Wednesday, 28 February 2018

One sided mobility issues

Hi all
I am relatively new to this blog and submitted my first post two days ago titled my daughters GBM.
She had a recurrence in September 17 and has remained stable since starting on some of the medications that i mentioned.
Mentally she seems well, no headaches or nausea, but has drastically deteriorated in her left side mobility.
Has anybody experienced this symptom, and if so are you able to shed any light on this condition.
Any help, greatly appreciated.

General question about supplements and interactions

Hey all, thanks for creating and maintaining this fantastic forum for patient-driven protocol development.  I wish I'd found this a year ago when my partner was first diagnosed with GBM.  I definitely would have pushed for adjuvant complementary therapies during the initial treatment phase (Stupp protocol plus Optune).  My partner was first diagnosed in Jan 2017 and the first recurrence showed up last month.  Two surgeries, two gross total resections.  The recovery from the first was fairly smooth, but this one has been rough.

I'm getting some pushback from doctors about using botanical extracts, and I'd like to know how people here handle that sort of thing.  The complaints are that these extracts are not standardized and poorly regulated, so varying dosages, contaminants, or even unknown active ingredients might cause side effects or unexpected interactions with other treatments.  A vascular specialist said he’s seen a lot of weird things happen with supplements, and our hematologist agreed.  My partner has a gnarly blood clot that requires intervention, which is why those doctors are involved.  For what it’s worth, our oncologist didn’t raise any of those concerns.

At my insistence, we’re crafting a custom treatment protocol for the recurrence.  Monotherapies and control arms make clinical trials less interesting to us.  We started CCNU and pembrolizumab last week.  Our oncologist is conservative with advice but is willing to let us try whatever is available.  I’ve been looking to add other treatment modalities through OTC supplements.  I got my partner on Vitamin D and calcium right away (not sure why every cancer patient isn’t put on these immediately), and I have melatonin and PSK ready to go.  I’m also strongly considering curcumin, ECGC, boswellia, THC/CBD, and lipoic acid.

How do people here deal with the sorts of concerns raised by these doctors?  Do you find that weird side effects and interactions are rare, or are they common but just worth the risk at this point?  Does everyone end up just ignoring some doctors sometimes?


Tuesday, 27 February 2018

My daughters GBM

Hi Stephen
Thank you for adding me to the authors list, the information available to all and from all is absolutely invaluable to everyone having to deal with this disease under the current medical regime.
My daughter was diagnosed while living in London in 2016.
She was 26 at the time and 22 weeks pregnant.
It was a large Bi frontal tumor, IDH1 mutation and Methylated 25%.
They completed a partial resection/debulking at the Royal London Hospital, but did not remove the majority of the tumor due to safety risks as they seen this at time.
After a month of recovery, we brought her home to Australia and made arrangements for her to undergo further surgery with a specialist Neurosurgeon in Sydney.
This was a lot more successful with 99% of remaining tumor removed.
Radiation and chemo had to be delayed for almost 2 months until her unborn child had developed sufficiently to be delivered by C section.
This also went well, and she started radiation and standard chemo (Temodar) in early December 2016.
She followed a few alternate treatments from early January 2017 including a vaccine clinical trial in Buffalo NY, followed by Hypothermia treatments in Germany before returning home to Australia in May 2017.
MRI's showed little if any progression up until August, and anything her surgeon could see he believed was residual from the radiation.
Her last MRI at that time was August 7th, which was supposedly still good, and by September 20 she was admitted to hospital with migraines and a temperature.
The following MRI and CT scan showed there was significant disease progression and oedema.
In October 17 i returned to the United States looking for a clinical trial that she may be eligible for.
It became more of a risk for her to undertake a long haul flight, so at the advice of every medical professional was that she start a maintenance treatment program of PCV (without Vincristine) and Avastin.
During this period, like many of you readers, we found the Ben William's story, and as we were not given any options that presented any hope, we have embarked on the same voyage as the followers on this blog.
She had her first standard Avastin treatment on November 14th followed by standard dose of Lomustine on November 20.
Her platelets and neutrophils went into free fall, requiring several platelet transfusions, and was unable to have Lomustine again (50% dose) for another 9 weeks, she continued on avastin at 3 weekly intervals.
As of January 15, i managed to persuade her oncologist to prescribe the Low dose avasin and i introduced the ACE inhibitor Trandolapril.
She is due again this Monday for the lower dose Lumustine.
The other prescription drugs that i have introduced since November are as follows;
20/11/17 Metformin 500mg twice daily
12/12/17  Tamoxifen 160mg daily split x 3 time a day
15/12/17 Low dose Naltrexone 4.5mg at night
15/12/17 Melatonin 20mg at night
15/12/17 Trandolapril 4mg morning
9/1/18 Celebrex 200mg daily (waited for her stop Dex)
17/1/18 Accutane 140mg daily split x 3 times a day 2 weeks on and 1 week off
19/1/18 Verapamil 480mg daily split morning and afternoon week of chemo only
Introducing Antabuse 400mg daily this Thursday prior to chemo next Monday.
We have been doing MRI's monthly since December 5 (at our own expense)
The last 3 MRI's have shown it as stable, no further disease progression.
My real concern presently is she has lost the majority of mobility in her left hand side, her left shoulder is drooping and her difficulty in walking is getting worse.
When the tumor reoccurred it came back in the ventricles, but she is mentally sharp without any headache or nausea. Has anybody else experienced the same symptom?
Can you tell me how people best target Disulfiram around chemo time (dosages) rather than daily dosages.
Her next MRI is on Monday 5th March
Kind Regards

Sunday, 25 February 2018

Strengthening the effect of CCNU + TMZ

My mom will soon take next course of Lomustine + 5 days of Temozolomide.

To enhance the effect of this combination only these days we want to take also:

1. Disulfiram 500 mg + Copper 4mg + DHA 1200mg / day
2. Verapamil 300-400 mg / day (doses of 40 mg every few hours, so that blood pressure does not go down much)
3. Curcumin Longvida 2000mg, EGCg 2000mg / day
4. Alfacalcidol 2 mg / day
According to this study:
Autophagy enhancement contributes to the synergistic effect of vitamin D in temozolomide-based glioblastoma chemotherapy.

Are there any other ideas that can enhance the effect? I have not forgotten anything?
Since my mother takes Lomustine and Temozolomide according to the Ceteg trial every 42 days, I do not want to miss anything.

In addition to these additives our main cocktail includes:
1. Delagil 300 mg / day
2. Bevacizumab 7,5mg/kg/3weeks
2. Sirolimus 2 mg / day (possibly, it will be reduced to 1 mg because of Varapamil)
3. Telmisartan 80 mg (will be canceled for this period because of Verapamil)
4. DCA + caffeine (will be canceled for this period because of Disulfiram)
5. Inhalation with perillic alcohol (will be canceled for this period because of Disulfiram).
    - After Disulfiram, when we can start inhalation again? Probably need a break.
    - Perhaps, for the effect of Disulfiram it is necessary to take it constantly, and not only in the days of Lomustine + Temozolomide? Perhaps, Disulfiram will not have an effect only in these 6 days?

I also found this research:
Lithium enhances the antitumour effect of temozolomide against TP53 wild-type glioblastoma cells via NFAT1/FasL signalling.
"Temozolomide combined with low-dose Li induces TP53wt glioma cell death via NFAT1/FasL signalling. This represents a potential therapeutic strategy for TP53wt glioma treatment."

However, I can not understand is the wild type TP53 our case?

Saturday, 24 February 2018

Perillyl alcohol. Full information about the treatment.

I've been in contact with dr. Clóvis Orlando, who is one of the main researchers in the treatment of perillic alcohol in Brazil. Email:
He was very kind, consulted us and wrote out a prescription for the purchase of  a finished solution in the Italian pharmacy in the city of Brescia. According to this recipe, I went to the pharmacy and bought a finished solution.
The finished solution is stored at a temperature of 2 to 8 degrees Celsius, in a yellow glass bottle.

The composition of 1 bottle:
Ethyl alcohol 96% - 45 g., Glycerin - 45 g., Perillic alcohol 96% - 10 g.
How to use:
Add to the inhaler 3 ml of mineral water PH>7. Then add 23 drops of the finished solution.
Inhaler (nebulizer) needs to be compressor. Not ultrasonic! Breathe through the nose. So repeat 4 times a day, every 6 hours.
You will need to choose a nebulizer with such performance that the procedure does not take more than 15 minutes. Now we already are experiencing the second nebulizer, so as the first worked too slowly and procedure borrowed 25 minutes.

1. We specifically bought an inhaler with a nozzle for the nose. I sent the video to the doctor and he said I could use this nozzle (see photo). So much more convenient! Unpleasant sensations - NO. The solution has a pleasant smell of lemon! We did not expect, but the procedure is quite pleasant. We've been doing this for a week.

2. The doctor recommended that we start a ketogenic diet! This is due to this research:
"Efficacy of a ketogenic diet with concomitant intranasal perillyl alcohol as a novel strategy for the therapy of recurrent glioblastoma."

In Stephen's library you can find a lot of documents on perillol alcohol studies with glioblastoma.
In the photo, you can see the perillyl alcohol and the finished solution that I bought on the prescription by dr. Clóvis Orlando.

Thursday, 22 February 2018

My father has GBM - What should he take?

My father has GBM, 71 years old from Israel.

Right now he is going to finish radiation, and taking with it TMZ. (protocol)

He is also taking this supplements

1. PSP (Psk)
3. Melatonin 
4. Boswellia 
5. Longvida (Curcumin) 
He can’t use celebrex  ince medical problems.
Any other suggestions what to do? Add something? Remove?
Any idea will be great! any tip will be very appreciated  !

Thank you very much!


Friday, 16 February 2018

Stable MRI!

I had a stable MRI on Monday. The doctors were nervous because I’ve had no follow up treatments since surgery on Nov. 10. A relief, for sure. It is a grade 3 AA.


Wednesday, 14 February 2018

DNX-2401 oncolytic adenovirus phase 1 trial results

Phase I Study of DNX-2401 (Delta-24-RGD) Oncolytic Adenovirus: Replication and Immunotherapeutic Effects in Recurrent Malignant Glioma (click here for abstract)

I've uploaded the full PDF to the Brain Tumor Library -> 1. Therapies - human studies -> DNX-2401

In group A, 5 out of 25 patients (20%) lived for at least 3 years post-injection of DNX-2401, and three of these (12%) had dramatic responses (at least 95% reduction in cross-sectional area of enhancing tumor) and at least three years of progression-free survival.

This therapy is currently being tested in combination with pembrolizumab (anti-PD-1).

Need recommendations for consulting for CCNU+Temozolomide for my mom

Hi folks,

My mother is a GBM patient who was diagnosed in September. Her GBM is IDH1/IDH2 -ve, is methylated and she almost had a complete resection. She has completed her 6 weeks of radio/chemotherapy and has complete 2 cycles of 5/23 temozolomide. The following study about using a combination of CCNU(Lomustine) + Temozolomide for methylated GBMs has had me interested for quite a while now:

I wish to switch to the CCNU + Temozolomide cycles for my mom since this protocol, I see it brings about a significant improvement in life expectancy for methylated GBM patients.

However, when I brought this up to my oncologist, I received quite some discouragement on doing this protocol because he said it wasn't global standard of care, which is why I began with the usual temozolomide cycles. I recently got to know that this is almost standard treatment given by oncologists in Germany with methylated GBMs.

I reached out to several oncologists in Germany to consult on this protocol via skype/call, but they refused to do so since it is a toxic therapy and they don't want to do it from distance.

I'm stuck. I probably know this protocol will definitely help improve my mom's life expectancy but I don't have an oncologist to do this protocol under.

My questions

- Can somebody with a good oncologist/hospital in/outside Germany which can consult me on skype/call for this chemotherapy protocol? It shall be of great help for me.

- If you don't know of one, would you recommend switching to the Lomustine+Temozolomide cycles by myself? I don't really want to self medicate since I don't know the answers to the following questions:

a. Whether it is okay to switch from temozolomide to temozolomide+lomustine cycles
b. What are the possible side effects that can happen with this chemotherapy regime and how to tackle them(Low blood counts, nausea, weakness, headache etc)
c. How many more cycles of Lomustine+Temozolomide cycles should I really do, and how should I dose them.
d. Reactions with the supplements that my mom already is on.

I really look forward to your response.

Dabrafenib and trametinib in BRAFV600E mutated glioma.

I started looking for information about Trametinib and found encouraging information about the treatment of BRAFV600E mutant tumors with a combination of Dabrafenib and trametinib.

"BRAF V600E mutations have been successfully treated with targeted therapy in melanoma, non–small cell lung cancer, and thyroid cancer. Interestingly, these mutations have also been identified in a subset of pediatric and adult brain tumors, with several cases reportedly responding to targeted therapy. However, these reports have been limited to single-agent BRAF inhibitor therapy and recurrent disease. Herein, we report dramatic clinical and radiographic responses to combination dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor) in 2 adults with high-grade gliomas (HGGs), with 1 patient treated in the first-line setting. These observations, together with prior case reports, advocate for routine screening of BRAF point mutations in adult HGGs, and suggest that treatment with dual-targeted therapy, even in newly diagnosed cases, is safe and effective."

"BRAFV600E mutations have been identified in a number of glioma subtypes, most frequently in pleomorphic xanthoastrocytoma, ganglioglioma, pilocytic astrocytoma, and epithelioid glioblastoma. Although the development of BRAF inhibitors has dramatically improved the clinical outcome for patients with BRAFV600E mutant tumors, resistance develops in a majority of patients due to reactivation of the MAPK pathway. Addition of MEK inhibition to BRAF inhibition improves survival. Here we report successful treatment of two patients with BRAFV600E mutant pleomorphic xanthoastrocytoma using the BRAF inhibitor dabrafenib in combination with the MEK inhibitor trametinib."

"A phase I/II clinical trial suggests that dabrafenib shrinks or stabilizes low-grade gliomas in children with the BRAF V600E mutation. Objective, durable responses occurred in 38% of patients, and the side effects were less severe than with chemotherapy. The researchers have started a second trial for patients with glioma and other BRAF-mutant tumor types, this time evaluating dabrafenib combined with trametinib."

To determine which dose of Trametinib can be tolerated and effective, for my mother who does not have the BRAF mutation, I began to look for reports on the treatment of patients. I found two such reports. Unfortunately the articles are paid:

Have you seen information about the used doses of trametinib in these reports and clinical trial?

I also found a pediatric clinical trial:
But here too, unfortunately, no dose is indicated.

In this studies, not related to the brain, such doses are suggested:
Dabrafenib is a 150 mg twice daily capsule administered orally on a continuous basis.
Trametinib is a 2 mg once daily tablet administered orally on a continuous basis.
Trametinib Dose-Escalation: Trametinib is administered orally once daily (OD) under fasting conditions. The starting dose of trametinib (0.0125 milligram per kilogram per dose [mg/kg/dose]) is 50% of the recommended fixed dose in adults (2 mg OD). The second dose level (0.025 mg/kg) is equivalent to the recommended dose in adults (2 mg PO daily). The third dose level (0.040 mg/kg) is equivalent to the maximum tolerated dose [MTD] in adults (3 mg PO daily).

Tuesday, 13 February 2018

IDH1 R132H Mutation Enhances Cell Migration by Activating AKT-mTOR Signaling Pathway, but Sensitizes Cells to 5-FU Treatment as NADPH and GSH Are Reduced!po=0.595238
Has this been shared here yet?

The AKT/mTor pathway is related to glucose metabolism. 5- Fu is the chemo ancient used in the Tocagen trials which have had complete responses in all IDH1 patients. It’s probably safe to assume that these patients had IDH1 mutations.

It is also interested to me because I’ve been in contact with a number of IDH1 mut patients who are having good success with a keto diet. It was been a little counter intuitive since it’s said that IDHmut tumours use glutamine as their metabolic preference. I have read that rather than using glutamine to profilerate perhaps they use it to invade surrounding cells but this seems to have lost out in favourite of using it for their metabolism.


Saturday, 10 February 2018

Newly diagnosed family member hoping for some clarifications

My name is Ashley. My mom was diagnosed with GBM unmethylated December 2017. She is 54 and healthy with a huge loving family that wants her around longer. She went in for emergent surgery due to headaches/pressure and this is how the tumor was found. They have removed the majority of the tumor. She is half way through radiation/chemo right now. She is essentially doing great as she has only hair loss and fatigue at the moment with some cognitive delays at time. I have researched extensively Ben Williams info, the Musella foundation, articles, journals etc. to help find the best treatments. Right now she is on these supplements:
fish oil 3g
melatonin 20mg
PSK trying for 3g
Genistein 125mg
Curcumin 4g
green tea (one-two cups a day)
Boswellia 1000mg but will be going up to 4200mg
Resveratrol 100mg/kg roughly 6000mg
Silibinin 420mg

celebrex 200mg  BID (recently just started)
Metformin 2000mg (will start soon-introducing drugs one at a time)
Disulfiram (500mg on chemo days with 250 on non chemo days-4mg copper also with this)-starting soon
Aralen (chloroquinine) 150mg BID --starting soon
Doxycycline 100mg BID-unsure about starting this? (this was recommended by Ben but I just haven't seen many recent trials using this)

My biggest question is how long do we have our family members take this? Is it every day or on just chemo days? There isn't great detail on how long people should be taking these.


2016 Classification of Diffuse Gliomas

This is a handy diagram showing the current (2016) classification of diffuse gliomas. I snipped it from Chapter 6. Molecular Classification of Gliomas (Kenta Masui et al) from the Handbook of Clinical Neurology, volume 134 (2016) edited by Mitchel Berger and Michael Weller.

Friday, 9 February 2018

leucine restriction for IDH1mut?

Hi all,

This article here says that leucine is an activator of GLUD2.

This is the article they sited:

Leucine is an essential amino acid, which means we must eat it in order to get it. The first article seems to say that leucine is stored in IDH1 mutant gliomas…but I read another article that this depends on the concentrations of ADP and L-Leucine — which implies they can be diluted. Is there an ADP inhibitor? (An initial google search seems to say there is but I'm not sure how they will impact the brain or health in general. I'm going to search that when I have more time.)


Thursday, 8 February 2018

Do statins, ACE inhibitors or sartans improve outcome in primary glioblastoma?

This is a new paper (click here for abstract) brought to us by some of the same authors who earlier produced:

Does Valproic Acid or Levetiracetam Improve Survival in Glioblastoma? A Pooled Analysis of Prospective Clinical Trials in Newly Diagnosed Glioblastoma

The group concluded:

"This secondary analysis of two large glioblastoma trials thus was unable to detect evidence for an association of the use of statins, ACEI or sartans with outcome in patients with newly diagnosed glioblastoma."

As with the previous study, there are some important caveats.  Some of the most intriguing data supporting the potential for angiotensin system blockers was in combination with bevacizumab:

Effect of angiotensin system inhibitors on survival in newly diagnosed glioma patients and recurrent glioblastoma patients receiving chemotherapy and/or bevacizumab

It would have been interesting to look at outcomes in those using/not using ACE inhibitors or sartans in combination with bevacizumab, for example in the Avaglio and RTOG-0825 trials.

Angiotensin-II has been shown to increase tumor-promoting macrophages in preclinical models:

and these tumor-infiltrating myeloid cells may play a significant role in resistance to anti-VEGF therapies such as bevacizumab.

Monday, 5 February 2018

Our cocktail and report "OncoDeep". What do you recommend to pay attention to?

Since the tumor after surgery (removed 99%) increased again in the same size (3.5 x 5 x 5 cm) in 3 weeks and the tumor did not decrease after radiotherapy + TMZ, we probably have a very unusual cocktail for the first line:
- cycle 42 days: Avastin (3mg/kg/week) + CCNU (1 day 75mg/m2) + TMZ (5 days 90mg/m2),
- disulfiram 500mg (+Copper 5mg + DHA) and verapamil 200mg only on the days of TMZ + CCNU administration, and 2 days before and after.  I'm not sure, maybe it's advisable to take Disulfiram every day? Otherwise, disulfiram may not start to influence so quickly?
- every day: cloroquine phosphate 250mg, telmisartan 80mg, alfacalcidol 2mcg, oxaloacetate 100mg,  melatonin 20mg, curcumin longvida 2000mg,  Berberine 1000mg, DHA/EPA 1000mg, PSK / PSP 1800mg, Methimazole + T3, R-lipoic acid + hydroxycitrate + ketogenic diet, omeprazole 20mg + DCA 20mg/kg (10mg/kg/BID) + caffeine (2 cups of coffee and 5 cups of black tea) + vitamin B1 200mg

My mother has been responding well to taking DCA + caffeine for a week in the form of black tea and coffee. However, my mom's pulse increased to 90-95 after sleep or rest. To reduce it, we now take 10 mg of propranolol per day. An increase in the pulse may also be caused by the intake of the hormone T3.

Also I consider the addition of a low dose of naltrexone before bed.
We also ordered perillyl alcohol at and expect it soon.

Today we received a report from OncoDNA. The last 3 months I read and search for any information about glioblastoma, but unfortunately I find it difficult to understand this report. Doctors in Russia do not order such reports at all! Our doctor in Germany said that unfortunately, such reports will not help us in any way.

Maybe you can tell me what to look for in this report? Any comments?
For example, I can not understand, is there overexpression (amplification) of EGFR?
"Damaging TP53" = mutation of TP53? Not understanding this, I can not draw conclusions from this review ( other studies.
"Damaging PTEN" = loss or mutation PTEN? An interesting article in this case:
Which of the drugs on the list of potential clinical benefits to pay attention to ?

Here is a link to the report itself and some pictures of him:



Saturday, 3 February 2018

Inhibitors of autophagy

Given the increasing role of inhibitors of autophagy, I would like to discuss the choice of an inhibitor of autophagy, as well as the possibility of enhancing their effect.

This study focuses on the comparison of some of these inhibitors:
"...the authors of this study set out to investigate whether chloroquine (CQ) analogs, in particular clinically established antimalaria drugs, would also be able to exert antitumor properties, with a specific focus on glioma cells.
...the authors treated different glioma cell lines with quinine (QN), quinacrine (QNX), mefloquine (MFQ), and hydroxychloroquine (HCQ) and investigated endoplasmic reticulum (ER) stress–induced cell death, autophagy, and cell death.
All agents blocked cellular autophagy and exerted cytotoxic effects on drug-sensitive and drug-resistant glioma cells with varying degrees of potency (QNX > MFQ > HCQ > CQ > QN)."

Thus, it follows from the study that cloroquine (CQ) shows a weak effect, even lower, that hydroxychloroquine (HCQ) (?!) Maybe this explains the choice of hydroxychloroquine instead of chloroquine in some tests?

And another quotes from the study:

"Cytotoxicity of QBAs for Glioma Cells:
To determine whether other quinoline-based antimalarial (QBA) compounds could mimic the cytotoxic effects of CQ in glioma cells, we used MFQ and QNX. Results showed that these drugs effectively killed U251 cells at much lower concentrations than CQ."

Blocking Autophagy and Inducing Apoptosis in Glioma Cells:
Based on information that CQ induces apoptosis by blocking autophagy, we analyzed whether the other QBA compounds can function in a similar manner.
Quinacrine, the most potent QBA, not only blocked autophagy, but at 20 μM it completely disrupted U251 cellular functioning, which was evidenced by a high level of PARP cleavage, as well as the absence of CHOP/GADD-153 and LC3B expression.

In Vivo Antitumor Activity:
The TUNEL assay for apoptosis demonstrated a significant increase in the number of TUNEL-positive cells in QNX- and QN-> MFQ-> CQ-treated tumors, as compared with untreated controls."

There are also many reports of another inhibitor of autophagy - 3-methyladenine (3-MA).


Since many people here take chloroquine, I would like to discuss the possibility of enhancing its effect. While I see there are the following options:

chloroquine + cimetidine
"Cimetidine pre-treatment caused a 53% decrease in the clearance rate of chloroquine, and a 49% increase in the elimination half-life. Cimetidine inhibited the conversion of chloroquine to monodesethylchloroquine in terms of reductions in the AUC, Cmax, and urinary excretion of monodesethylchloroquine. The serum Cmax of chloroquine was increased by approximately 30% in the cimetidine pre-treated group."
The downside is that since there are many medicines in the cocktail, numerous unpredictable interactions with cimetidine are possible.

increase in the dose of Chloroquine
Instead of using cimetidine, can it be easier to increase the dose of Chloroquine? The standard is 250 mg / day.

chloroquine + hypoxia-inducing agents
"This work shows that inhibition of autophagy is a promising strategy against GBM and identifies ATG9 as a novel target in hypoxia-induced autophagy. Combination with hypoxia-inducing agents may provide benefit by allowing to decrease the effective dose of autophagy inhibitors."
What hypoxia-inducing agents are they talking about?

I also found several preliminary studies on the synergy of chloroquine and other drugs. It is interesting to study more ..

Dihydroartemisinin + Сhloroquine
Dihydroartemisinin Exerts Anti-Tumor Activity by Inducing Mitochondrion and Endoplasmic Reticulum Apoptosis and Autophagic Cell Death in Human Glioblastoma Cells.
"Co-treatment with chloroquine (CQ) significantly induced the above effects. Furthermore, ER stress and mitochondrial dysfunction were involved in the dihydroartemisinin-induced autophagy."

Asparaginase + Сhloroquine
"combination treatment with autophagy inhibitor CQ significantly enhanced anti-glioblastoma efficacy of asparaginase in U87MG cell xenograft model."

Sorafenib + Сhloroquine 
"we combined sorafenib treatment in GBM cells (U373 and LN229) and tumors with the autophagy inhibitor chloroquine. We found that blockage of autophagy further inhibited cell proliferation and migration and induced cell apoptosis in vitro and in vivo. These findings suggest the possibility of combination treatment with sorafenib and autophagy inhibitors for GBM."