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Nathan Goodyear

Mistletoe viscotoxins increase natural killer cell‐mediated cytotoxicity - Ta... - 0 views

febs.onlinelibrary.wiley.com/...j.1432-1033.2002.02932.x

cancer mistletoe NK NK cells

shared by Nathan Goodyear on 08 Jul 18 - No Cached
  • Nathan Goodyear on 08 Jul 18
     
    Study finds that mistletoe augments NK activity not via an increase in NK numbers.
Nathan Goodyear

High doses of multiple antioxidant vitamins: essential ingredients in improving the eff... - 0 views

www.ncbi.nlm.nih.gov/...10067654

antioxidant antioxidants vitamin C vitamin E vitamin A carotenoids cancer vitamins

shared by Nathan Goodyear on 28 Sep 18 - No Cached
  • Nathan Goodyear on 28 Sep 18
     
    only abstract available here from older study, finds antioxidants i.e. C, A, E, and carotenoids augment cancer therapies.
Nathan Goodyear

http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.538.3045&rep=rep1&type=pdf - 0 views

citeseerx.ist.psu.edu/...download

antioxidants vitamin C vitamin A Vitamin E carotenoids cancer vitamins

shared by Nathan Goodyear on 28 Sep 18 - No Cached
  • Nathan Goodyear on 28 Sep 18
     
    antioxidants reduce side effects of traditional cancer treatments and even augment their efficacy.
Nathan Goodyear

High-Dose Parenteral Ascorbate Enhanced Chemosensitivity of Ovarian Cancer and Reduced ... - 0 views

stm.sciencemag.org/...222ra18

ovarian cancer IV vitamin C vitamin C intravenous vitamin C

shared by Nathan Goodyear on 06 Feb 14 - No Cached
  • Nathan Goodyear on 06 Feb 14
     
    IV vitamin C shown to augment cancer killer effect of chemotherapy.  This study looked at ovarian cancer in animal models and in humans.  The effect--a synergistic effect was found that promoted tumor destruction.  The great thing about IV vitamin C is the benefit but also the very low side effect profile.
Nathan Goodyear

A Combined Preclinical Therapy of Cannabinoids and Temozolomide against Glioma | Molecu... - 0 views

mct.aacrjournals.org/...90.long

cancer THC medical marijuana glioblastoma CBD

shared by Nathan Goodyear on 18 Sep 18 - No Cached
  • Δ9-Tetrahydrocannabinol (THC; Supplementary Fig. 1), the main active component of the hemp plant Cannabis sativa
  • CB1, abundantly expressed in the brain and at many peripheral sites
  • CB2, expressed in the immune system and also present in some neuron subpopulations and glioma cells
  • ...3 more annotations...
  • antitumoral agents
  • Aside from THC, C. sativa produces approximately 70 other cannabinoids, although, unlike THC, many of them exhibit little affinity for CB receptors (10, 20). Of interest, at least one of these components, namely, cannabinol (CBD; Supplementary Fig. 1), has been shown to reduce the growth of different types of tumor xenografts including gliomas
  • the combined administration of THC and CBD is being therapeutically explored (10, 20, 26), although its effects on the proliferation and survival of cancer cells have only been analyzed in vitro
  • Nathan Goodyear on 18 Sep 18
     
    THC found to augment chemotherapy in the glioblastoma cell culture study.
Nathan Goodyear

Suppression of HSP27 increases the anti-tumor effects of quercetin in human leukemia U9... - 0 views

www.ncbi.nlm.nih.gov/...PMC4686121

quercetin cancer HSP heat shock proteins mTOR VEGF apoptosis

shared by Nathan Goodyear on 23 Feb 19 - No Cached
  • Nathan Goodyear on 23 Feb 19
     
    Quercetin effects in cancer i.e. decreased VEGF, apoptosis inhibition, mTOR inhibition... are augmented via HSP27 suppression
Nathan Goodyear

https://pdfs.semanticscholar.org/3f03/58787b2bfb3f9614df62f3c545e689fbccd4.pdf?_ga=2.15... - 0 views

pdfs.semanticscholar.org/...3f9614df62f3c545e689fbccd4.pdf

Picibanil dendritic cells cancer immunotherapy

shared by Nathan Goodyear on 01 Mar 19 - No Cached
hoangkimchi liked it
  • Nathan Goodyear on 01 Mar 19
     
    Picibanil augments Dendritic cell activation and signaling.
Nathan Goodyear

ScienceDirect - 0 views

www.sciencedirect.com/...S2212492618300745

"pancreatic cancer" cancer metformin chloroquine berberine

shared by Nathan Goodyear on 27 Nov 18 - No Cached
  • Nathan Goodyear on 27 Nov 18
     
    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

Inhibition of Wnt/β-catenin pathway by niclosamide: a therapeutic target for ... - 0 views

www.ncbi.nlm.nih.gov/...24736023

nicolsamide cancer Wnt ovarian cancer

shared by Nathan Goodyear on 28 Mar 18 - No Cached
  • Nathan Goodyear on 28 Mar 18
     
    niclosamide found to augment chemotherapy through blockad of Wnt/Beta-catenin pathway.
Nathan Goodyear

Anti-helminth compound niclosamide downregulates Wnt Signaling and elicits antitumor re... - 0 views

www.ncbi.nlm.nih.gov/...PMC3117125

Niclosamide Wnt cancer colon cancer

shared by Nathan Goodyear on 21 Mar 18 - No Cached
  • Others have reported that niclosamide inhibits the NF-κB pathway in leukemia cell lines (26) or mTOR signaling in MCF-7 breast cancer cells
  • niclosamide enhances the anti-tumor effect of oxaliplatin
  • In the more rapidly growing tumor (HCT116), a dose of 200 mg/kg of body weight was needed to suppress the tumor growth
  • ...13 more annotations...
  • however, 100 mg/kg of niclosamide could suppress the growth of the relatively slow-growing tumor (CRC039) to the same level
  • niclosamide was confirmed to inhibit the growth of human CRCs in NOD/SCID mice
  • niclosamide can inhibit Wnt pathway activation in CRC
  • The mechanism of action of the niclosamide in our studies is thought to be through internalization of Fzd1 and downregulation of Wnt pathway intermediaries
  • Recently, Jin et al. (26) reported that niclosamide inhibited the NF-κB pathway and increased reactive oxygen species levels to induce apoptosis in AML cells. In contrast, we did not observe any inhibitory effect of niclosamide on NF-κB signaling in our CRC model
  • oral administration of niclosamide does result in sufficient distribution of the drug into tumor tissue, to prove a prolonged inhibitory effect on Wnt/ß-catenin signaling, resulting in tumor growth inhibition
  • we required higher doses (100 ~ 200 mg/kg body weight) of niclosamide in order to demonstrate significant inhibition of tumor growth in NOD/SCID mice
  • niclosamide concentrations in tumor tissue showed good correlation with those in plasma, suggesting the efficient distribution of niclosamide from blood to tumor tissue
  • we observed downregulation of Dvl2 and ß-catenin cytosolic expression in niclosamide-treated tumor cells in vivo
  • One potential concern for the use of niclosamide as an anticancer therapy is the poor absorption of this drug
  • The Wnt signaling pathway, fundamental to embryonic tissue patterning, is also activated in stem-like cells
  • The canonical Wnt pathway is activated in approximately 80% of sporadic CRC primarily due to mutations in the APC gene
  • recent observations reveal that Wnt ligands or inhibitors may affect the growth and survival of colon cancer cells in spite of the presence of APC or CTNNB1 mutations
  • Nathan Goodyear on 21 Mar 18
     
    Niclosamide found to inhibit Wnt/B-catenin signaling pathway, and thus promotion of apoptosis, in colorectal cancer cells in Vivo study.  It was also found to augment chemotherapeutic.
Nathan Goodyear

Cortisol Exerts Bi-Phasic Regulation of Inflammation in Humans - 0 views

www.ncbi.nlm.nih.gov/...PMC3186928

cortisol glucocorticoids inflammation hormones

shared by Nathan Goodyear on 12 Oct 16 - No Cached
  • GCs induce increased cellular expression of receptors for several pro-inflammatory cytokines including interleukin (IL)-1 (Spriggs et al. 1990), IL-2 (Wiegers et al. 1995), IL-4 (Paterson et al. 1994), IL-6 (Snyers et al. 1990), and IFN-g (Strickland et al. 1986), as well as GM-CSF
  • GCs have also been shown to stimulate effector cell functions including phagocytosis by monocytes (van der Goes et al. 2000), effector cell proliferative responses (Spriggs et al. 1990), macrophage activation (Sorrells and Sapolsky 2010), and a delay of neutrophil apoptosis
  • a concentration- and time-dependent range of GC effects that are both pro- and anti-inflammatory
  • ...13 more annotations...
  • basal (diurnal) concentrations of cortisol do not exert an anti-inflammatory effect on several pro-and anti-inflammatory mediators of the human immune inflammatory response
  • withdrawal of cortisol activity in vivo did not lead to increased inflammatory responsiveness of immune effector cells
  • maximal suppression of inflammation was achieved by a stress-associated, but still physiologic, cortisol concentration. There was no greater anti-inflammatory effect at higher cortisol concentrations (Yeager et al. 2005) although IL-10 concentrations continued to increase with increasing cortisol concentrations as we and others have shown
  • acutely, physiological cortisol concentrations are anti-inflammatory and, as proposed, act to limit over expression of an inflammatory response that could lead to tissue damage
  • Acutely, cortisol has anti-inflammatory effects following a systemic inflammatory stimulus (Figure 4). However, a cortisol concentration that acts acutely to suppress systemic inflammation also has a delayed effect of augmenting the inflammatory response to subsequent, delayed stimulu
  • 1) GCs can exert pro-inflammatory effects on key inflammatory processes and, 2) GC regulation of inflammation can vary from anti- to a pro-inflammatory in a time-dependent manner
  • The immediate in vivo effect of both stress-induced and pharmacological GC concentrations is to suppress concurrent inflammation and protect the organism from an excessive or prolonged inflammatory response
  • GCs alone, in the absence of an inflammatory stimulus, up-regulate monocyte mRNA and/or receptors for several molecules that participate in pro-inflammatory signaling, as noted above and in the studies presented here.
  • In humans, as shown here, if in vivo GC concentrations are elevated concurrent with an inflammatory stimulus, anti-inflammatory effects are observed
  • In sharp contrast, with a time delay of 12 or more hours between an increased GC concentration and the onset of an inflammatory stimulus, enhancing effects on inflammation are observed. These effects have been shown to persist in humans for up to 6 days
  • GC-induced enhancement of inflammatory responses is maximal at an intermediate concentration, in our studies at a concentration that approximates that observed in vivo following a major systemic inflammatory stimulus
  • In addition to enhanced responses to LPS, recently identified pro-inflammatory effects of GCs also show enhanced localization of effector cells at inflammatory sites
  • we hypothesize that pre-exposure to stress-associated cortisol concentrations “prime” effector cells of the monocyte/macrophage lineage for an augmented pro-inflammatory response by; a) inducing preparative changes in key regulators of LPS signal transduction, and b) enhancing localization of inflammatory effector cells at potential sites of injury
  • Nathan Goodyear on 12 Oct 16
     
    very interesting read on the effects of inflammation on cortisol and visa versa.
Nathan Goodyear

A guide to perioperative nutrition - ScienceDirect - 0 views

www.sciencedirect.com/...S1090820X04001189

nutrition IV nutrition surgery IV therapy

shared by Nathan Goodyear on 13 Jul 17 - No Cached
  • Nathan Goodyear on 13 Jul 17
     
    Nutritional supplementation pre/post operative will reduce bruising, swelling, inflammation, promote wound healing, augment immune system, reduce surgical induced oxidation.
Nathan Goodyear

Adjuvant histamine in cancer immunotherapy, Seminars in Cancer Biology | 10.1006/scbi.2... - 0 views

www.deepdyve.com/...ancer-immunotherapy-6XEaCggcvx

histamine IL-2 NK NK cells immunotherapy cancer

shared by Nathan Goodyear on 12 May 18 - No Cached
  • Nathan Goodyear on 12 May 18
     
    histamine dihydrochloride augments IL-2 stimulation of NK and blocks the monocyte/macrophage inhibition of IL-2 stimulation of NK cells.
Nathan Goodyear

Histamine: A Novel Approach to Cancer Immunotherapy: Cancer Investigation: Vol 18, No 4 - 0 views

www.tandfonline.com/...07357900009012178

histamine NK IL-2 cancer immunotherapy

shared by Nathan Goodyear on 12 May 18 - No Cached
  • Nathan Goodyear on 12 May 18
     
    histamin augments NK activation with IL-2 therapy. Histamine blocks the monocyte/macrophate inhibition of IL-2 induced NK activity.
Nathan Goodyear

Effect of germanium, poly-trans-[2-carboxyethyl] germasesquioxane on natural killer (NK... - 0 views

www.ncbi.nlm.nih.gov/...12237519

cancer germanium NK cells

shared by Nathan Goodyear on 30 May 18 - No Cached
  • Nathan Goodyear on 30 May 18
     
    Germanium found to augment NK cell activity both normal dogs and dogs with adenocarcinoma.
Nathan Goodyear

Effect of High-dose Vitamin C Combined With Anti-cancer Treatment on Breast Cancer Cells - 0 views

ar.iiarjournals.org/...751.short

vitamin c breast cancer

shared by Nathan Goodyear on 20 Aug 19 - No Cached
  • Nathan Goodyear on 20 Aug 19
     
    cell study finds high dose vitamin C (up to 20 mM) augments conventional chemo.
Nathan Goodyear

Hyperthermia as an immunotherapy strategy for cancer - 1 views

www.ncbi.nlm.nih.gov/...PMC2828267

cancer hyperthermia

shared by Nathan Goodyear on 29 Nov 18 - No Cached
  • the notion of treating human cancers with heat dates back to the writings of Hippocrates
  • enhance the efficiency of standard cancer therapies, such as chemotherapy and radiation treatment
  • After antigen uptake at tumor sites, APCs have the ability to create a robust response by entering lymphoid compartments and programming lymphocytes
  • ...36 more annotations...
  • Hyperthermia differs fundamentally from fever in that it elevates the core body temperature without changing the physiological set point
  • hyperthermia is induced by increasing the heat load and/or inactivating heat dissipation
  • mor cells [2]. Although significant cell killing could be achieved by heating cells or tissues to temperatures > 42°C for 1 or more hours, the application, measurement and consistency of this temperature range within the setting of cancer clinical trials
  • mild temperature hyperthermia (ie, within the fever-range, 39–41°C)
    • Nathan Goodyear
      Nathan Goodyear on 04 Aug 19
       
      101.2 to 105.8
  • moderate hyperthermia (41°C)
    • Nathan Goodyear
      Nathan Goodyear on 04 Aug 19
       
      105.8 F
  • Hsps are a family of stress-induced proteins
  • they are key regulators of cellular protein activity, turnover and trafficking
  • Hsps ensure appropriate post-translational protein folding, and are able to refold denatured proteins, or mark irreversibly damaged proteins for destruction
  • the ability of fever-range hyperthermia to induce reactive immunity against tumor antigens through DCs and NK-cells is likely mediated by Hsps
  • thermotolerance
  • Hsps support the malignant phenotype of cancer cells by not only affecting the cells’ survival, but also participating in angiogenesis, invasion, metastasis and immortalization mechanisms
  • Hsps released from stressed or dying cells activate dendritic cells (DCs), transforming them into mature APCs
  • In theory, fever-range hyperthermia may take advantage of tumor cell Hsps by inducing their release from tumor cells and augmenting DC priming against tumor antigens
  • In several models of hyperthermia, heat-treated tumors exhibited improved DC priming and generation of systemic immunity to tumor cell
  • hyperthermia alone can enhance antigen display by tumor cells, thus rendering them even more susceptible to programmed immune clearance
  • Fever-range hyperthermia may also induce Hsps
  • Hsps may exert an adjuvant effect by bolstering MHC class II and co-stimulatory molecule expression by DCs
  • thermal ablation of liver tumors in particular has demonstrated an ability to potentiate immune responses [57, 58] and elicit robust T-cell infiltrates at ablation sites
  • specific Hsp, Hsp70, directly inhibits apoptosis pathways in cancer cells, as demonstrated in human pancreatic, prostate and gastric cancer cells
  • Cross-priming is the ability of extracellular Hsps complexed to tumor peptides to be internalized and presented in the context of MHC class I molecules on APCs, thus allowing potent priming of CTLs against tumor antigens
  • It has been reported that Hsps are generated from necrotic tumor cell lysates, but not from tumor cells undergoing apoptosis
  • tumor cells exposed to hyperthermia in the heat shock range (42°C for 4h) prior to lysing, DC activation and cross-priming were significantly enhanced with the application of heat
  • Due to the ability of Hsps to activate DCs directly by chaperoning tumor antigens upon their release [28], it is possible that both local and regional immune stimulation can be achieved with hyperthermia.
  • support the use of hyperthermia as an inducer of Hsps to serve as ‘danger signals’, activating antitumor immune responses
  • whole-body hyperthermia not only augments immune responses, but also stimulates the migration of skin-derived DCs to draining lymph nodes
    • Nathan Goodyear
      Nathan Goodyear on 04 Aug 19
       
      This allows for the activation of lymphocytes by the activated dendritic cells.
  • suggest a valuable role of hyperthermia in DC cancer vaccine strategies
  • In mice treated with fever-range whole-body hyperthermia, tumor growth was significantly inhibited and NK-cell infiltration increased
    • Nathan Goodyear
      Nathan Goodyear on 04 Aug 19
       
      Hyperthermia increased NK cell activation, proliferation, and infiltration, which equals increased cytotoxicity.
  • exposure to fever-range hyperthermia resulted in improved endogenous NK-cell cytotoxicity to several cancer types
  • improved activation and function of DCs and NK cells following hyperthermia
  • Hyperthermia increases the expression ICAM-1 a key adhesion molecule,
  • The combined effects of hyperthermia on lymphoid tissue endothelium and lymphocytes can promote immune surveillance and increase the probability of naive lymphocytes leaving the circulation and encountering their cognate antigen displayed by DCs in lymphoid organs.
  • In independent clinical studies, whole-body hyperthermia resulted in a transient decrease in circulating lymphocytes in patients with advanced cancer [12, 94, 99, 100], a finding which mirrored observations in animal models in which lymphocyte entry into lymph noeds was increased following hyperthermia treatment [93]. Enhanced recruitment of lymphocytes to lymphoid tissues may be exploited in the treatment of malignancies.
  • The initial tumor antigen presentation and initiation of clonal expansion of CTLs transpires in the lymph nodes and cannot take place outside this specialized compartment
  • the ability of DCs present in the lymph nodes to stimulate an anti-tumor immune response is critical
  • hyperthermia has been shown to improve immune surveillance by T-cell
  • and to increase DC trafficking to lymph nodes
  • Nathan Goodyear on 29 Nov 18
     
    Great review of hyperthermia.
Nathan Goodyear

High-dose ascorbic acid synergizes with anti-PD1 in a lymphoma mouse model - 0 views

www.ncbi.nlm.nih.gov/...PMC6983418

check point inhibitors CTL lymphoma cytotoxic T cells PD-1 vitamin C immune check point inhibitors IV vitamin C NK cells NK

shared by Nathan Goodyear on 01 Apr 21 - No Cached
  • Nathan Goodyear on 01 Apr 21
     
    high dose vitamin C shown to augment PD-1 immune check point inhibitors in Lymphoma mouse model.
Nathan Goodyear

High-dose vitamin C enhances cancer immunotherapy - 0 views

sci.bban.top/...scitranslmed.aay8707.pdf

"Vitamin C" "IV vitamin cancer immunotherapy immune system

shared by Nathan Goodyear on 02 Apr 21 - No Cached
  • Nathan Goodyear on 02 Apr 21
     
    Absolute must read. IVC augments immune system and immunotherapy.
Nathan Goodyear

Phosphodiesterase 5 Inhibitors Enhance Chemotherapy Killing in Gastrointestinal/Genitou... - 0 views

www.ncbi.nlm.nih.gov/...PMC3935155

chemotherapy phosphodiesterase 5 inhibitors repurposed drugs PDE inhibitors PDE5I phosphodiesterase inhibitors cancer PDE5 inhibitors

shared by Nathan Goodyear on 08 Mar 21 - No Cached
  • Nathan Goodyear on 08 Mar 21
     
    PDE inhibitors repurposed to augment chemotherapy in treatment of cancer.
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