Friday, 30 September 2016


Thank you Stephen and many others for passing on your helpful knowledge of GBM.

Unfortunately, I failed in my attempts to help make my daughter one of the longer term survivors of this dreadful disease.

So with a very heavy heart and great sadness I have to say my beautiful, very special 18yr old daughter Maddie lost her 13 month battle with GBM on Mon 26th Sept 2016.

Thursday, 29 September 2016

Avastin Infusion

My husband just had his third Avastin infusion, his protocol is once every two weeks at 1/2 the usual dose. Sadly, he is that 10% of those who use Avastin that the treatment has completely kicked him in the butt. On the plus side, it seems to have done an excellent job reducing his inflammation (see MRI below). I'm checking with this group on those who have used Avastin and what were the side-effects, if any. Also, what was the upside? Just FYI, Greg's neuro-onc is recommending that he has 3 more rounds before we decide to give Greg a break.
For background, Greg is 62 yrs old, diagnosed with GBM on May 1, 2015. The tumor is in his right temporal lobe. Resection was not an option. He had 5 rounds of Temodar, his MGMT is methylated but his IDH1 is non-mutated.

The right scan is August, then yesterday's MRI, then August, then yesterday's

Wednesday, 28 September 2016

MRI notes... biopsy pending. What do you think it sounds like?

Hi -

My friend had her biopsy Monday which went very well.  She is now waiting on the diagnosis and advice from the tumor review board, likely next Tuesday.  I am reading her MRI notes and would love your insights.  I suspect GBM based on "high-grade" and the impression notes.  Anyone else want to take a look and weigh in?  I haven't told her that I think it will be GBM.  We are still hopeful for MS, lymphoma, <anything else>...

Redemonstration of bilateral enhancing lesions, grossly unchanged:
Subcortical enhancing lesion in the right parietal lobe measures approximately
27 x 17 mm (9/139).
Peripherally enhancing and centrally necrotic left occipital lesion measuring
20 x 17 mm (9/84). Grossly unchanged T2/FLAIR abnormality about the left
occipital lesion.

These lesions demonstrated diffusion projection on the previous MRI,
suggestive of high-grade, highly cellular tumors.

Additionally, there is masslike, T2 hyperintense cortical expansion of the
left anterior temporal pole, unchanged.

The ventricles are symmetric. Basal cisterns are patent. No midline shift. No
acute infarction. No intracranial hemorrhage. No extra-axial fluid collection.

Orbits and soft tissues are unremarkable. Visualized vascular flow voids are
maintained. The calvarium is intact. Visualized paranasal sinuses and mastoid
air cells are clear.


Redemonstration of bilateral enhancing lesions in the left occipital and right
parietal lobes, as well as infiltrating T2 hyperintense cortical expansion of
the left anterior temporal pole. The left temporal pole lesion is worrisome
for primary malignancy, with the additional lesions possibly representing
multifocal primary glioma versus less likely metastatic disease. Presence of
some diffusion restriction involving the bilateral enhancing lesions on the
previous exam is suggestive of some high-grade, highly cellular components.

Wednesday, 21 September 2016

Temsirolimus in Recurrent GBM

Hi All,

Has anyone tried Temsirolimus in addition to avastin in recurrent GBM? Was it successful? Thanks!!

Effects of metformin treatment on glioma-induced brain edema

"Finally, metformin treatment dose-dependently reduced glioma induced vascular permeability and cerebral edema in vivo in rats. Thus, our results suggested that metformin may protect endothelial cell tight junction, prevent damage to the blood brain barrier induced by brain tumor growth, and alleviate the formation of cerebral edema."

The rats were fed metformin dissolved in their daily drinking water.

Fat as fuel source

Monday, 19 September 2016

PD-1 explanation

Can someone explain to me what exactly PD-1 is/means.  Is it a biomarker that is determined by the genotyping of tumors?   Thanks.


Can you take metformin if you are unable to eat properly for GBM recurrence?

My daughter's recurrence means she is now stuck in bed can't swallow much.
I am trying to think of what medications would be best to try to get her to take if she can't eat much or swallow very easily?
I can't just leave her without meds to deteriorate even more.

Sunday, 18 September 2016

PD1 inhibitor and supplements

Due to reoccurrence we are self funding PD1 therapy and I'm so confused as to what supplements to use if any. Before we were using usual cocktail drugs in high doses but now we are looking at the supplements from an immune response point of view and it seems that many of the drugs can negatively impact the immune system in some way or maybe it's just my lack of understanding(which is highly probable) that is the problem.. I'm way out of my depth trying to decipher most pubmed articles.

Anyone else using PD-1 inhibitor that can help with supplement choice would be much appreciated?

Resveratrol and curcumin suppress immune response through CD28/CTLA-4 and CD80 co-stimulatory pathway

Saturday, 17 September 2016

For Caregivers: Reposting from Minsha on the Inspire (ABTA) site

This morning I read this post from Inspire (ABTA) site. I thought Minsha did a great job encapsulating GBM from a caregiver's experience. I'm sharing this with her permission. 

"I thought I share my thoughts after 10 months (and continuing) intense research and my husband’s brave fight against this dreadful disease.

My pearls of wisdom, as a simple caregiver (and generally relentless person):

- Look this disease straight in the eye and do not give up. If you don’t win the battle at the end, at least you have put up a good fight, and helped future patients learn from your experience.
- Trust your body. Don’t feel it has disappointed you. 
- Treat your body (and soul) well. You’re body is fighting HARD, even though you can’t sometimes see it. Rest, stay active, do supplements, eat right, and “meditate”, and let people take care of you.
- Most likely, the chance of dying from GBM is much greater than any of these treatments (FOR NOW), but this is changing very rapidly and patients ARE living much beyond the 14 months …. all the statistics are getting to be “obsolete”. 
- For you not to be part of the lucky few of the past, you need to take advantage of the NEW TREATMENTS in addition to SOC, and for the moment most of these are offered “trials” and off label. 
- Trust new treatments, but be very cautious of “new things” (Phase I-II) studies were they are trying to get the safety and dose escalation done (unless you are desperate, or the same drug has passed Phase II in similar trial). 
- Try to find a trail that is Open Label and Non Randomized, if it is available.
- Every drug company wants “IN” on this lucrative business. Do not go for treatments that have not shown good results at least in 100s of people tested. 
- Do not let comments on drugs/treatments scare you. Comments like "Temodar weakens your immune system”, “Temodar does not work on un-methylated”, “Use of Avastin, or immunotherapy will disqualifies you from X and Y future trials.” These may be partially correct, but NOT by any means the “General Rule”. 
- Make the best decision “at the time” you need the drug/treatment to have the odds in your favor. 
- All decisions need to be made based on Risk/Rewards. Nothing about this disease or fight is guaranteed. If the Rewards outweigh the Risk, that is is GOOD in the world of GBM.
- Once you make a decision, do NOT look back. You never know what you will do next. A decision that may seem wrong, may actually work to your advantage as you continue other treatments. 
- Trials come and go, and change inclusion/exclusion criteria, Trials should be "Used by You" (if they fit the circumstances and your needs), and not the other way around.
- Don’t try to be your own, or your loved one’s scientist/doctor. The good doctors and scientists in this field have dedicated their whole career (sometimes life) to it, and they are on your side. 
- All these sites and what we discuss, should give you thoughts to ask questions, and discuss with your NO. 
- Do take your health in your own hands and make your own decisions, but let your doctors guide you.
- Ultimately you need to find a doctor and team that you “trust" and can guide you in making your decisions. There are “many" fabulous, highly experienced NOs out there.
- Every patient is “different”, and as we use treatments in addition to SOC, our paths are different. You want a team that is the "expert in the path you’re taking".
- Your NO knows you the best, and he/she is most knowledgeable in your particular situation. If this is not the case, change your doctor. Doctors like all other have their own biases and styles that may or may not fit you.
- If the side effects scare you, first and foremost inform your doctor, then you can look into our group for advice and help through experience.

I don’t know if all this helps, but this has guided us so far, and god willing we have KILLED all the cancer cells left behind after surgery (with RT, Temodar, PD-1 inhibitor). But we ARE continuing this fight following the same guidelines.

Please do share your own pearls of wisdom. It is greatly appreciated, and all the best to you and your loved ones!"

Friday, 16 September 2016

flash-freezing tumor in liquid nitrogen

Does anyone know where this is being done? It's probably too late for us as my wife is having a resection on Wednesday sept 21st. We asked Kaiser Redwood City about this and they don't have liquid nitrogen nor any way to store it if they did. How important is it to do this and where can it be done?  FYI the surgeon and NO believe she has a Low Grade Glioma at this point.

Thanks, Justin

Thursday, 15 September 2016

We meet again

Hi. Just a quick post to share because I am stunned right now.  I received word this AM that one of my best friends is in the hospital and was told she has brain cancer.  I don't know details yet, she hasn't had a biopsy, just MRI (which leads me to believe her 'diagnosis' to be irresponsible and cruel) has anyone been diagnosed without a biopsy?  I didn't believe that to be possible.

Anyway, more details as I know them.  I'm not looking forward to this but do feel quite thankful to have all of you.

xoxo Annie

Wednesday, 14 September 2016

Article "Glioma-induced caspase-3 inhibition in microglia promotes a tumor-supportive phenotype."

"Glioblastomas are one of the most malignant forms of brain tumour and are difficult to surgically remove because the tumour cells invade the surrounding healthy brain tissue. Glioblastomas also affect the microglia -- immune cells of the brain -- in such a way that they stimulate the tumour cells instead of attacking them.
The multi-national research group has previously shown that pro-inflammatory activation of microglia is controlled by a group of enzymes called caspases. In the present study, they sought to examine if the way the cancer cells affect microglia also includes similar mechanism. By cultivating microglia and glioblastoma cells together, the researchers were able to show that the cancer cells inhibit caspase-3 activity in the microglia.
"We show that it's the same inhibition of caspase-3 that causes the microglia to stimulate the tumour cells instead of attacking them," says Bertrand Joseph, Principal Investigator at Karolinska Institutet's Department of Oncology-Pathology. "When we removed caspase-3 from the microglia in a glioblastoma mouse model, the tumours grew more quickly."
According to the study authors, their results demonstrate that the glioma cells use a nitric oxide-dependent mechanism to force microglia to modify caspase-3 to form a tumour-stimulating form of these cells.
"Two things surprised us," says Bertrand Joseph. "First and foremost, that affecting the signalling mechanism between glioblastoma cells and microglia that we discovered has such a major effect on tumour growth. Secondly, that basal caspase-3 activity, which is often considered to be an absence of activity, fulfills essential function in regulating microglia cell behavior."

Link to news article:

Link to scientific journal:

Saturday, 10 September 2016

Virtual Trial

Most of you are probably already aware of the valuable website created by Al Musella.   That site got its name from the Virtual Trial, which tracks the outcomes of patients who are trying many different experimental therapies beyond the standard-of-care.  The way to gain access this de-identified database is to join the virtual trial oneself.

"The Brain Tumor Virtual TrialTM is a new concept in collecting and analyzing outcomes data for brain tumor patients. We collect information from brain tumor patients - or their friends / family, over the internet. Participants are not told what treatments to do - we just record and analyze the outcomes of the treatments you and your doctors decide to try. The idea is to enable us to quickly identify which treatments or combinations of treatments look the most promising. We will then perform a traditional multi-center study on the best combinations of treatments."

Click here for more details and to register.

Wednesday, 7 September 2016

Clinical Trials and Avastin

Dear Stephen and BT community, 
I tried to look this up in our google drive BT library but I didn't see it. Is anyone aware of this clinical trial? A person on Inspire shared it with me. Thoughts?

"A new PD-L1 trial + Avastin that takes patients that have had avastin before: ank=3"
Hi there everyone. My husband was dx in Jan 2016 with Astrocytoma grade 2 after biopsy. Seizures were the presenting symptom.The tumor has a  diffuse gliomatosis cerebri growth pattern, in at least 3 lobes. He just turned 79, but is super healthy and very active..(except for a bad back). He is a super bright still practicing professional. He opted to try Temodar alone, 5-23-cycle, no radiation bc of cognitive side effects. He has scans every 2 months and NO says all have been stable with possible shrinkage in an area. The MRI on 8/1/16 showed stable disease as well, BUT they also did a Spectroscopy which showed a long TE sequence with Cho/Cr ratio 2.25:1, and a short TE portion with Cho/Cr ratio at 1.96:1.  I've read that indicates higher grade tumor, growth etc. The NO said it is not reliable test in grade 2, bc the tumor tissue in grade 2's and normal tissue is a lot alike. This doesn't make sense to me.  Also, this spike was not present on study the last time spectroscopy was done, which was on 02/24/16.  Ive called Duke for another opinion and am waiting to hear back. We live near Orlando, and have been going to Mayo in Jacksonville, and have been happy, but our NO is leaving Mayo. He has been feeling very tired and awful last 3-4 days. I don't know if I am being paranoid, but I worry what if it is starting to grow or transform...So, all that to ask...does anyone have experience with Choline / Creatine Ratio? Thank you!!  Angela

Tuesday, 6 September 2016


Stephen and others

Anyone familiar with this drug?  Looks like it is in phase 1 trials, but on the Inspire board, someone was given Marizomib.  Does not sound like this was part of a clinical trial.  But this is a guess.

Timing of follow up MRI

For those using avastin or avastin and a cytotoxic drug, how long after the initial infusion of avastin before an MRI was completed to check for signs of tumor stabilization.  Dr. Benkers at Swedish says after the 2nd infusion, but before the 3rd (which would mean MRI between weeks 2 and 4 after the initial avastin infusion) and Dr. Lai at UCLA say just before the next dose of (in Jeremys case) CCNU.  In Jeremys case that means about 6 weeks after the initial dose of avastin.  Just wondering what others are doing.

Avastin decision

I am very confused after two discussions with my daughters NO regarding Avastin and am seeking opinions.
First discussion he said to try to get Avastin through insurance, this wasn't possible as not licensed in the UK for GBM.
So we said we would try to raise money to finance. NO then said he wouldn't use Avastin as her recurrence was diffuse and he didn't think it would work as well as it does for solid tumors or edema, and that it could make things worse.
He also said trials show it doesn't work with children or young adults.
We are now unsure weather to go ahead with Avastin or not? Where can you get impartial advice?
We know it isn't a cure and there are pros and cons like a lot of medications.

Monday, 5 September 2016

On-line pharmacy recommendation

Has anyone has experience with ordering from on-line pharmacies? Husband's NO agreed with him taking Antabuse (disulfiram) with temozolomide before leaving on his vacation, but did not write an RX for it and we forgot to ask before leaving the office. Now he is gone and the next round of temo will start on Wednesday. I can order disulfiram via an on-line pharmacy without the RX but want to make sure they are legit. Thoughts or recommendations?

Friday, 2 September 2016

Low Dose Naltrexone

As mentioned above, one of the main endogenous opioids with increased production following low dose naltrexone is met-enkephalin (also known as methionine enkephalin, and as opioid growth factor). A Chinese study published online in August 2016 examined the effects of met-enkephalin on microglial cells in culture [46]. As explained in this study and elsewhere, microglia (the resident macrophages of the nervous system) and macrophages infiltrating from the systemic circulation are actively recruited into tumors, polarized to a tumor-promoting M2 phenotype and away from a tumor-fighting M1 phenotype, and can make up as much as 30% of a GBM tumor. The investigators found that at the optimal concentration of met-enkephalin (1 picomolar), M1-type cytokine production and surface proteins were increased in the microglia, including interleukin-12, TNF-alpha, CD86, CD40, and iNOS. In contrast, M2 cytokines and markers were not affected, including interleukin-10, TGF-beta, CD163, and arginase. Phagocytosis (a main function of M1 macrophages) and cytotoxicity towards U87 glioblastoma cells was increased by met-enkephalin treatment. Thus, met-enkephalin (opioid growth factor), an endogenous opioid whose production is increased in humans following transient opioid receptor blockade by low dose naltrexone, may aid glioma patients by reverting tumor-associated microglia to an M1 anti-tumor phenotype.
View common questions and answers about the use of low dose naltrexone at LDN Science. Especially interesting areinterviews with Dr. Ian Zagon, who discovered the clinical benefits of naltrexone in very low doses.
The effective dose of low dose naltrexone ranges from 2.5 – 10 mg, with the most common dose being 4.5 mg daily. LDN may be taken in the morning or evening. Some individuals may experience sleep disturbances (such as nightmares) caused by LDN and these people may choose to take their daily dose in the morning.

Thursday, 1 September 2016

CUSP9 without being in a trial

I have asked my daughters NO to prescribe the drugs used in the CUSP9 'Concept of Treatment Trial', he has agreed to try to get them prescribed  minus the Auranofin.

He has agreed this as they can't offer anything else. Her recurrence is diffuse in cerebellum, extends to the brain stem and shows small area of enhancement round original site of left temporal lobe.
 He said Gamma knife not an option, no trials available and she is not fit to fly for magnetic or any other therapy due to lack of mobility, tiredness etc.

At present I am trying to get health insurance co to pay for Avastin, which they are saying isn't licenced in UK.

My concern is,  that apart from twice weekly blood tests I am going to have to try to oversee her treatment with these drugs and I'm very nervous. But there doesn't seem to be an alternative.

NO has said to stop Valproic Acid, presumably because of interaction.

Any thoughts gratefully received.