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Nathan Goodyear

Improved liver function after high dose intravenous vitamin C and Helxior SC injections... - 0 views

www.researchgate.net/...chemotherapy-and-radiation.pdf

metastasis high dose vitamin C IV vitamin C High dose IV vitamin C hepatocellular carcinoma cancer hepatocellular cancer vitamin C

shared by Nathan Goodyear on 09 Mar 21 - No Cached
  • Nathan Goodyear on 09 Mar 21
     
    HDIVC plus mistletoe SQ improved and stabilized a patient with advanced hepatocellular carcinoma.
Nathan Goodyear

Clinical significance of therapy using branched-chain amino acid granules in patients w... - 0 views

onlinelibrary.wiley.com/...full

hepatitis C hepatitis BCAA amino acids liver disease cancer hepatocellular

shared by Nathan Goodyear on 20 May 15 - No Cached
  • Nathan Goodyear on 20 May 15
     
    BCAA reduces incidence of hepatocellular cancer in patients with HCV.
Nathan Goodyear

Phase II Randomized Trial of Autologous Formalin-Fixed Tumor Vaccine for Postsurgical R... - 0 views

clincancerres.aacrjournals.org/...1574

immunotherapy cancer hepatocellular cancer liver cancer

shared by Nathan Goodyear on 24 May 18 - No Cached
  • Nathan Goodyear on 24 May 18
     
    Specific immunotherapy from patient the specific antigens of cancer cells fixed in formalin improves survival in hepatocellular cancer.
Nathan Goodyear

N-acetylcysteine improves antitumoural response of Interferon alpha by NF-kB downregula... - 0 views

www.ncbi.nlm.nih.gov/...PMC3539937

IFN-alpha N-acetylcysteine hepatocellular cancer liver cancer NAC hepatocellular carcinoma

shared by Nathan Goodyear on 03 Mar 21 - No Cached
  • Nathan Goodyear on 03 Mar 21
     
    NAC for treatment of hepatocellular cancer.
Nathan Goodyear

Oral supplementation with branched-chain amino acid granules prevents hepatocarcinogene... - 0 views

www.ncbi.nlm.nih.gov/...23607436

BCAA amino acids liver disease cancer HCV hepatitis C hepatocellular cirrhosis hepatitis

shared by Nathan Goodyear on 20 May 15 - No Cached
  • Nathan Goodyear on 20 May 15
     
    Study finds 12 g/day BCAA reduced the incidence of hepatocellular carcinoma in those patients with HCV.
Nathan Goodyear

Increased serum reverse triiodothyronine levels at diagnosis of hepatocellula... - 0 views

www.deepdyve.com/...els-at-diagnosis-of-cpaqYxUZKS

rT3 non-thyroidal illness syndrome hepatocellular carcinoma hepatitis C cancer hepatocellular cancer cirrhosis euthyroid sick syndrome

shared by Nathan Goodyear on 15 Mar 21 - No Cached
  • Nathan Goodyear on 15 Mar 21
     
    Elevated rT3 as a part of non-thyroid all illness syndrome
Nathan Goodyear

The effect of testosterone and fenofibrate, administered alone or in combination, on ca... - 0 views

www.ncbi.nlm.nih.gov/...26031507

Testosterone hormones cardiovascular disease hsCRP insulin insulin resistance insulin sensitivity

shared by Nathan Goodyear on 04 Jun 15 - No Cached
  • Nathan Goodyear on 04 Jun 15
     
    This study looked at oral Testosterone plus fenofibrate (tricor).  That is not the purpose of this post.  This study found that oral Testosterone decanoate reduced hsCRP and improved insulin sensitivity.  One caveat--Testosterone should not be given orally due to increased risk of hepatocellular cancer.
Nathan Goodyear

The effect of long-term supplementation with branched-chain amino acid granules in pati... - 0 views

www.ncbi.nlm.nih.gov/...23090049

BCAA amino acids HCV hepatitis hepatitis C liver disease cancer hepatocellular

shared by Nathan Goodyear on 20 May 15 - No Cached
  • Nathan Goodyear on 20 May 15
     
    BCAA improve overall survival in HCV related liver cancer.
Nathan Goodyear

Testosterone in Men with Advanced Li... [J Gastroenterol Hepatol. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...25087838

Testosterone men male hormone hormones cirrhosis liver disease

shared by Nathan Goodyear on 05 Aug 14 - No Cached
  • Nathan Goodyear on 05 Aug 14
     
    published ahead of print.  The authors conclude that the Testosterone therapy in hypogonadal men with cirrhosis requires further study.  They, the authors, state that the risk of Testosterone and hepatocellular carcinoma is overstated.  This risk is associated with oral Testosterone replacement and thus in that light is not overstated.  The majority of treatment strategies today employ none oral routes of administration which would support their statement.
Nathan Goodyear

Vitamin C preferentially kills cancer stem cells in hepatocellular carcinoma via SVCT-2... - 0 views

www.nature.com/...s41698-017-0044-8

cancer cancer stem cells liver cancer vitamin C IV vitamin C oncology

shared by Nathan Goodyear on 30 Jan 18 - No Cached
  • Chen et al. have revealed that ascorbate at pharmacologic concentrations (0.3–20 mM) achieved only by intravenously (i.v.) administration selectively kills a variety of cancer cell lines in vitro, but has little cytotoxic effect on normal cells.
  • Ascorbic acid (the reduced form of vitamin C) is specifically transported into cells by sodium-dependent vitamin C transporters (SVCTs)
  • SVCT-1 is predominantly expressed in epithelial tissues
  • ...41 more annotations...
  • whereas the expression of SVCT-2 is ubiquitous
  • differential sensitivity to VC may result from variations in VC flow into cells, which is dependent on SVCT-2 expression.
  • high-dose VC significantly impaired both the tumorspheres initiation (Fig. 4d, e) and the growth of established tumorspheres derived from HCC cells (Fig. 4f, g) in a time-dependent and dose-dependent manner.
  • Hepatocellular carcinoma (HCC)
  • The antioxidant, N-acetyl-L-cysteine (NAC), preventing VC-induced ROS production (a ROS scavenger), completely restored the viability and colony formation among VC-treated cells
  • DNA double-strand damage was found following VC treatment
  • DNA damage was prevented by NAC
  • Interestingly, the combination of VC and cisplatin was even more effective in reducing tumor growth and weight
  • Consistent with the in vitro results, stemness-related genes expressions in tumor xenograft were remarkably reduced after VC or VC+cisplatin treatment, whereas conventional cisplatin therapy alone led to the increase of CSCs
  • VC is one of the numerous common hepatoprotectants.
  • Interestingly, at extracellular concentrations greater than 1 mM, VC induces strong cytotoxicity to cancer cells including liver cancer cells
  • we hypothesized that intravenous VC might reduce the risk of recurrence in HCC patients after curative liver resection.
  • Intriguingly, the 5-year disease-free survival (DFS) for patients who received intravenous VC was 24%, as opposed to 15% for no intravenous VC-treated patients
  • Median DFS time for VC users was 25.2 vs. 18 months for VC non-users
  • intravenous VC use is linked to improved DFS in HCC patients.
  • In this study, based on the elevated expression of SVCT-2, which is responsible for VC uptake, in liver CSCs, we revealed that clinically achievable concentrations of VC preferentially eradicated liver CSCs in vitro and in vivo
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      the authors here made similar mistakes to the Mayo authors i.e. under doses here in this study.  They dosed at only 2 grams IVC.  A woefully low dose of IVC.
  • Additionally, we found that intravenous VC reduced the risk of post-surgical HCC progression in a retrospective cohort study.
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      positive results despite a low dose used.
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      Their comfort zone was 1mM.  They should have targeted 20-40 mM.
  • Three hundred thirty-nine participants (55.3%) received 2 g intravenous VC for 4 or more days after initial hepatectomy
  • As the key protein responsible for VC uptake in the liver, SVCT-2 played crucial roles in regulating the sensitivity to ascorbate-induced cytotoxicity
  • we also observed that SVCT-2 was highly expressed in human HCC samples and preferentially elevated in liver CSCs
  • SVCT-2 might serve as a potential CSC marker and therapeutic target in HCC
  • CSCs play critical roles in regulating tumor initiation, relapse, and chemoresistance
  • we revealed that VC treatment dramatically reduced the self-renewal ability, expression levels of CSC-associated genes, and percentages of CSCs in HCC, indicating that CSCs were more susceptible to VC-induced cell death
  • as a drug for eradicating CSCs, VC may represent a promising strategy for treatment of HCC, alone or particularly in combination with chemotherapeutic drugs
  • In HCC, we found that VC-generated ROS caused genotoxic stress (DNA damage) and metabolic stress (ATP depletion), which further activated the cyclin-dependent kinase inhibitor p21, leading to G2/M phase cell cycle arrest and caspase-dependent apoptosis in HCC cells
  • we demonstrated a synergistic effect of VC and chemotherapeutic drug cisplatin on killing HCC both in vitro and in vivo
  • Intravenous VC has also been reported to reduce chemotherapy-associated toxicity of carboplatin and paclitaxel in patients,38 but the specific mechanism needs further investigation
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      so, exclude the benefit to patients until the exact mechanism of action, which will never be fully elicited?!?!?
  • Our retrospective cohort study also showed that intravenous VC use (2 g) was related to the improved DFS in HCC patients after initial hepatectomy
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      Terribly inadequate dose.  Target is 20-40 mM which other studies have found occur with 50-75 grams of IVC.
  • several clinical trials of high-dose intravenous VC have been conducted in patients with advanced cancer and have revealed improved quality of life and prolonged OS
  • high-dose VC was not toxic to immune cells and major immune cell subpopulations in vivo
  • high recurrence rate and heterogeneity
  • tumor progression, metastasis, and chemotherapy-resistance
  • SVCT-2 was highly expressed in HCC samples in comparison to peri-tumor tissues
  • high expression (grade 2+/3+) of SVCT-2 was in agreement with poorer overall survival (OS) of HCC patients (Fig. 1c) and more aggressive tumor behavior
  • SVCT-2 is enriched in liver CSCs
  • these data suggest that SVCT-2 is preferentially expressed in liver CSCs and is required for the maintenance of liver CSCs.
  • pharmacologic concentrations of plasma VC higher than 0.3 mM are achievable only from i.v. administration
  • The viabilities of HCC cells were dramatically decreased after exposure to VC in dose-dependent manner
  • VC and cisplatin combination further caused cell apoptosis in tumor xenograft
  • These results verify that VC inhibits tumor growth in HCC PDX models and SVCT-2 expression level is associated with VC response
  • qPCR and IHC analysis demonstrated that expression levels of CSC-associated genes and percentages of CSCs in PDXs dramatically declined after VC treatment, confirming the inhibitory role of VC in liver CSCs
  • Nathan Goodyear on 30 Jan 18
     
    IV vitamin C in vitro and in vivo found to "preferentially" eradicate cancer stem cells.  In addition, IV vitamin C was found to be adjunctive to chemotherapy, found to be hepatoprotectant.  This study also looked at SVCT-2, which is the transport protein important in liver C uptake.
Nathan Goodyear

Hyperthermia Inhibits Recombination Repair of Gemcitabine-Stalled Replication Forks - 0 views

www.ncbi.nlm.nih.gov/...PMC4155430

chemoresistance gemzar hepatocellular cancer hyperthermia liver cancer hepatocellular carcinoma chemotherapy"

shared by Nathan Goodyear on 30 Mar 21 - No Cached
  • Nathan Goodyear on 30 Mar 21
     
    Hyperthermia helps to overcome HCC gemzar resistance. Exact mechanism undetermined.
Nathan Goodyear

Myeloid derived suppressor cells inhibit natural killer cells in patients with hepatoce... - 0 views

aasldpubs.onlinelibrary.wiley.com/...hep.23054

MDSC liver cancer NK cells cancer hepatocellular carcinoma myeloid-derived suppressor cells

shared by Nathan Goodyear on 11 Nov 20 - No Cached
  • Nathan Goodyear on 11 Nov 20
     
    In liver cancer, MDSCs suppress NK cells. Other studies show this effect is more than Treg cells.
Nathan Goodyear

A case of amoxicillin-induced hepatocellular liver injury with bile-duct damage - 0 views

www.ncbi.nlm.nih.gov/...PMC3304646

amoxil amoxicillin liver antiobioitic liver enzymes

shared by Nathan Goodyear on 16 Apr 15 - No Cached
  • Nathan Goodyear on 16 Apr 15
     
    amoxil induced liver injury manifest with elevated liver enzymes.
Nathan Goodyear

High dose vitamin K3 infusion in advanced hepatocellular carcinoma - Sarin - 2006 - Jou... - 0 views

onlinelibrary.wiley.com/...abstract

vitamin K cancer therapy treatment

shared by Nathan Goodyear on 09 Feb 11 - No Cached
  • Vitamin K has been shown to have antitumor effect
  • Nathan Goodyear on 09 Feb 11
     
    Vitamin K therapy and cancer 
Nathan Goodyear

Effects of vitamin C and E on liver enzymes ... [Vet Hum Toxicol. 2004] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...15303390

liver enzymes vitamin C hepatocellular damage injury toxin

shared by Nathan Goodyear on 15 Oct 11 - No Cached
  • Nathan Goodyear on 15 Oct 11
     
    vitamin c prevented increase in liver enzymes from aflatoxin
Nathan Goodyear

Effects of vitamin C on liver enzymes an... [Gen Physiol Biophys. 2005] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...15900086

liver enzymes vitamin C hepatocellular injury

shared by Nathan Goodyear on 15 Oct 11 - No Cached
  • Nathan Goodyear on 15 Oct 11
     
    Vitamin C protects the liver against injury and lowers enzymes
Nathan Goodyear

Transarterial Chemoembolization With Doxorubicin-Eluting Microspheres for Inoperable He... - 0 views

www.ncbi.nlm.nih.gov/...PMC3070282

TACE DEB-TACE liver liver cancer cancer

shared by Nathan Goodyear on 26 Jul 18 - No Cached
  • Nathan Goodyear on 26 Jul 18
     
    Transarterial chemoembolization with micropheres called DEB-TACE for liver tumors.
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
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  • 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
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