Kalorirestriktiv ketogen diett (høy fett, lav karb og moderat med protein).
- Boswellia 3-4 g og bromelain
- Curcumin fra Doctors best 6-8 g
- Edelfosine/miltefosine (L)
- GLA 1-4 g
- Selenium 800-1000 ug (helst i form av selenite)
- Vitamin D3 (5000 iu daglig)
- Vitamin E (Delta Tocotrienols)
- Cantron/Protocel 50
- Chaga (Betulinic acid)
- Chlorella (N)
- Chloroquine (L)
- Germanium 132
- Melatonin (15-40 mg daglig) (N), (R)
- Newcastle Virus (L)
- Perillyl Alcohol (POH)
- Sodium Phenylbutyrate/Anti-neoplastons
- Thalidomide (L)
- Valgancylcovir (L)
- Cyclopamine + lovastatin
- In Search of a Breakthrough Therapy for Glioblastoma Multiforme. Neuroglia 2018, 1(2), 292-307
In vitro and in vivo efficacy of edelfosine-loaded lipid nanoparticles against glioma.
J Control Release. 2011 Jul 28.
Our results showed that Tween® 80 coated Compritol® and Precirol® LN can effectively inhibit the growth of C6 glioma cells in vitro and suggest that edelfosine-loaded LN represent an attractive option for the enhancement of antitumor activity on brain tumors in vivo.
A phase 1/2 study of orally administered synthetic hypericin (Johannesurt) for treatment of recurrent malignant gliomas.
Cancer. 2011 Mar 31. doi: 10.1002/cncr.26123. [Epub ahead of print]
Synthetic hypericin administered orally appeared to provide stabilization or a slight (<50%) decrease in tumor volume (coded as stable disease) at 3 months for 7 of 42 patients (17%) and produced a tumor reduction >50% (partial response) in 2 patients (5%). Seventeen patients (40%) survived for 3 months on daily synthetic hypericin at dose levels of 0.33 ± 0.070 mg/kg daily. The mean maximum tolerated dose was 0.40 ± 0.098 mg/kg daily. Twelve patients continued on hypericin therapy beyond 3 months. The median survival was 26 weeks (Kaplan-Meier method).
Inhibitive effect of artemether on tumor growth and angiogenesis in the rat C6 orthotopic brain gliomas model.
Integr Cancer Ther. 2009 Jun;8(2):195.
There were remarkably inhibitory effects of artmeter on brain glioma growth and angiogenesis in SD rats and the mechanism that artemether inhibited brain glioma growth might be penetrating the blood-brain barrier and inhibiting angiogenesis.
Lactate promotes glioma migration by TGF-β2–dependent regulation of matrix metalloproteinase-2
Neuro Oncol. 2009 August; 11(4): 368–380.
Lactate dehydrogenase type A (LDH-A) is a key metabolic enzyme catalyzing pyruvate into lactate and is excessively expressed by tumor cells. Transforming growth factor-β2 (TGF-β2) is a key regulator of invasion in high-grade gliomas, partially by inducing a mesenchymal phenotype and by remodeling the extracellular matrix.
Metabolic management of glioblastoma multiforme using standard therapy together with a restricted ketogenic diet: Case Report.
Nutr Metab (Lond). 2010 Apr 22;7:33.
This is the first report of confirmed GBM treated with standard therapy together with a restricted ketogenic diet. As rapid regression of GBM is rare in older patients following incomplete surgical resection and standard therapy alone, the response observed in this case could result in part from the action of the calorie restricted ketogenic diet. Further studies are needed to evaluate the efficacy of restricted ketogenic diets, administered alone or together with standard treatment, as a therapy for GBM and possibly other malignant brain tumors.
Targeting energy metabolism in brain cancer through calorie restriction and the ketogenic diet.
J Cancer Res Ther. 2009 Sep;5 Suppl 1:S7-15.
We propose a different approach to brain cancer management that exploits the metabolic flexibility of normal cells at the expense of the genetically defective and less metabolically flexible tumor cells. This approach to brain cancer management is supported from recent studies in orthotopic mouse brain tumor models and in human pediatric astrocytoma treated with calorie restriction and the ketogenic diet. Issues of implementation and use protocols are discussed.
The ERGO trial: A pilot study of a ketogenic diet in patients with recurrent glioblastoma.
J Clin Oncol 28, 2010 (suppl; abstr e12532)
Conclusions: This ketogenic diet is feasible and safe and has antitumor activity in glioma patients. The combination of the diet with antiangiogenic agents appears promising according to theoretical considerations and our preliminary data. Randomized trials evaluating the therapeutic potential of ketogenic diets in tumor patients are warranted.
Modulation of glioma risk and progression by dietary nutrients and anti-inflammatory agents
Nutr Cancer. 2011;63(2):174-84.
Scientific evidence suggests that certain natural dietary components, such as phytoestrogens, flavonoids, polyunsaturated fatty acids, and vitamins, may exert a protective effect against gliomas by changing the nature of the interaction between genetics and environment. Similarly, certain antiinflammatory drugs and dietary modifications, such as methionine restriction and the adoption of low-calorie or ketogenic diets, may take advantage of glioma and normal glial cells’ differential requirements for glucose, methionine, and ketone bodies and may, therefore, be effective as part of preventive or treatment strategies for gliomas.