By Keir Liddle
Dr Burzynskis Antineoplasteon (ANP) therapy has a tragically impressive list of failures but he appears to have a few success stories (even after you account for those who didn’t actually survive). But do these prove the effectiveness of ANPs as a treatment for cancer or is there perhaps something else that could explain the lucky few who his treatment appears to help?
The Burzynski clinic provides information for new patientsabout what treatment involves and what drugs patients will be taking alongside ANP treatment. This document explains how ANPs Atengenal (A10) and Astugenal (AS2-1) are to be delivered via an infusion pump. It details how ANP should be stored and shipped, they should be at a controlled temperature within the storage range (15-30 degrees Celsius or 59-86 degrees Fahrenheit) and tells the patients nurses will demonstrate the process the patients should use themselves for dressing changes, flushing, disconnecting, and reconnecting and medication administration via Hickman line.
Among other details the information provided to patients also details the other kinds of drugs they may also be prescribed alongside their course of ANP: anticonvulsants and steroids. Which are fairly standard types of drug to prescribe someone with a brain tumour, alongside treatment, as they aid recovery and assist with common side effects.
Anticonvulsants and steroids are routinely prescribed to combat the side effects of brain tumours including intercranial swelling fluid leaking into surrounding brain areas causing edema (pressure that disrupts the function of surrounding brain regions). These drugs are used to deal with side effects as diverse as grand mal seizures, language difficulties and other cognitive impairments.
However certain steroids used in cancer patients can have another surprising result, one that has implications when attempting to determine if Dr Burzynskis patients response on Magnetic Resonance Imaging (MRI) scans.
Dexamethasone, a steroid commonly used to combat the symptoms of tumour growth and brain swelling, is the steroid listed in Burzynskis patient information as being administered alongside ANP. Dexamethasone has become the steroid of choice in brain oedema due to its minimal salt retention and its relative potency when compared with other steroids.
A number of studies have revealed that prescription of dexamethasone has interesting implications when it comes to determining tumour progression or remission using MRI scans. As it can make it appear as if tumours are shrinking, or indeed vanishing, when they are not.
In a case reported in the Journal of Neurology, Neurosurgery and Psychiatry in 1997 a 56 year old man was treated for a left frontoparietal mass with oedema (brain tumour with swelling) with 2 mg dexamethasone three times daily. This treatment resulted in a resolution of his symptoms and after the patients brain was scanned and the oedema and the tumour had apparently disappeared (even with the use of contrast enhancement) the patient was sent home. The patient was scheduled for a biopsy three weeks later and was readmitted and rescanned. Having been removed from steroid treatment the tumour was again visible on the scan and massive brain swelling has occurred. The histology of the tumour showed it was a glioblastoma multiforme. He was admitted to intensive care and tragically he died within a few hours.
The doctors concluded that:
“You cannot be sure what the lesion is unless you have tissue for histology. It also shows that steroids can reduce the peritumorous oedema and apparent tumour size so that the tumour effectively disappears on the scans.”
A similar case is reported in the Journal of Clinical Neuroscience where a 59-year-old man presented with a history of headache and confusion. A CT scan of the brain showed a tumour on the left parietal lobe adjacent to the posterior horn of the lateral ventricle. Again the patient received dexamethasone (16 mg/day), again the enhancing lesion seen on CT scan faded following dexamethasone therapy and again teh subsequent biopsy revealed the tumour to be a glioblastoma multiforme. The study authors note that:
“Various intrinsic cerebral lesions have been noted to disappear on CT imaging after the administration of corticosteriods,1 but it is less common for a glioma to do so.”
They further conclude that:
“This report reiterates the potential pitfall of presumptive diagnosis and highlights the importance of MRI guided biopsy in patients where a tumor fades on CT imaging after corticosteroid therapy. We also highlight the need to clarify the actions of corticosteroids on specific tumor types.”
Again highlighting that one cannot rely on MRI scans as reliable proof of remission in cases of brain cancer other factors, such as the impact of steroid treatment, may make these scans less than fully reliable.
A paper published as recently as July of this year further highlights the diagnostic dilemma faced by physicians and oncologists in interpreting MRI results where the steroids that are prescribed may give rise to a situation where an MRI gives the false impression that a patients tumour is shrinking or has even vanished when it hasn’t.
Could Burzynskis much touted MRI scans showing dramatic improvement in tumour size, and indeed vanishing tumours, be simply down to the effects of Dexamethasone or could he have stumbled upon dexamethasone as an as of yet undiscovered effective treatment for brain stem cancers?
Research published in the Journal of Clinical Neuroscience throws cold water on the second interpretation as the authors undertook a search of the literature and found:
“only three other similar cases of rapidly vanishing glioblastomas after steroid treatment  and  (Table 1). All three cases were histologically proven glioblastoma multiforme and were given high doses of dexamethasone over a few weeks. Serial imaging performed within a few weeks of commencement of steroids showed a significant degree of resolution of the tumor
From the review, the daily dexamethasone dose ranged from 6 mg to 16 mg per day. The recurrence of the tumor typically was very aggressive and occurred within 1–4 weeks from the time of disappearance.
The glioblastomas that vanish rapidly are frequently multicentric with a predilection for the corpus callosum and are associated with rapid clinical deterioration and demise of the patient.”
The authors conclude that despite indications from MRI scans the prognosis of patients on high dose Dexamethasone remains poor and deterioration is often rapid.
It seems tragically plausible that Dr Burzynskis reported success and tumour reductions are nothing more miraculous than the clinically understood and scientifically reported side effects of steroid treatment. This might explain why so many family and patient blogs happily report successful treatment before going on to report rapid and unexpected deterioration.
Whether Dr Burzynski is aware of the effects and implications of prescribing high dose dexamethasone in determining tumour progression remains unknown. If he is unaware this implies nothing more than incompetence on his part but if he is aware it implies something much more sinister: that he is perhaps knowingly misleading his patients.
Whatever the truth of the matter it will remain unknown until the day Dr Burzynski decides to properly record and publish his results and submit them to the scrutiny of medical science.
Though given he has steadfastly avoided doing so for over 35 years I wouldn’t advise anyone hold their breath.