoxib) was synthesized by these USC researchers.

Contact Florence Hofman for more information on it.

http://keckfac.usc.e....php?person=468


USC researchers identify strong new anti-cancer compound

http://theweekly.usc...recordnum=16491


Calcium-activated endoplasmic reticulum stress as a major component of tumor cell
death induced by 2,5-dimethyl-celecoxib, a non-coxib analogue of celecoxib


http://mct.aacrjourn...t/6/4/1262.full


Dimethyl-Celecoxib (DMC), a derivative of celecoxib that lacks cyclooxygenase-2
Inhibitory function, potently mimics the anti-tumor effects of celecoxib on burkitt’s
lymphoma in vitro and in vivo

http://www.landesbio...t/article/1699/

[joelcairo]

But the main benefit of this analogue seems to be fewer side effects resulting from COX-2 inhibition, not a stronger cancer-fighting effect. The side effects of Celebrex are already quite minor. At cancer-therapeutic doses (600-800 mg/day) there can be cardiac risks after several years of use, but this seems inconsequential compared with the immediate threat from malignant cancer.

[1kgcoffee]

How are things Kim? You're probably very busy & stressed, but if you can find the time I'm sure many people are curious. What does your current regimen look like after this flood of suggestions?

[tham]

As posted in the Neurofibromatosis 2 thread below, these activate merlin :

Curcumin
Sodium valproate

Combine the above with pterostilbene, which penetrates the blood-brain barrier far better
than resveratrol, to knock down the rest of the downstream components.



Merlin Is a Potent Inhibitor of Glioma Growth


" ..... merlin reexpression inhibits glioma cell proliferation and promotes apoptosis in vivo. "

" ..... merlin is a potent inhibitor of high-grade human glioma. "


In the present study, we show, for the first time, that merlin expression is dramatically
reduced in high-grade human malignant gliomas. Furthermore, reexpression of merlin
inhibits the growth of human glioma cells in vitro and in vivo, whereas NF2 knockdown
promotes glioma growth in vivo.

The demonstration that merlin is a critical negative regulator of glioma growth coupled
with the identification of novel downstream effectors will provide new targets for the
development of future brain tumor treatments.


" Together, we found a 93% concordance between loss of merlin RNA and protein
expression in these GBM tumors ..... merlin expression was absent in 27.4%
of the GBM tumors. Interestingly, we did not observe any reduction in merlin
expression in anaplastic astrocytoma (WHO grade 3 tumors), suggesting that
loss of merlin is associated with grade 4 glioma (GBM). "


http://cancerres.aac...68/14/5733.full






Neurofibromatosis Type 2 Tumor Suppressor Protein, NF2, Induces
Proteasome-Mediated Degradation of JC Virus T-Antigen in Human Glioblastoma.

http://www.plosone.o...al.pone.0053447


Merlin/Neurofibromatosis Type 2 Suppresses Growth by Inhibiting the
Activation of Ras and Rac.

http://cancerres.aac...t/67/2/520.long



Moesin-ezrin-radixin-like protein (merlin) mediates protein interacting with the carboxyl
terminus-1 (PICT-1)-induced growth inhibition of glioblastoma cells in the nucleus.

http://www.ncbi.nlm....ubmed/21167305/



Critical Role of PICT-1, a Tumor Suppressor Candidate, in Phosphatidylinositol
3,4,5-Trisphosphate Signals and Tumorigenic Transformation

http://www.molbiolce...17/11/4888.long