Skip to main content

Home/ Dr. Goodyear/ Group items tagged C

Rss Feed Group items tagged

Nathan Goodyear

http://www.spectracell.com/media/uploaded/2/0e2938319_1393442221_2132abstract2014nzmedj... - 0 views

  •  
    IV vitamin C at 50 grams twice weekly shown to reduce side effects associated with chemotherapy.  Granted, this is a single case study without comparison, but this is supported by other studies.
Nathan Goodyear

Intravenous vitamin C administration improve... [In Vivo. 2011 Nov-Dec] - PubMed - NCBI - 0 views

  •  
    IV vitamin C in women with breast CA in Germany found to benefit from less side effects and improved quality of life in those receiving chemo/radiation.  Again, IV vitamin C proven to be well tolerated in very ill individuals.
Nathan Goodyear

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

  •  
    Nice study that reveals the pharmacologic mechanism of vitamin C as a pro-oxidant in cancer cells.  Obviously, this effect is opposite that found blood.   In this study they looked at high dose IV vitamin C in the treatment of ovarian, pancreatic, and glioblastoma cancer.  Treatment was beneficial and well tolerated.
Nathan Goodyear

Altered Deoxyribonuclease Activity in Cancer Cells and its Role in Non Toxic Adjuvant C... - 0 views

  •  
    Combination of IV vitamin C and K3 in ratio of 100:1 shown to provide mechanism to induce cancer cell death through a process called autoschizis.
Nathan Goodyear

The association of vitamins C and K3 kills ca... [Eur J Med Chem. 2003] - PubMed - NCBI - 0 views

  •  
    IV vitamin C and K3 show synergistic cancer cell death via autoschizis.
Nathan Goodyear

Intravenous Vitamin C in the treatment of shingles: Results of a multicenter prospectiv... - 0 views

  •  
    IV vitamin C shown to be beneficial in the treatment of Shingles.
Nathan Goodyear

Interference of Intravenous Vitamin C With Blood Glucose Testing - 0 views

  •  
    Case study highlighting the "false" elevations of glucose on strip testing with IV vitamin C.
Nathan Goodyear

European Journal of Clinical Nutrition - Abstract of article: Effect of vitamin C on co... - 0 views

  •  
    vitamin C shown to reduce the # of colds over a 5 year period.  Showing a long-term immune enhancing effect of vitamin C
Nathan Goodyear

Pharmacological ascorbate induces cytotoxic... [Anticancer Drugs. 2012] - PubMed - NCBI - 0 views

  •  
    IV vitamin C induces cell death of prostate cancer cell lines via H2O2, which is not new, but what is new is the ascorbate-insensitive cell line.
Nathan Goodyear

MECHANISMS OF ASCORBATE-INDUCED CYTOTOXICITY IN PANCREATIC CANCER - 0 views

  •  
    Good discussion of the mechanism of action of IV vitamin C in cancer therapy.
Nathan Goodyear

JAMA Network | JAMA | Destruction of Vitamin B12 by Ascorbic Acid - 0 views

  •  
    old study finds oral vitamin C destroyed substantial amount of B12.  This is the reason vitamin B 12 is given when vitamin C is given.
Nathan Goodyear

Effect of intravenous ascorbic acid in hemod... [Am J Kidney Dis. 2006] - PubMed - NCBI - 0 views

  •  
    High dose IV vitamin C shown to be well tolerated in those on hemodialysis.  Liver enzymes were followed throughout the course of the 6 month trial.  In fact, IV vitamin C was shown to improve the response of the EPO therapy.
Nathan Goodyear

Hepatoprotective Effect of Vitamin C (Ascorbic Acid) - 0 views

  •  
    Vitamin C is hepatoprotective.  This review highlights the proposed methods by which vitamin C reduces ALT, AST, alkaline phosphatase, LDH, malondialdegyde...
Nathan Goodyear

The ROS-induced cytotoxicity of ascorbate is attenuated by hypoxia and HIF-1alpha in th... - 0 views

  •  
    vitamin C effects decreased by hypoxia which increases HIF-1alpha.  The authors propose oxygen therapy, hyperbaric, to improve and augment the cytotoxic effects of vitamin C.
Nathan Goodyear

The river blindness drug Ivermectin and related macrocyclic lactones inhibit WNT-TCF pa... - 0 views

  • WNT signaling
  • early colon cancers commonly display loss of function of the tumor suppressor Adenomatous polyposis coli (APC), a key component of the β-CATENIN destruction complex
  • Other cancers also show an active canonical WNT pathway; these include carcinomas of the lung, stomach, cervix, endometrium, and lung as well as melanomas and gliomas
  • ...31 more annotations...
  • In normal embryogenesis and homeostasis, the canonical WNT pathway is activated by secreted WNT ligands produced in highly controlled context-dependent manners and in precise amounts. WNT activity is transduced in the cytoplasm, inactivates the APC destruction complex, and results in the translocation of activate β-CATENIN to the nucleus, where it cooperates with DNA-binding TCF/LEF factors to regulate WNT-TCF targets and the ensuing genomic response
  • beyond the loss of activity of the APC destruction complex, for instance throughAPC mutation, phosphorylation of β-CATENIN at C-terminal sites is required for the full activation of WNT-TCF signaling and the ensuing WNT-TCF responses in cancer.
  • The WNT-TCF response blockade that we describe for low doses of Ivermectin suggests an action independent to the deregulation of chloride channels
  • involve the repression of the levels of C-terminally phosphorylated β-CATENIN forms and of CYCLIN D1, a critical target that is an oncogene and positive cell cycle regulator.
  • the Avermectin single-molecule derivative Selamectin, a drug widely used in veterinarian medicine (Nolan & Lok, 2012), is ten times more potent acting in the nanomolar range
  • Ivermectin also diminished the protein levels of CYCLIN D1, a direct TCF target and oncogene, in both HT29 and H358 tumor cells
  • Activated Caspase3 was used as a marker of apoptosis by immunohistochemistry 48 h after drug treatment. Selamectin and Ivermectin induced up to a sevenfold increase in the number of activated Caspase3+ cells in two primary (CC14 and CC36) and two cell line (DLD1 and Ls174T) colon cancer cell types (Fig​(Fig2C).2C). All changes were significative
  • The strong downregulation of the expression of the intestinal stem cell genesASCL2 andLGR5 (van der Flieret al, 2009; Scheperset al, 2012; Zhuet al, 2012b) by Ivermectin and Selamectin (Fig​(Fig2D)2D) raised the possibility that these drugs could affect WNT-TCF-dependent colon cancer stem cell behavior
  • Pre-established H358 tumors responded to Ivermectin showing a ˜ 50% repression of growth
  • Ivermectin hasin vivo efficacy against human colon cancer xenografts sensitive to TCF inhibition with no discernable side effects
  • Ivermectin (Campbellet al, 1983), an off-patent drug approved for human use, and related macrocyclic lactones, have WNT-TCF pathway response blocking and anti-cancer activities
  • these drugs block WNT-TCF pathway responses, likely acting at the level of β-CATENIN/TCF function, affecting β-CATENIN phosphorylation status.
  • anti-WNT-TCF activities of Ivermectin and Selamectin
  • Ivermectin has a well-known anti-parasitic activity mediated via the deregulation of chloride channels, leading to paralysis and death (Hibbs & Gouaux, 2011; Lynagh & Lynch, 2012). The same mode of action has been suggested to underlie the toxicity of Ivermectin for liquid tumor cells and the potentiation or sensitization effect of Avermectin B1 on classical chemotherapeutics
  • the specificity of the blockade of WNT-TCF responses we document, at low micromolar doses for Ivermectin and low nanomolar doses for Selamectin, indicate that the blockade of WNT-TCF responses and chloride channel deregulation are distinct modes of action
  • What is key then is to find a dose and a context where the use of Ivermectin has beneficial effects in patients, paralleling our results with xenografts in mice.
  • Cell toxicity appears at doses greater (> 10 μM for 12 h or longer or > 5 μM for 48 h or longer for Ivermectin) than those required to block TCF responses and induce apoptosis.
  • Our data point to a repression of WNT-β-CATENIN/TCF transcriptional responses by Ivermectin, Selamectin and related macrocylic lactones.
  • (i) The ability of Avermectin B1 to inhibit the activation of WNT-TCF reporter activity by N-terminal mutant (APC-insensitive) β-CATENIN as detected in our screen
  • (ii) The ability of Avermectin B1, Ivermectin, Doramectin, Moxidectin and Selamectin to parallel the modulation of WNT-TCF targets by dnTCF
  • (iii) The finding that the specific WNT-TCF response blockade by low doses of Ivermectin and Selamectin is reversed by constitutively active TCF
  • (iv) The repression of key C-terminal phospho-isoforms of β-CATENIN resulting in the repression of the TCF target and positive cell cycle regulator CYCLIN D1 by Ivermectin and Selamectin
  • (v) The specific inhibition ofin-vivo-TCF-dependent, but notin-vivo-TCF-independent cancer cells by Ivermectin in xenografts.
  • These results together with the reduction of the expression of the colon cancer stem cell markersASCL2 andLGR5 (e.g., Hirschet al, 2013; Ziskinet al, 2013) raise the possibility of an inhibitory effect of Ivermectin, Selamectin and related macrocyclic lactones on TCF-dependent cancer stem cells.
  • the capacity of cancer cells to form 3D spheroids in culture, as well as the growth of these, is also WNT-TCF-dependent (Kanwaret al, 2010) and they were also affected by Ivermectin treatment
  • If Ivermectin is specific, it should only block TCF-dependent tumor growth. Indeed, the sensitivity and insensitivity of DLD1 and CC14 xenografts to Ivermectin treatment, respectively, together with the desensitization to Ivermectin actionin vivo by constitutively active TCF provide evidence of the specificity of this drug to block an activated WNT-TCF pathway in human cancer.
  • Ivermectin has a good safety profile since onlyin-vivo-dnTCF-sensitive cancer xenografts are responsive to Ivermectin treatment, and we have not detected side effects in Ivermectin-treated mice at the doses used
  • previous work has shown that side effects from systemic treatments with clinically relevant doses in humans are rare (Yang, 2012), that birth defects were not observed after exposure of pregnant mothers (Pacquéet al, 1990) and that this drug does not cross the blood–brain barrier (Kokozet al, 1999). Similarly, only dogs with mutantABCB1 (MDR1) alleles leading to a broken blood–brain barrier show Ivermectin neurotoxicity (Mealeyet al, 2001; Orzechowskiet al, 2012)
  • Indications may include treatment for incurable β-CATENIN/TCF-dependent advanced and metastatic human tumors of the lung, colon, endometrium, and other organs.
  • Ivermectin, Selamectin, or related macrocyclic lactones could also serve as topical agents for WNT-TCF-dependent skin lesions and tumors such as basal cell carcinomas
  • they might also be useful as routine prophylactic agents, for instance against nascent TCF-dependent intestinal tumors in patients with familial polyposis and against nascent sporadic colon tumors in the general aging population
  •  
    Ivermectin, a common anti-parasitic, found to inhibit WTF-TCF pathway and decrease c-terminal phosophorylaiton of Beta-CATENIN all resulting in increased aptosis and inhibition of cancer growth in colon cancer cell lines and lung cancer cell lines.
Nathan Goodyear

Increasing the Effectiveness of Intravenous Vitamin C as an Anticancer Agent - ISOM - 0 views

  •  
    Good review of ways to increase the anti-cancer efficacy of IV vitamin C.
Nathan Goodyear

High dose intravenous vitamin c and metastatic pancreatic cancer: Two cases - 0 views

  •  
    2 case studies of high dose vitamin C in pancreatic cancer with good results.  The important thing here is the imaging and biomarkers were initiated and followed.  Progressive cancers, like pancreatic cancer, require more frequent dosing of IVC.
Nathan Goodyear

Supplemental ascorbate in the supportive treatment of cancer: Reevaluation of prolongat... - 0 views

  •  
    This is the republication of the original Pauling and Cameron study. This re-analysis actually revealed better outcomes than the original. Also, they found that vitamin C likely is responsible for the release of Fe from ferritin required for the cytotoxicity with vitamin C.
Nathan Goodyear

Vitamin C: An Epigenetic Regulator | IntechOpen - 0 views

  •  
    Great chapter review of the effects of vitamin C on epigenetics.
Nathan Goodyear

Weekly ascorbic acid infusion in castration-resistant prostate cancer patients: a singl... - 0 views

  •  
    Look at this BS study. 60 grams!!! Create a study to underdose the patients and then declare the "alternative treatment" without evidence. They lack such an understanding of the pharmacokinetics of vitamin C. They also lack a basic experience with IV vitamin C! Also, serious adverse events with the 60 grams IVC?!?!?
« First ‹ Previous 81 - 100 of 864 Next › Last »
Showing 20 items per page