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Nathan Goodyear

Increasing incidence of glioblastoma multiforme and meningioma, and decreasing incidenc... - 0 views

www.ncbi.nlm.nih.gov/...PMC3263004

brain tumor tumors brain tumor meningioma glioblastoma multiforme Schwannoma australian study

shared by Nathan Goodyear on 05 Feb 13 - No Cached
  • Nathan Goodyear on 05 Feb 13
     
    Granted, this is an Australian study, but they found an increasing incidence of certain tumors: significant increase in glioblastoma multiforme in both men and women and increasing trends of meningioma's in men.  The good news, is they found a decreasing incidence of Schwannoma in women.
Nathan Goodyear

Metabolic management of glioblastoma multiforme using standard therapy together with a ... - 0 views

www.ncbi.nlm.nih.gov/...PMC2874558

ketogenic ketogenic diet cancer ketones ketone bodies

shared by Nathan Goodyear on 17 Nov 16 - No Cached
  • Nathan Goodyear on 17 Nov 16
     
    case study highlights the use of a calorie restricted, ketogenic diet to augment glioblastoma multiforme.  In incomplete resection, at 2 months no brain tumor was visualized via PET and MRI.
Nathan Goodyear

Glutamate release promotes growth of malignant gli... [Nat Med. 2001] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...11533703

glutamate glutamic acid MSG cancer glioblastoma multiforme

shared by Nathan Goodyear on 10 Feb 11 - No Cached
  • Nathan Goodyear on 10 Feb 11
     
    some tumors, glioblastoma multiforme, secrete glutamate, which increases aggressive nature of cancer
Nathan Goodyear

British Journal of Cancer - A pilot clinical study of [Delta]9-tetrahydrocannabinol in ... - 0 views

www.nature.com/...6603236a.html

THC cannabinoids cancer Tetrahydrocannabinol CBD

shared by Nathan Goodyear on 15 Dec 14 - No Cached
  • Nathan Goodyear on 15 Dec 14
     
    Pilot study of THC for advanced, recurrent glioblastoma multiforme.  The infused THC appeared to be safe and provide some anti proliferative activity, but all patients died within 1 year.
Nathan Goodyear

Frontiers | Management of Glioblastoma Multiforme in a Patient Treated With Ketogenic M... - 0 views

www.frontiersin.org/...full

press-pulse therapy hyperbaric ketogenic metabolic therapy cancer ketogenic diet Glioblastoma glioblastoma multiforme HBOT nutrition

shared by Nathan Goodyear on 01 Apr 18 - No Cached
  • The SOC for GBM was modified in this patient to initiate KMT prior to surgical resection, to eliminate steroid medication, and to include HBOT as part of the therapy
  • the greatest therapeutic benefit for patients (near 1.0)
  • The observed reduction in blood glucose in our patient would reduce lactic acid fermentation in the tumor cells, while the elevation of ketone bodies would fuel normal cells thus protecting them from hypoglycemia and oxidative stress
  • ...30 more annotations...
  • Previous studies showed that GBM survival and tumor growth was correlated with blood glucose levels
  • Evidence indicates that glioma cells cannot effectively use ketone bodies for energy due to defects in the number, structure, and function of their mitochondria
  • The accuracy of the GKI as a predictor for therapeutic efficacy, however, is better when ketone bodies are measured from the blood than when measured from the urine
  • A reduction of glucose-driven lactic acid fermentation would not only increase tumor cell apoptosis, but would also reduce inflammation and edema in the tumor microenvironment thus reducing tumor cell angiogenesis and invasion
  • Besides serving as a metabolic fuel for GBM, glutamine is also an essential metabolite for normal immune cells
  • therapies that inhibit glutamine availability and utilization must be strategically employed to avoid inadvertent impairment of immune cell functions
  • we used the non-toxic green tea extract, EGCG, and chloroquine in an attempt to limit glutamine availability to the tumor cells
  • EGCG is thought to target the glutamate dehydrogenase activity that facilitates glutamine metabolism in GBM cells
  • Chloroquine, on the other hand, will inhibit lysosomal digestion thus restricting fermentable amino acids and carbohydrates from phagocytosed materials in the tumor microenvironment
  • HBOT to increase oxidative stress in the tumor cells
  • As glucose and glutamine fermentation protect tumor cells from oxidative stress, reduced availability of these metabolites under ketosis could enhance the therapeutic action of HBOT, as we recently described
  • Prior to subtotal tumor resection and standard of care (SOC), the patient conducted a 72-h water-only fast
  • Following the fast, the patient initiated a vitamin/mineral-supplemented ketogenic diet (KD) for 21 days that delivered 900 kcal/day
  • KD (increased to 1,500 kcal/day at day 22
  • the patient received metformin (1,000 mg/day), methylfolate (1,000 mg/day), chloroquine phosphate (150 mg/day), epigallocatechin gallate (400 mg/day), and hyperbaric oxygen therapy (HBOT) (60 min/session, 5 sessions/week at 2.5 ATA)
  • Biomarkers showed reduced blood glucose and elevated levels of urinary ketones with evidence of reduced metabolic activity (choline/N-acetylaspartate ratio) and normalized levels of insulin, triglycerides, and vitamin D
  • This is the first report of confirmed GBM treated with a modified SOC together with KMT and HBOT, and other targeted metabolic therapies
  • Glioblastoma multiforme (GBM) is the most common and malignant of the primary adult brain cancers
  • less than 20% of younger adults generally survive beyond 24 months
  • glucose and glutamine are the primary fuels that drive the rapid growth of most tumors including GBM
  • Glucose drives tumor growth through aerobic fermentation (Warburg effect), while glutamine drives tumor growth through glutaminolysis
  • The fermentation waste products of these molecules, i.e., lactic acid and succinic acid, respectively, acidify the tumor microenvironment thus contributing further to tumor progression
  • Glucose and glutamine metabolism is also responsible for the high antioxidant capacity of the tumor cells thus making them resistant to chemo- and radiotherapies
  • The reliance on glucose and glutamine for tumor cell malignancy comes largely from the documented defects in the number, structure, and function of mitochondria and mitochondrial-associated membranes
  • These abnormalities cause the neoplastic GBM cells to rely more heavily on substrate level phosphorylation than on oxidative phosphorylation for energy
  • dexamethasone not only increases blood glucose levels but also increases glutamine levels through its induction of glutamine synthetase activity
    • Nathan Goodyear
      Nathan Goodyear on 21 May 18
       
      use mannitol instead
  • Calorie restriction and restricted KD are anti-angiogenic, anti-inflammatory, anti-invasive, and also kill tumor cells through a proapoptotic mechanism
  • Evidence also shows that therapeutic ketosis can act synergistically with several drugs and procedures to enhance cancer management improving both progression free and overall survival
  • hyperbaric oxygen therapy (HBOT) increases oxidative stress on tumor cells especially when used alongside therapies that reduce blood glucose and raise blood ketones
  • The glutamine dehydrogenase inhibitor, epigallocatechin gallate (EGCG) is also proposed to target glutamine metabolism
  • Nathan Goodyear on 01 Apr 18
     
    Case study of Glioblastoma treated with ketogenic metabolic therapy as an adjuct to modified standard therapy.
Nathan Goodyear

Management of Glioblastoma Multiforme in a Patient Treated With Ketogenic Metabolic The... - 0 views

www.ncbi.nlm.nih.gov/...PMC5884883

glioblastoma glioblastoma multiforme "brain cancer" cancer ketogenic diet

shared by Nathan Goodyear on 23 Dec 18 - No Cached
  • Nathan Goodyear on 23 Dec 18
     
    Great case study of Glioblastoma
Nathan Goodyear

Artesunate enhances the therapeutic response of glioma cells to temozolomide by inhibit... - 0 views

www.ncbi.nlm.nih.gov/...PMC5341871

Cancer artesunate temodar glioblastoma glioblastoma multiforme

shared by Nathan Goodyear on 19 Dec 18 - No Cached
  • Nathan Goodyear on 19 Dec 18
     
    Artesunate augments Temodar in animal model of glioblastoma.
Nathan Goodyear

Corticosteroids compromise survival in glioblastoma in part through their elevation of ... - 0 views

academic.oup.com/...2715227

glioblastoma glioblastoma multiforme "brain cancer" cancer glucose

shared by Nathan Goodyear on 23 Dec 18 - No Cached
  • Nathan Goodyear on 23 Dec 18
     
    Corticosteroids elevate glucose in patients with glioblastomas, compromising treatment and shortening survival.
Nathan Goodyear

The current state and future perspectives of cannabinoids in cancer biology - 0 views

www.ncbi.nlm.nih.gov/...PMC5852356

Cancer CBD THC cannabinoids

shared by Nathan Goodyear on 19 Sep 18 - No Cached
hoangkimchi liked it
  • The activation of each of them leads to an inhibition of adenylyl cyclase via G proteins (Gi/o), which in turn activates many metabolic pathways such as mitogen‐activated protein kinase pathway (MAPK), phosphoinositide 3‐kinase pathway (PI3K), cyclooxygenase‐2 pathway (COX‐2), accumulation of ceramide, modulation of protein kinase B (Akt), and ion channels
  • phytocannabinoids, endocannabinoids, and synthetic cannabinoids
  • Action of THC in human organism relies on mimicking endogenous agonists of CB receptors—endocannabinoids
  • ...8 more annotations...
  • The upregulated expression of CB receptors and the elevated levels of endocannabinoids have been observed in a variety of cancer cells (skin, prostate, and colon cancer, hepatocellular carcinoma, endometrial sarcoma, glioblastoma multiforme, meningioma and pituitary adenoma, Hodgkin lymphoma, chemically induced hepatocarcinoma, mantel cell lymphoma)
  • concentration of endocannabinoids, expression level of their receptors, and the enzymes involved in their metabolism frequently are associated with an aggressiveness of cancer
  • CB2 receptor contributes to human epidermal growth factor receptor (HER2) pro‐oncogenic signaling and an overexpression of CB2 increases susceptibility for leukemia development after leukemia viral infection
  • endocannabinoid‐degrading enzymes are upregulated in cancer cell lines and in human tumors
  • Many cannabinoids, ranging from phytocannabinoids (THC, CBD), endocannabinoids (2‐arachidonoylglycerol, anandamide), to synthetic cannabinoids (JWH‐133, WIN‐55,212‐2), have shown ability to inhibit proliferation, metastasis, and angiogenesis in a variety of models of cancer
  • Despite some inconsistent data, the main effect of cannabinoids in a tumor is the inhibition of cancer cells’ proliferation and induction of cancer cell death by apoptosis
  • CB1 and CB2 receptor agonists stimulate apoptotic cell death in glioma cells by induction of de novo synthesis of ceramide, sphingolipid with proapoptotic activity
  • process of autophagy is upstream of apoptosis in mechanism of cell death induced by cannabinoids
Nathan Goodyear

Hexokinase 2 is a key mediator of aerobic glycolysis and promotes tumor growth in human... - 0 views

jem.rupress.org/313

Hexokinase "hexokinase 2" "hexokinase II" glioblastoma cancer

shared by Nathan Goodyear on 19 Jan 19 - No Cached
  • Nathan Goodyear on 19 Jan 19
     
    to be read: hexokinase II and glioblastoma
Nathan Goodyear

Imp2 controls oxidative phosphorylation and is crucial for preserving glioblastoma canc... - 0 views

www.ncbi.nlm.nih.gov/...PMC3435496

cancer glioblastoma glioblastoma multiforme "brain cancer" CSC cancer stem cells oxidative phosphorylation

shared by Nathan Goodyear on 28 Nov 18 - No Cached
  • Nathan Goodyear on 28 Nov 18
     
    Glioblastoma's CSCs found to rely on oxidative phosphorylation metabolism and not aerobic glycolysis.
Nathan Goodyear

Anticancer Effects of Niclosamide in Human Glioblastoma | Clinical Cancer Research - 0 views

clincancerres.aacrjournals.org/...4124.long

Niclosamide cancer Glioblastoma glioblastoma multiforme NOTCH mTOR Wnt

shared by Nathan Goodyear on 16 Apr 18 - No Cached
  • glioblastoma remains a fatal disease with a median overall survival time of only 15 months
  • inter- and intrapatient tumor heterogeneity
  • cellular and genetic diversity that characterizes glioblastoma
  • ...5 more annotations...
  • This broad effect could be a result of niclosamide's pleiotropic activity, similarly affecting signaling pathways that are known to be overly active in human malignant cells (i.e., mTOR, NOTCH, WNT/CTNNB1; refs. 44–46)
  • It is a salicylanilide that was introduced as a molluscide in 1959
  • Studies in animals suggested no mutagenic, oncogenic, or embryotoxic activity and no cumulative effects
  • its rate of absorption from the intestinal tract was estimated at only 33%
  • the potential mechanism of synergy between temozolomide and niclosamide as a “natural inducer” of NFKBIA
  • Nathan Goodyear on 16 Apr 18
     
    Niclosamide pilot animal study useful in the treatment of Glioblastoma.  Found to inhibit NOTCH, mTOR, and WNT and cancer signaling. Also found to reduce the malignant potential through cytostatic, cytotoxic and antimigratory effects of niclosamide on GBM
Nathan Goodyear

The anti‐hypertensive drug prazosin inhibits glioblastoma growth via the PKCδ... - 0 views

embomolmed.embopress.org/...511

Glioblastoma glioblastoma multiforme hypertension prazosin cancer

shared by Nathan Goodyear on 14 May 18 - No Cached
  • glioblastoma‐initiating cells (GICs)
  • Nathan Goodyear on 14 May 18
     
    prazosin promotes apoptosis of gliobastoma-initiating cells in mouse model via Akt pathway.
Nathan Goodyear

Hypertension as a biomarker in patients with recurrent glioblastoma treated with antian... - 0 views

www.ncbi.nlm.nih.gov/...23075631

hypertension glioblastoma multiforme Glioblastoma

shared by Nathan Goodyear on 14 May 18 - No Cached
  • Nathan Goodyear on 14 May 18
     
    treatment with anti-angiogenesis meds often are associated with the SE of HTN; What is interesting about this is that this is associated with improved survival.
Nathan Goodyear

First results on survival from a large Phase 3 clinical trial of an autologous dendriti... - 0 views

translational-medicine.biomedcentral.com/...s12967-018-1507-6

dendritic cells cancer glioblastoma multiforme glioblastoma brain cancer

shared by Nathan Goodyear on 01 Jun 18 - No Cached
  • Nathan Goodyear on 01 Jun 18
     
    Dendritic therapy, I think the use of vaccine is completely inappropriate here, found to extend life in those with methylated MGMT.  This phase III trial is still on going, but this is a very positive future therapy in the immunotherapy attack against cancer.
Nathan Goodyear

Curcumin decreases malignant characteristics of glioblastoma stem cells via induction o... - 0 views

bmccancer.biomedcentral.com/...s12885-017-3058-2

STAT3 ROS MAPK curcumin glioblastoma multiforme

shared by Nathan Goodyear on 17 Apr 21 - No Cached
  • Nathan Goodyear on 17 Apr 21
     
    Curcumin increases ROS in glioblastoma.
Nathan Goodyear

Metronomic capecitabine as an immune modulator in glioblastoma patients reduces myeloid... - 0 views

pubmed.ncbi.nlm.nih.gov/31600167

myeloid-derived suppressor cells glioblastoma multiforme metronomic chemotherapy low-dose chemotherapy MDSC glioblastoma

shared by Nathan Goodyear on 08 Nov 20 - No Cached
  • Nathan Goodyear on 08 Nov 20
     
    Low-dose, metronomic chemotherapy induces suppression of MDSCs in the TME in glioblastoma.
Nathan Goodyear

VEGF receptor inhibitors block the ability of metronomically dosed cyclophosphamide to ... - 0 views

www.ncbi.nlm.nih.gov/...PMC3294103

low-dose chemotherapy glioblastoma multiforme VEGF glioblastoma cancer metronomic chemotherapy

shared by Nathan Goodyear on 11 Nov 20 - No Cached
  • Nathan Goodyear on 11 Nov 20
     
    CPA administered on an intermittent, every 6-day metronomic schedule stimulates tumor recruitment of macrophages, natural killer (NK) cells, and dendritic cells with regression of large established tumors, as seen in several implanted glioma models; also of note, VEGF inhibition inhibited this effect.
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