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Nathan Goodyear

Control of inducible chemoresistance: enhanced anti-tumor therapy through increased apo... - 0 views

pubmed.ncbi.nlm.nih.gov/10202930

chemotherapy NF-kappaB chemoresistance cancer

shared by Nathan Goodyear on 28 Aug 20 - No Cached
  • Nathan Goodyear on 28 Aug 20
     
    Chemotherapy induces chemoresistance via activation of NF-kappaB. Resistant therapy increases metastatic potential which = cause of 90% of mortality
Nathan Goodyear

Ivermectin reverses the drug resistance in cancer cells through EGFR/ERK/Akt/... - 0 views

jeccr.biomedcentral.com/...s13046-019-1251-7

NF-kappaB ivermectin Akt EGFR cancer chemoresistance ERK

shared by Nathan Goodyear on 01 Oct 20 - No Cached
  • Nathan Goodyear on 01 Oct 20
     
    Ivermectin restores chemosensitivity in chemoresistant cancer cells through inhibition of EBFR and its downstream ER/Akt/NF-kappaB signaling.
Nathan Goodyear

The Potential Role of Systemic Buffers in Reducing Intratumoral Extracellular pH and Ac... - 0 views

cancerres.aacrjournals.org/...2677.long

pH acid tumor cancer alkaline NaHCO3

shared by Nathan Goodyear on 19 Nov 18 - No Cached
  • Nathan Goodyear on 19 Nov 18
     
    Great diagram of the pH in/around solid tumors. Cancer exists in an obvious hypoxic environment which favors the HIF-1alpha which favors lactate production which drops the pH in the tumor extracellular environment effecting chemoresistance, radioresistance, angiogenesis, invasion, aggressiveness, metastasis, immune evasion...
Nathan Goodyear

Role of Growth Hormone in Breast Cancer - 0 views

academic.oup.com/...3098660

breast cancer growth hormone GH

shared by Nathan Goodyear on 12 Aug 19 - No Cached
  • Nathan Goodyear on 12 Aug 19
     
    Growth hormone plays critical role in breast cancer: promotes angiogenesis, stimulated mTOR, promotes chemoresistance, promotes breast stem activity, promotes metastasis via increase in epithelial to mesenchymal transition...
Nathan Goodyear

Nrf2 inhibition reverses the resistance of cisplatin-resistant head and neck cancer cel... - 0 views

www.ncbi.nlm.nih.gov/...PMC5198738

head and neck cancer MDR heme-oxygenate-1 artesunate multi-drug resistance Nrf2 HO-1

shared by Nathan Goodyear on 28 Jun 19 - No Cached
  • Nathan Goodyear on 28 Jun 19
     
    Nrf2 inhibition decreased chemoresistance to artesunate in Patients with head and neck cancer resistant to cisplatin.
Nathan Goodyear

Inhibition of tumor angiogenesis as a strategy to circumvent acquired resista... - 0 views

onlinelibrary.wiley.com/...bies.950130106

chemotherapy angiogenesis

shared by Nathan Goodyear on 25 Sep 20 - No Cached
  • Nathan Goodyear on 25 Sep 20
     
    Even with cancer chemoresistance to chemo, the move to inhibit angiogenesis i.e. via lower dose, allows a bypass of the resistance to another means of action.
Nathan Goodyear

Chemoresistant KM12C Colon Cancer Cells Are Addicted to Low Cyclic AMP Levels in a Phos... - 0 views

cancerres.aacrjournals.org/...5248

phosphodiesterase colorectal cancer chemoresistance PDE phosphodiesterase inhibitors

shared by Nathan Goodyear on 16 Feb 21 - No Cached
  • Nathan Goodyear on 16 Feb 21
     
    PDE inhibition increases cAMP to restore chemosensitivity in this cell study.
Nathan Goodyear

Phosphoinositide 3-kinase accelerates postoperative tumor growth by inhibiting apoptosi... - 0 views

pubmed.ncbi.nlm.nih.gov/15741161

metastasis local recurrence surgery

shared by Nathan Goodyear on 13 Aug 20 - No Cached
  • Nathan Goodyear on 13 Aug 20
     
    Again, surgical upregulation of PI3k stimulates local recurrence via anti-apoptosis and induction of chemoresistance.
Nathan Goodyear

Bisphenol A at Low Nanomolar Doses Confers Chemoresistance in Estrogen Recept... - 0 views

www.ncbi.nlm.nih.gov/...PMC2649216

ER-alpha estrogen receptor Bisphenol A toxins cancer breast

shared by Nathan Goodyear on 18 Oct 12 - No Cached
  • Nathan Goodyear on 18 Oct 12
     
    How do environmental chemicals interfere?  This study shows how Bisphenol A actually interferes at the site of the estrogen receptor alpha.  Bisphenol A decreased the efficacy of chemotherapy in ER +/- breast cancer.  Again, the focus is on the interaction with ER alpha.
Nathan Goodyear

Anti-cancer effects of artesunate in a panel of chemoresistant neuroblastoma cell lines... - 0 views

www.ncbi.nlm.nih.gov/...19698702

Artesunate cancer neuroblastoma

shared by Nathan Goodyear on 18 Oct 18 - No Cached
  • Nathan Goodyear on 18 Oct 18
     
    Artesunate found to be effective agains neuroblastoma cell lines.
Nathan Goodyear

Leptin signaling and cancer chemoresistance: Perspectives - 0 views

www.ncbi.nlm.nih.gov/...PMC5385432

Leptin Cancer

shared by Nathan Goodyear on 20 Feb 19 - No Cached
  • Nathan Goodyear on 20 Feb 19
     
    Leptin and cancer
Nathan Goodyear

Oncotarget | Preclinical evaluation of a nanoformulated antihelminthic, niclosamide, in... - 0 views

www.oncotarget.com/index.php

Niclosamide cancer ovarian cancer

shared by Nathan Goodyear on 16 Apr 18 - No Cached
  • Ovarian cancer is the most lethal gynecologic malignancy in the world
  • paclitaxel represents a breakthrough in the treatment of ovarian cancer, the overall 5-year survival rate of patients with stage III disease is still approximately 40%
  • Targeting cancer stem cells is an emerging concept in cancer therapy
  • ...8 more annotations...
  • Ovarian cancer stem cells play an important role in chemoresistance and cancer recurrence
  • Furthermore, recent studies indicate that niclosamide exhibits anticancer effects against various human cancer cells by acting on multiple cell signaling pathways and inducing mitochondrial uncoupling [16–21]
  • has low systemic bioavailability (~10%) when administered orally, which is beneficial for treating local parasitic infections of the intestines while minimizing systemic exposure
  • The nano-NI demonstrated significantly higher inhibitory effects on sphere formation than the original niclosamide did
  • the nano-NI formulation decreased the metabolic activity of ovarian cancer cells and caused a metabolic shift from oxidative phosphorylation to glycolysis
  • This toxicity evaluation showed that oral nano-NI had no toxic effect on either group of mice in terms of weight, plasma albumin levels, and blood cell counts, and revealed no adverse effects on vital organ function in the rodents, which suggests that nano-NI is safe for animals
  • niclosamide inhibits tumor cell growth by interrupting multiple pathways (Wnt, Notch, STAT3, NF-κB, and mTORc1) and the generation of reactive oxygen species in several cancer cells
  • The current standard therapy for ovarian cancer includes taxanes and platinum-based chemotherapy after cytoreductive surgery. Among treated patients, nearly 70 to 80% will experience disease recurrence
  • Nathan Goodyear on 16 Apr 18
     
    nano-Niclosamide more effective than traditional Niclosamide in in vitro and in vivo ovarian cancer.
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.
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