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Nathan Goodyear

The Long-term Survival of a Patient With Pancreatic Cancer With Metastases to the Liver... - 0 views

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    IV ALA + po LDN found to be effective in pancreatic cancer-case study.
Nathan Goodyear

Revisiting the ALA/N (a-Lipoic Acid/Low- Dose Naltrexone) Protocol for People With Meta... - 0 views

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    3 case studies of the use of ALA and LDN to treat pancreatic cancer.
Nathan Goodyear

PO-238 Dichloroacetate (DCA) treatment affects mitochondrial activity and ste... - 0 views

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    DCA shown to decrease tumor size in mouse model of pancreatic cancer stem cells.
Nathan Goodyear

Revisiting the ALA/N (a-Lipoic Acid/Low- Dose Naltrexone) Protocol for People With Meta... - 0 views

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    3 case studies on the benefit of IV ALA and po LDN in the treatment of pancreatic cancer.
Nathan Goodyear

Effect of Small Interference RNA Targeting HIF-1α Mediated by rAAV Combined L... - 0 views

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    Vitamin C "restrains" HIF-1 expression according to authors of this in vivo study of pancreatic cancer.
Nathan Goodyear

Treatment of pancreatic cancer with intravenous vitamin C: a... : Anti-Cancer Drugs - 0 views

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    High dose vitamin C found to be effective in partial regression of pancreatic cancer.
Nathan Goodyear

Hypereosinophilia Induced by High-Dose Intratumoral and Peritumoral Mistletoe Applicati... - 0 views

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    IV and Intratumoral mistletoe induced hypereosinophilia in pancreatic cancer case study.
Nathan Goodyear

Frontiers | Antitumor Effects of Cannabinoids in Human Pancreatic Ductal Adenocarcinoma... - 0 views

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    dose-dependent trigger of pancreatic cancer apoptosis in mouse model. They dosed up to 10 mg/kg at a ratio of THC:CBD of 1:6.
Nathan Goodyear

Cannabinoids Inhibited Pancreatic Cancer via P-21 Activated Kinase 1 Mediated Pathway -... - 0 views

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    THC:CBD target pancreatic cancer which expresses KRAS mutation appx 90% of time.
Nathan Goodyear

Mechanisms of Pancreatic β-Cell Death in Type 1 and Type 2 Diabetes - 0 views

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    inflammation leads to death of pancreatic beta cells and result in diabetes.
Nathan Goodyear

Cytokines in the Progression of Pancreatic β-Cell Dysfunction - 0 views

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    inflammatory cytokines lead to progressive pancreatic Beta islet cells dysfunction and resultant diabetes.
Nathan Goodyear

Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive ... - 0 views

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    high dose IV vitamin C shown to be treatment option in Cancer.  Granted in a mouse study, but high dose IV vitamin C shown to decrease growth rates of ovarian, pancreatic, and glioblastoma cancers.
Nathan Goodyear

The role of octreotide and somatostatin in acute a... [Digestion. 1999] - PubMed - NCBI - 0 views

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    Octreotide useful in pancreatitis.
Nathan Goodyear

Interaction of gonadal status with syste... [Support Care Cancer. 2011] - PubMed - NCBI - 0 views

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    pancreatic cancer survival risk is shorted by 2.43 with elevated estradiol in women.  This risk is linked to an increase in TNF alpha.  In contrast, men survival risk was worse by 1.96 odds ratio with low Testosterone.  Again, inflammation was the culprit.
Nathan Goodyear

Efficacy of liposomal curcumin in a human pan... [Anticancer Res. 2013] - PubMed - NCBI - 0 views

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    liposomal curcumin at 20 mg/kg reduced pancreatic tumor growth by 42% in in vitro and xenograft studies.  The curcumin, the most prevalent polyphenol in tumeric, was given intraperitoneal in this study.
Nathan Goodyear

Nuclear factor-kappaB and IkappaB kinase are constitu... [Cancer. 2004] - PubMed - NCBI - 0 views

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    curcumin down regulates NF-kappaB in pancreatic cancer.
Nathan Goodyear

Boswellic Acid Suppresses Growth and Metastasis of Human Pancreatic Tumors in an Orthot... - 0 views

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    Study finds that acetyl-11-keto-Beta-boswellic acid (AKBA) reduced growth of pancreatic cancer and metastasis in mouse model.  AKBA also inhibits NF-kappaB and induced apoptosis.  AKBA is found in Frankinsense. 
Nathan Goodyear

Anticancer mechanisms of cannabinoids - 0 views

  • modulating key cell signalling pathways involved in the control of cancer cell proliferation and survival
  • cannabinoids inhibit angiogenesis and decrease metastasis in various tumour types in laboratory animals
  • Cannabis sativa L. (marijuana)
  • ...41 more annotations...
  • of the approximately 108 cannabinoids produced by C. sativa, Δ9-tetrahydrocannabinol (thc) is the most relevant because of its high potency and abundance in plant preparations
  • Tetrahydrocannabinol exerts a wide variety of biologic effects by mimicking endogenous substances—the endocannabinoids anandamide3 and 2-arachidonoylglycerol4,5—that engage specific cell-surface cannabinoid receptors
  • the cb2 receptor was initially described to be present in the immune system6, but was more recently shown to also be expressed in cells from other origins
  • transient receptor potential cation channel subfamily V, member 1
  • orphan G protein–coupled receptor 55
  • Most of the effects produced by cannabinoids in the nervous system and in non-neural tissues rely on cb1 receptor activation
  • two major cannabinoid-specific receptors—cb1 and cb2
  • cardiovascular tone, energy metabolism, immunity, and reproduction
  • cannabinoids are well known to exert palliative effects in cancer patients
  • best-established use is the inhibition of chemotherapy-induced nausea and vomiting
  • thc and other cannabinoids exhibit antitumour effects in a wide array of animal models of cancer
  • cannabinoid receptors and their endogenous ligands are both generally upregulated in tumour tissue compared with non-tumour tissue
  • cb2 promotes her2 (human epidermal growth factor receptor 2) pro-oncogenic signalling in breast cancer
  • pharmacologic activation of cannabinoid receptors decreases tumour growth
  • endocannabinoid signalling can also have a tumour-suppressive role
  • pharmacologic stimulation of cb receptors is, in most cases, antitumourigenic. Nonetheless, a few reports have proposed a tumour-promoting effect of cannabinoids
  • most prevalent effect is the induction of cancer cell death by apoptosis and the inhibition of cancer cell proliferation
  • impair tumour angiogenesis and block invasion and metastasis
  • thc and other cannabinoids induce the apoptotic death of glioma cells by cb1- and cb2-dependent stimulation
  • Autophagy is primarily a cytoprotective mechanism, although its activation can also lead to cell death
  • autophagy is important for cannabinoid antineoplastic activity
  • autophagy is upstream of apoptosis in the mechanism of cannabinoid-induced cell death
  • the effect of cannabinoids in hormone- dependent tumours might rely, at least in part, on the ability to interfere with the activation of growth factor receptors
  • glioma cells), pharmacologic blockade of either cb1 or cb2 prevents cannabinoid-induced cell death with similar efficacy
  • other types of cancer cells (pancreatic48, breast24, or hepatic43 carcinoma cells, for example), antagonists of cb2 but not of cb1 inhibit cannabinoid antitumour actions
  • thc promotes cancer cell death in a cb1- or cb2-dependent manner (or both) at lower concentrations
  • cannabidiol (cbd), a phytocannabinoid with a low affinity for cannabinoid receptors15, and other marijuana-derived cannabinoids57 have also been proposed to promote the apoptotic death of cancer cells acting independently of the cb1 and cb2 receptors
  • In cancer cells, cannabinoids block the activation of the vascular endothelial growth factor (vegf) pathway, an inducer of angiogenesi
  • In vascular endothelial cells, cannabinoid receptor activation inhibits proliferation and migration, and induces apoptosis
  • cb1 or cb2 receptor agonists (or both) reduce the formation of distant tumour masses in animal models of both induced and spontaneous metastasis, and inhibit adhesion, migration, and invasiveness of glioma64, breast65,66, lung67,68, and cervical68 cancer cells in culture
  • the ceramide/p8–regulated pathway plays a general role in the antitumour activity of cannabinoids targeting cb1 and cb2
  • cbd, by acting independently of the cb1 and cb2 receptors, produces a remarkable anti-tumour effect—including reduction of invasiveness and metastasis
  • cannabinoids can also enhance immune system–mediated tumour surveillance in some contexts
  • ability of thc to reduce inflammation75,76, an effect that might prevent certain types of cancer
  • recent observations suggest that the combined administration of cannabinoids with other anticancer drugs acts synergistically to reduce tumour growth
  • combined administration of gemcitabine (the benchmark agent for the treatment of pancreatic cancer) and various cannabinoid agonists synergistically reduced the viability of pancreatic cancer cells
  • Other reports indicated that anandamide and HU-210 might also enhance the anticancer activity of paclitaxel89 and 5-fluorouracil90 respectively
  • Combined administration of thc and cbd enhances the anticancer activity of thc and reduces the dose of thc needed to induce its tumour growth-inhibiting activity
  • Preclinical animal models have yielded data indicating that systemic (oral or intraperitoneal) administration of cannabinoids effectively decreases tumour growth
  • Combinations of cannabinoids with classical chemotherapeutic drugs such as the alkylating agent temozolomide (the benchmark agent for the management of glioblastoma80,84) have been shown to produce a strong anticancer action in animal models
  • pharmacologic inhibition of egfr, erk83, or akt enhances the cell-death-promoting action of thc in glioma cultures (unpublished observations by the authors), which suggests that targeting egfr and the akt and erk pathways could enhance the antitumour effect of cannabinoids
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    Good review of the anticancer effects of cananbinoids.
Nathan Goodyear

ScienceDirect - 0 views

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    metformin augments chemotherapy in the treatment of pancreatic cancer. It promotes the anti-proliferative effects of mTORC and inhibits the proliferative PI3k/mTOR. It also works synergistically with the known anti-tumor anti-malarial drugs chloroquine and with the herb berberine.
Nathan Goodyear

From the Cover: Pharmacologic doses of ascorbate act as a prooxidant and decrease growt... - 0 views

  • An extensive panel of 43 tumor and 5 normal cell lines were exposed to ascorbate in vitro for ≤2 h to mimic clinical pharmacokinetics
  • effective concentration that decreased survival 50% (EC50) was determined. EC50 was <10 mM for 75% of tumor cells tested, whereas cytotoxicity was not evident in normal cells with >20 mM ascorbate
  • The addition of catalase to the medium ameliorated death of ovarian carcinoma (Ovcar5), pancreatic carcinoma (Pan02), and glioblastoma (9L) cells exposed to 10 mM ascorbate (1 h), indicating cytotoxicity was mediated by H2O2
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  • A treatment dose of 4 g ascorbate/kg body weight either once or twice daily did not produce any discernible adverse effects
  • Xenograft experiments showed that parenteral ascorbate as the only treatment significantly decreased both tumor growth and weight by 41–53%
  • Peak plasma concentrations of ascorbate approached 30 mM
  • Pharmacologic concentrations of ascorbate decreased tumor volumes 41–53% in diverse cancer types known for both their aggressive growth and limited treatment options.
  • Our findings showed that pharmacologic ascorbic acid concentrations were cytotoxic to many types of cancer cells in vitro (Fig. 1A) and significantly impeded tumor progression in vivo without toxicity to normal tissues
  • The amelioration of ascorbate cytotoxicity in vitro by the addition of catalase was consistent among sensitive cancer cells (Fig. 1B) and points unambiguously to H2O2 generation in the extracellular medium
  • the current in vivo data support that pharmacologic ascorbate concentrations, which can readily be achieved in humans (Fig. 3E), diminished growth of several aggressive cancer types in mice (Fig. 2) without causing apparent adverse effects.
  • These intratumoral H2O2 concentrations of >125 μM persisted for >3 h after ascorbate administration
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    Tumor xenograft model in mice finds reduction in growth rates of ovarian cancer, pancreatic cancer, and glioblastoma with daily IV vitamin C.
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