Ultrasound -- wave of the future?

Very interesting article - http://www.pbs.org/wgbh/nova/next/body/hifu/

Metecurcumin and NovaSOL

Does anyone use these brands? And if so what do you use for a dosage?  Thank you.

Fat not Sugar

WOW! I know this is merely from models at this point and not clinic, but it seems this is a radical revelation if verified! Am I missing something or is this as revolutionary as it appears? Again, I know the scientific process has a long way to go, but the claim seems like a whole new world would be opened.
http://m.huffpost.com/uk/entry/uk_5774e95de4b08b8610d782bc?edition=uk

Grace and peace,

Danny

cachexia

Any one here no ways of treating and preventing cachexia?

Hard fought battle.

After almost 22 months of courageously fighting this horrible disease, my very brave husband Roger lost his battle. I am devastated and heartbroken beyond belief, but grateful he is at peace.
I wish each of you all the best as you so bravely fight on. You will remain in my thoughts and prayers.
Sincerely,
Jaki

Columbia University GBM Webcast tomorrow- Thursday 6/30/16 1:30PM-2:30PM EST

Hi Everyone,

I think you can use the links below to register for this free seminar (listen on phone or connect to the webcast online).  I think they will accommodate international callers too.

Speakers-

Dr. Jeffrey Bruce (Neurosurgery)

Dr. Eric Wong (Neuro-Oncology)

Thursday, June 30, 2016, 1:30 – 2:30 pm, Eastern Time

Dr. Jeffrey Bruce- Edgar M. Housepian Professor of Neurological Surgery, Vice Chairman, Department of Neurosurgery, Columbia University College of Physicians and Surgeons, Co-Director, Brain Tumor Center, Director, Bartoli Brain Tumor Research Laboratory

http://www.cancercare.org/connect_workshops/536-update_on_glioblastoma_2016 -06-30

media.cancercare.org

Best,

Mike B

Liquid Aspirin

Did anyone see this? Maybe a future addition to the cocktail.

Grace and Peace,
Danny

http://medicalxpress.com/news/2016-06-breakthrough-brain-tumour.html

recent comments

Hi Stephen,
Any luck in restoring the' recent comments' column.

Looking for an improvisational N-O in Boston

Can anyone out there recommend an NO in the Boston area that isn't afraid to think outside the cancer/medical complex, buttoned-up box?  Someone along the lines who is open to off-label and re-purposed drugs, and other treatment ideas. Thanks!

Liposomal Curcumin and Resveratrol

Can anyone recommend a brand of Liposomal Curcumin and or
Resveratrol?  Is anyone taking them together?    Thank you!

First Steps

Hello,

My dad (age 64) was recently diagnosed with stage four GBM. We are still awaiting pathology information regarding MGMT, etc. He had a biopsy, but the tumor is inoperable at this time. He started chemo and radiation on Friday, but I want to start him on additional supplements and medications to improve his chances. I am sifting through the blog and more. 

Could you outline your suggestions for first steps please? I have already ran into opposition with his neuro-oncologist, so I am frustrated and overwhelmed and looking for where to start.

I truly appreciate all of the information you have already made available.

Thank you.

Stephanie

Nivo dosing

I am curious if anyone that is using Nivo (Opdivo) is on a different schedule than every two weeks.  My son is using Nivo outside of a clinical trial and is scheduled for infusion every two weeks at 240 mg for 4 months, then 480 mg monthly thereafter.  His NO said this is the way Nivo is now being used in clinical trials.  I have not heard of anyone else on this dosing schedule.

Vadym and Tania.

Hello!
Couple of words about my husband Vadym.
16 July he finished radiotherapy with tmz.Vadim feels changeable - there are headaches, speech and memory problems, and control emotions, weight loss.
But as a whole - a positive trend, although barely noticeable.
Vadym"s protocol till yesterday.
Metformine 2,5 g per day,
Dexametazone 3 mg,
Cereblex 200 mg per day,
Chlorochine 250 mg per day,
Boswellia serrata Life extention 5-6 capsules x 3 time per day.
Milk Thistle 250 mg x 3times per day
DCA 1 gr x 2 times per day
Maitake
CLO
Whey protein,
Phosphatidile serine.
Quercetine 1600 mg 3 times per day,
Bromelain 2 cuplets x 2 times per day
Resveratrol 500 mg once per day
Chlorella 500 mg 3 times per day
Rhodiola
Befungin ( chaga mushroom)
Gentle Iron 1 capsule 3 time a day ( low iron in blad tests)
Genistin
Curcuma longa 2400-3000 mg,
Minocycline ( Now he doesnt accept it, we started it and Vadym had a headache and rash at dose 100 mg 2 time per day. We stopped, maybe we will restart it again).
Today we stopped all supplements and medicines as Vadym has swelling on the left side of the face and redness ( place of radiation). Doctor said to take diuretics and antihistamine, but if he has temperature increase, it will be a reason to suspect an infection and start antibiotics.
Im going to restart all supplements step by step after.
Did someone such a situation?
Im affraid, that Vadym vill be without support....

Also i would like ask advise about German Clinics for ImmunoTherapy. Can anyone recommend me any of them?
My warmest greetings to all!
Tania.

Introduction and introductory thoughts

Call me Steve C.  I trained and practiced as a family physician.  Subsequently ended up in administrative work; I don't practice now.  But I've read more research articles about clinical topics than most family docs.

In early May, my wife had a stroke-like episode and was diagnosed with a 4 cm brain tumor, left parietal lobe.  Grade IV glioma = glioblastoma.  Full excision with clinically excellent post-op status, care at Johns Hopkins (to be highly recommended).

She's on the standard Stupp protocol.  However, we were fortunate enough to get into a trial with nivolumab (Opdivo).

The Opdivo is a bit of an immune shotgun approach.  It is a "checkpoint inhibitor," or PD-1 inhibitor.  It tones down some of the body's (including tumor's) ability to avoid being attacked by the immune system.  The main side effects are thus from the immune system attacking tissues other than the tumor.  That may sound like a shot in the dark for killing tumor cells, but some tumors are fairly susceptible to being attacked by the immune system.  Melanoma, for example, is especially "antigenic," and susceptible to being attacked.  An agent very much like Opdivo eliminated Jimmy Carter's metastatic melanoma.  

I recall sadness on hearing about Jimmy Carter's diagnosis of metastatic melanoma.  I was confident that the next news to be heard was to be of his passing away.  I was floored when the next news instead was that he was cancer-free, because of an Opdivo-like treatment.  I knew then that we've entered a whole new era of cancer treatment.

Glioblastoma isn't quite as antigenic as melanoma, but our oncologist tells us that it's more antigenic than most other tumors.  Opdivo may make a huge difference.

Opdivo is an antibody.  She got the first dose (236 mg) by IV yesterday, with no side effects.  She's scheduled to get another dose every 2 weeks *indefinitely*.  Levels should build up steadily over several months (antibodies have a very long lifespan, months, in the bloodstream).  We met another patient on indefinite Opdivo, who looked great and has had no side effects.  We're hopeful.

I've been reading lots and lots of "preclinical" research reports.  An interesting recurrent theme is that many different agents with modest anti-glioma effects in animals seem to have additive effects with other agents against the tumor cells.  This is seen also in the 60 Minutes report, where polio-treated tumors became extremely sensitive to ordinary chemotherapy.

We conclude that an optimum approach would include a wide range of additive adjunctive strategies, to include diet (ketogenic), exercise, mental health, and cautious use of some supplements--those with a reasonably solid base of research to show some evidence of benefit.
Thus, we're still pursing DIY adjunctive approaches.  Among the more promising non-toxic options includes:
http://www.ncbi.nlm.nih.gov/pubmed/27298767
http://www.ncbi.nlm.nih.gov/pubmed/26637846
http://www.ncbi.nlm.nih.gov/pubmed/10902853

I find Pubmed to be an invaluable resource to help sift through promising avenues and avoiding all the snake oil nostrums and charlatanry that dominate the realm of alternatives for cancer treatment.
It's frustrating that we can't rely on the oncologists' assistance with this.  Physicians, especially oncologists, really can't ethically endorse unproven treatments, and so few potential treatments have been adequately studied in humans.  We''ll offer them the opportunity to veto anything they think is hazardous, but we can't expect them to encourage anything.  It was really striking when when we asked their opinion of medical marijuana, whether for symptom relief or for the laboratory-demonstrated anti-tumor effects, and the response was "we have no opinion on medical marijuana."  It's frustrating, but I do respect them for their strict ethical standards here.  I have no doubt that, were they to sit on the other side of the consultation desk, they'd personally be using a range of such agents.

Advice on MGMT unmethylated tumor

Hi,

My father (67 years) was recently diagnosed with GBM in the cerebellum after a sub-total resection. The neurosurgeon said they were able to remove almost all of the tumor mass except for some minor residue.

There were two tumors, one in the middle of the cerebellum (vermis area) and one in the left hemisphere.

The result from the histopathology says:
* High staining of Ki67 marker.
* EGFR positive staining (but doesn't say how much nor whether EGFRvIII mutated or not)
* GFAP positive staining
* Vimentin positive staining
* Mainly cytoplasmic staining of MAP II.
* No staining of IDH1 R132H mutation.
* Only few cells show staining of p53 and NSE.
* No loss of 1p36 or 19q13.
* MGMT unmethylated (9% methylation as measured with pyro sequencing)

Father has just finished 6 weeks of radio+TMZ therapy and we're scheduled to meet the oncologist on Thursday to plan the next step. I recon she will order the standard 5/23 schedule TMZ chemotherapy per the Stupp protocol.

I have tried to read up on GBM and the treatment options available. However if I understand correctly, my father's unmethylated MGMT means the 5/23 TMZ schedule is likely not effective, but maybe a metronomic TMZ schedule would be.

I have put together a cocktail of supplements:
* Curcumin (Longvida) 1000 mg/day
* Zinc 30 mg/day
* Vitamin D3 5000 IU/day
* Silibinin 800 mg/day
* Berberine 1000 mg/day
* Garlic (AGE extract) 600 mg/day
* Lycopene 20 mg/day
* Selenium (as L-selenomethionine) 200 mcg/day

I'm also looking at adding PSK/PSP as well as Pterostilbene, but haven't yet found a good supplier that delivers to Sweden.

I'm thankful to any input or advice you can give me on how to proceed.

A few questions/thoughts:

1. Would you add or remove anything from the supplement cocktail, or change the dosage?
I read that some supplements could have both negative or positive effect depending on the dosage, i.e. Quercetin. Is there a list somewhere on known/suspected supplements to avoid?

2. My father is reluctant to do anything outside of the doctor's recommendation, so I have to try to keep the supplement cocktail as simple as possible. If I understand correctly curcumin and vitamin D are considered to be two of the most promising supplements. If I have to prioritize, which of the supplements should I keep (or exchange for something else)?

3. I've noticed that many of the supplement cocktails contain three different mushrooms - Reishi, Maitake, Corioulus versicolor. Are the mushrooms basically the same (i.e. source of PSK/PSP) or do they contain completely different agents?

4. When meeting the oncologist on Thursday, should I press for some alternative to the 5/23 TMZ schedule? I.e. addition of Keppra or some other MGMT "sensitizing" drugs or should I try to press for a metronomic TMZ schedule (or both)?

5. Should I try to press for additional meds (i.e Celebrex or others) when meeting the onc? Which ones would be most important?

6. Does the pathology report give any additional useful information to help treat this or meds that I should press for/supplements to add? I'm not able to make much out of it except for the MGMT status.

7. Should I ask for any additional (selective) gene testing done on the tumor sample? If I understand the pathological report correctly, the sample is a paraffin fixed type (not frozen) so that makes it inelligible for immunovaccine samples.

8. Anything else I should think of or that you would do/recommend? As we live in Sweden, the possibility of entering trials may be limited, but I'll nevertheless ask the onc about Optune etc.

Thanks,
Peter

"Aggressive" treatment or "Watch and Wait" for grade 2 glioma

I had a gross total resection of a grade 2 glioma. Now I have 2 options. “Aggressive treatment”, chemo radiation followed by chemo or to “watch and wait”. The tumor is IDH1 mutated but not MGMT mutated. 

My NO says they always to Temodar with radiation.My feeling is with the threat of hypermutation and without the MGMT mutation I’d be better off deferring treatment, though the radiation might kill remaining cells. 

My NO thinks the best course is to wait since it’s likely to take years to regrow at which time new treatments will be available. Though I think he's overly optimistic. The tumor was partially resected in 2005, fully resected in 2011 and fully resected again this year after a 2nd recurrence.
Any thoughts on whether to be aggressive or to watch and wait would be appreciated. I’m also going to find another NO for a 2nd opinion.

Peak authors

As it turns out, there is a limit of 100 authors to any one blog, which this blog has now reached.  I will unfortunately need to start removing previous authors that are not actively posting in order to make room for newer authors.  If this happens to you and you'd like to author a post in the future, please send in a new request to be re-added to the author list.

Chemo-Radiotherapy failed: Recurrence

All -

Mom's tumor has recurred in multiple areas in the operating bed right in the middle of first round of chemo and radiation. We had started her cocktail as well. Doctors have stopped chemo and radiation, calling it failure.

I need to decide on the next possible treatment option. We are still waiting for her genetic report. But this news is a huge setback as it does not leave time for us to try various things over a longer period of time. Surgery will not be feasible. I believe doctors will be cooperative in letting us avail of other treatments on compassionate use basis as well. But something probably needs to work more immediately now.

Please advise what options we should be pursuing here in US or in Germany.

best,
Jinesh

Cannabis oil and GBM treatment group

Here is a link to  a facebook group for Glioblastoma  and Cannabis Oil treatment for anyone interested.  




https://www.facebook.com/groups/glioNOmore/

Methadone a possible addition to the cocktail?

             BioFabNet Telemedicine BW                        

Hi Stephen and all

I came across this article about methadone from a Belgian  blog GBM patient who is using Methadone as a part of his cocktail and doing well, he is also doing immunotherapy etc so as usual you can never be sure what is working. There is some interesting research regarding GBM and Methadone in the article below.  The article is mainly about leukaemia but does include some GBM investigations near the end. I wonder if Methadone works along the same lines as Noscapine? Below is a link to the blog.

http://www.slideshare.net/pjmuller/glioblastoma-go-for-the-cocktail-approach

1. Methadone the last step to becoming an anti-cancer drug

Methadone – the last step to becoming an anti-cancer drug

It all began several years ago with a surprising discovery in the laboratory. Claudia Friesen, a chemist at Ulm University, discovered that leukaemia cells that were exposed to methadone died within a relatively short period of time. Seven years on and many papers later, what was once a rather exotic substance is now undergoing clinical testing in cancer patients.

Dr. Claudia Friesen has been extremely interested in anti-cancer drugs ever since she studied chemistry at Heidelberg University. She has been with the University Hospital in Ulm since 1998 and when she joined Professor Erich Miltner’s group at the university’s Institute of Legal Medicine in September 2007, she started to look more closely at potential drugs for cancer treatment, with a particular focus on drugs with a cytotoxic effect. She made rapid progress and only three months after starting her investigations, Friesen made a groundbreaking discovery that she has been working on ever since.

Surprising death in the test tube

Cancer researcher Claudia Friesen found that methadone is a promising new potential therapy for leukaemia. © Pytlik/BioRegionUlm

When Friesen and her team tested methadone in leukaemia cells, they were surprised to find that methadone effectively killed leukaemia cells in a comparatively short time; until now methadone has usually only been used for managing severe pain and as an anti-addictive preparation for use in patients with opioid (e.g. heroin) dependence. At the time of Friesen’s discovery, little was known about methadone and its mechanism of action. What was known was that it exerts its analgesic effect by binding to opioid receptors and that tumour cells express many opioid receptors on their surface.
Friesen and her team found that methadone induced apoptosis in leukaemia cells, a finding that Friesen was able to deduce from the presence of typical membrane-enclosed vesicles outside the cancer cells. It goes without saying that Friesen was aware that the process of apoptosis is often defective in cancer cells, and is the reason why such cells grow in an uncontrolled manner. The excitement of the hunt had got its hold on her.
In 2008, Friesen published her findings and caused quite a stir in the scientific and non-scientific press, probably because her findings were unusual in the context of mainstream cancer research. The binding of methadone to opioid receptors on cancer cells induces apoptosis, i.e. programmed cell death; the process is triggered by protein-degrading enzymes (caspase 9 and 3), which quickly sweep obstacles such as Bcl-xL and XIAP (X-linked inhibitor of apoptosis protein) out of the way. Moreover, methadone does not have any toxic effects on healthy, non-leukaemic blood cells.
Friesen and her team discovered that the binding of methadone to an opioid receptor leads to the activation of inhibitory G-proteins. These inhibit the enzyme adenylate cyclase, which in turn leads to the downregulation of cyclic adenosine monophosphate (cAMP). This improves the effectiveness of anti-cancer drugs in treating cancer. 

Opioid receptors and cell death

Opioid receptors appear to play a key role in the induction of cell death, but little is yet known about them. They are found in the brain and spinal cord of mammals including humans, and bind to endogenous and exogenous opioids such as methadone. They have seven transmembrane-spanning domains and are usually found in areas involved in pain control and regulation of emotional response. Methadone binds to μ receptors.

Cancer cells carry a large number of opioid receptors on their surface. Healthy cells only carry a few. The more opioid receptors a cell has, the easier it is to trigger its death. A cancer cell that has a particularly large number of opioid receptors can be driven to suicide by methadone alone. Unfortunately, as Friesen has found, most tumour cell types do not carry enough opioid receptors for methadone to be effective on its own. However, she has also found that cells with a median density of opioid receptors can be driven to suicide by exposing them simultaneously to methadone and cytostatic drugs, which increases the drugs' cytotoxic potential.

Ex vivo experiments with patient cancer cells and human cancer cell lines confirmed the apoptotic effect of methadone (“the speed with which cell death occurs depends on the type of tumour”), and animal models were used to confirm the results in vivo. The scientists tested the effect of methadone in combination with a chemotherapeutic drug in mice bred to have human leukaemia and found that the tumour stopped growing, and did in fact shrink and disappear completely.

Mutual increase in cytotoxic potential makes the clinical application of methadone more likely

But this was not the only thing Friesen and her team discovered. They also observed a phenomenon that has brought their findings closer to clinical application (Friesen 2013). When methadone binds to opioid receptors, cancer cells not only take up greater amounts of the anti-cancer drug than without methadone, they also reduce the efflux of the drug. In addition, the anti-cancer drug used leads to an increase in the number of opioid receptors that are expressed on the cancer cell surface, with the result that more methadone can bind. In other words, methadone and the anti-cancer drug mutually increase their cytotoxic potential. Friesen has already shown this “dual synergism” for several substance classes with a cytotoxic effect (e.g. platinum complexes, anthrocyclines).

Friesen strongly believes that the mutual increase of the agents’ cytotoxic potential improves the therapeutic outcome: significantly lower amounts of cytostatic drugs would be required, which in turn would reduce the number of adverse drug effects. Methadone also has the potential to sensitise resistant cancer cells to anti-cancer drugs and give ‘untreatable’ patients another chance of treatment with a better outcome.

Even cancer stem cells capitulate in vitro

Glioblastoma cells survive treatment with an anti-cancer drug. © Friesen/University Hospital Ulm

Recently, Friesen’s research group (Friesen 2014) has once again come up with findings that highlight the positive effect of methadone in the treatment of cancer. The researchers found that methadone breaks chemo- and radioresistance in leukaemia cells expressing opioid receptors and sensitises leukaemia cells for doxorubicin treatment, and hence apoptosis.
Unexpectedly, Friesen and her team also succeeded in doing the same with glioblastoma stem cells. This project was supported with funds from German Cancer Aid. Glioblastoma is the most common malignant brain tumour in adults and has a bad prognosis. It cannot currently be cured.

Methadone can break the resistance of glioblastoma cells to anti-cancer drugs and induce apoptosis. Apoptosis leads to a typical granular cell shape. © Friesen/University Hospital of Ulm

There have already been a few clinical cases that substantiate Friesen’s findings. For example, Friesen knows of a cancer patient who was no longer responding to conventional chemotherapies and was given palliative chemotherapy in combination with methadone. The combined administration of methadone and anti-cancer drug led to a strong reduction in tumour volume. The administration of methadone therefore appears to have led to the sensitisation of tumours cells. Some of the patient’s tumours even disappeared completely. It goes without saying that methadone has dramatically increased the patient’s quality of life.
Despite undergoing several chemotherapies, another cancer patient nevertheless developed liver metastases. Eventually, the combined administration of anti-cancer drug and methadone led to the destruction of the metastases. A patient from Florida, USA, with small-cell lung cancer contacted Friesen to tell her that he was given methadone to relieve cancer pain and has survived for 12 years instead of the predicted six months. Friesen has also received reports of successes from Westphalia-Lippe where palliative doctors prescribe methadone as standard for the treatment of peritoneal carcinomatosis.

Ulm University Hospital to initiate clinical trial

In the meantime, the scientific world is becoming less sceptical about the use of methadone in cancer treatment. Friesen reported on the observed effects of methadone at the German Cancer Congress earlier this year. Something that seemed unthinkable seven years ago, will become reality in 2014: Professor Thomas Seufferlein, medical director in the Department of Internal Medicine I at Ulm University Hospital, in cooperation with Professor Ralf-Dieter Hofheinz, head of the TagesTherapieZentrum at the Interdisciplinary Tumour Centre at the Mannheim University Medical Centre, will continue Friesen’s work and carry out a clinical trial with the aim of providing evidence that methadone, when given in combination with an anti-cancer drug, acts as a chemosensitiser or resistance breaker in patients undergoing conventional chemotherapy.

The clinical trial will also include patients who barely or no longer respond to conventional chemotherapies. The study design is not yet ready, but it is planned to include a broad range of patients with different types of tumours. The trial has the major goal of improving the effect of anti-cancer drugs and the quality of life of cancer patients.

A new helper for conventional cancer therapy?

Despite all positive results achieved so far, Claudia Friesen knows that the use of methadone in the treatment of cancer patients has its limits. The effect of methadone will depend on the dose used and on the condition of the patient treated. Nevertheless, it would be considered successful from the patient’s perspective if methadone was shown to improve upon conventional cancer treatment.

Although the use of methadone as an anti-cancer drug has already reached the clinical trial stage, Claudia Friesen will continue to have plenty of work to do and she is planning to focus specifically on the molecular processes that are ignited in tumour cells when methadone binds to opioid receptors. Understanding these processes might help scientists to elucidate how methadone is able to effectively trigger cellular apoptosis.

<sup>References:

Friesen, C. et al.: Methadone, Commonly Used as Maintenance Medication for Outpatient Treatment of Opioid Dependance, Kills Leukemia Cells and Overcomes Chemoresistance, Cancer Research 2008, 68, 6059-6064.
Friesen, C. et al.: Cell death sensitization of leukemia cells by opioid receptor activation, Oncotarget 2013, 4, 655-690.

Friesen, C. et al.: Opioidrezeptoraktivierung verstärkt Effektivität von Chemotherapeutika, Ärztliches Journal Onkologie, 4, 2013, 26-27.

Friesen, C. et al.: Opioid receptor activation triggering downregulation of cAMP improves effectiveness of anti-cancer drugs in treatment of glioblastom Cell Cycle 2014, 13:10, 1560–1570.</sup>

 

Boswellia?

I'm a little confused about Boswellia. Should I be adding this to the cocktail during radiation? Hes not currently taking any steroids.....

Lab test may predict glioblastoma aggression and spread

https://www.sciencedaily.com/releases/2016/06/160609134259.htm

Vision damage

Hi all
Dad's tumor has been stable for about 4-5months now however his symptoms have been getting worse especially his vision.
Could chorquine course this?
If so is there anything we can do to try make this better ?
He can barley see at all

High above normal Gamma GT few hours after consuming cocktail drugs ?

Hi All,

Need help in this confusion. My brother, aged 29, just got diagnosed for GBM 4 grade months ago, with unmethylated MGMT and positive EFGR. Currently his on 30x radiotherapy along with 120mg temodal a day, Mon - Fri. Just two days ago he started the cocktail drugs regime with drugs as follow:

Celebrex 400mg/day
Verapamil HCL 240mg/day (Isoptin)
Cimetide (Xephamet) 400mg/day  (the pharmacist Tagamet claimed not produced anymore?)
Metformin 500mg/day (Glucophage)

all taken an hour after taking temodal. He take a blood test during that first day of consuming all those drugs, and the next day when the blood test result out it shows that his gamma gt is 84 which is above normal as normally it should be below 62. He shows symptom of what the oncologist said to be kind of 'liver damage', which are fatigue, nauseating feeling, and a few feeling to vomit. We are confused as to what cause such a high Gamma GT is it possibly the drugs or temodal? Have any of you experienced this? If yes how to recover it? Should we stop some of the cocktail drugs or lessen the dosage? Thank you very much for the time and reply!

MRI results

Hi everyone,

My husband, Corneliu had his MRI, and we are wery grateful because his clear MRI....

it only sees  the surgery hole... ))

wish you all great recovery and much health!

Melinda

Carboplatine + Avastin

Hi all,

Anyone had any sustained success with Avastin and carboplatine combination? Stephen, would appreciate your views please. We are struggling with decisions and my husband just had another recurrence less than 2 months after the last recurrence. Would carboplatine add any benefit? Did it show any efficacy? Many thanks. 

Ipilimumab with Opdivo

Hi All,

Anyone here has had experience with Ipilimumab ( Yervoy) along with Nivolumab ( Opdivo)? I know the earlier study showed severe toxicity but I heard that later on, when the yervoy dose was reduced from 3mg/kg to 1mg/kg, the safety profile became much better and the combination became much better tolerated. Stephen, Any thought on efficacy or on whether it is worth trying in GBM? Many thanks for the help.
Noha

Potassium bad for glioblastoma

Hi all
I was on the web searching and researching as always the other night and I came across something that was new to me anyway. There was a blog inspire.com I think it was on and there was a Gbm patient there her and her husband where both scenitescs, and they came to the conclusion that they was going to cut out all potassium in order to inhibit prolife and migration.
I think that was in 2011 and she is now cancer free.
Since reading this I have reasearched it some more and apparently it's correct that potassium channels do indeed play a role in prolife and migration of Gbm
So I question is
She did it by completely not eating anything that contained potassium.
I no there are drugs for potassium channel blockers would these be as effective.
And Stephen I would love to hear your views on the matter
Hope all u guys are well

New trial at MD Anderson (Houston) for newly diagnosed or first recurrent GBM

A Phase I/II Clinical Trial of Autologous Cytomegalovirus (CMV)-Specific Cytotoxic T Cells for Glioblastoma (GBM) Patients (click here to view detailed trial description)

This is a phase 2, non-randomized, open-label trial.

There are 3 arms: first, a dose expansion study to find the maximum tolerated dose of the CMV-specific T-cells in recurrent GBM at first relapse, along with dose-dense temozolomide.

After finding the maximum tolerated dose, the second arm of recurrent GBM patients undergoes temozolomide treatment for 21 days followed by the first administration of CMV-specific T-cells, followed by surgery for the recurrent tumor on day 30.  After surgery patients undergo another 3 cycles of dose-dense temzolomide followed by T-cell infusions.  Temozolomide is continued for a maximum of 12 cycles or until disease progression.

The third arm consists of newly diagnosed GBM patients treated with dose-dense temozolomide and CMV-specific T-cells, after conventional radiochemotherapy.

All patients undergo a leukapheresis procedure to obtain T-cells, which are reinjected after conditioning.

Chance Gilford's Debut on YouTube

Hi Friends,

We've been through it the last months, but recently Chance has been making a comeback and we just recorded his first YouTube. I wanted to share it here because Stephen, this site, all of you, have been such a blessing to us. We have gone from no conversation to deep and meaningful ones. Tomorrow is not promised but I would have given everything to have such quality time with him and I feel blessed beyond measure. Don't give up, don't give in...

https://www.youtube.com/watch?v=s5LIwwQTQGY

Drop in White Blood Counts and Neutrophils: Need cocktail update advice

Stephen and all --
Mom's white blood cell counts and Neutrophils dropped below lower threshold after 4 weeks of radio-chemotherapy and our cocktail which included many things... but I am suspecting this due to one of the following:  Temodar, Celebrex, Chloroquine, Minocycline, Metformin or Artimisinin.

Our NO asked us to discontinue Temodar. She is not aware of our cocktail. I read online the Celebrex affects Neutrophils counts.

Any guess as to this is primarily due to Temodar or any other drugs? What medicines out of the above would you recommend us continue along with Radiation in case if we must drop Temodar for now?

thx

New Chloroquine trial set to start in July

A Phase I Trial for the Addition of Chloroquine, an Autophagy Inhibitor, to Concurrent Chemoradiation for Newly Diagnosed Glioblastoma

NCT02378532

Hives - Rash

Hello all,

I am on my currently progressing thru my maintenance cycles of Temador.  The 1st 6 cycles were done with a trial drug, Velibipar.

Now with cycles 7 and 8 of just my 400 mg of Temador, I have had hives break out the day after taking my last pills.  Benadryl has helped reduce the welts and itchiness.

Anyone else experience this?

Marc

Phase 1 trial results for tumor resection + Toca511 and TocaFC

Study results were just published today in Science Translational Medicine.  Find the study in the main area of the Library.

Partially metronomic TMZ schedule

Hi all!

I would be happy to hear your advice on metronomic TMZ administration. That has been widely discussed here already but I've got a specific question.

My dad's GBM is MGMT unmethylated (and there is some contrast enhancement after the radiochemotherapy). Our oncologist obviously doesn't have anything else to offer so she proposed cycles of monotherapy with 300 mg TMZ daily in the standard schedule 5/23, i.e. 3x100 mg TMZ capsules daily.

Is there any sense of switching to some "partial" metronomic schedule, i.e. he would take 1 capsule of 100 mg TMZ every day for 15 days. After 15 days we'll run out of TMZ (we've got 1500 mg in 100-mg-capsules for one cycle). The oncologist wouldn't agree to put him on full metronomic schedule as this is not allowed officially...
So to conclude, it would be 15 days on (100 mg daily), 13 days off.

High five from Poland!