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Nathan Goodyear

Cancer-Expanded Myeloid-Derived Suppressor Cells Induce Anergy of NK Cells th... - 0 views

www.jimmunol.org/...240.long

NK cells MDSC cancer myeloid-derived suppressor cells

shared by Nathan Goodyear on 11 Nov 20 - No Cached
  • Nathan Goodyear on 11 Nov 20
     
    Myeloid-derived suppressor cells decrease NK cell activity
Nathan Goodyear

Histamine dihydrochloride and low-dose interleukin-2 as post-consolidation im... - 0 views

www.academia.edu/...rapy_in_acute_myeloid_leukemia

AML leukemia acute myeloid leukemia IL-2 histamine cancer NK cells

shared by Nathan Goodyear on 31 May 18 - No Cached
  • IL-2 is a central T cell-derived cytokine, which induces NK cell and T cell proliferation, differentiation and activation, and also stim-ulates the production of secondary immunostimulatory cytokines
  • combination of histamine and IL-2 thus triggers efficient NK cell-mediated killing of several types of leukemic cells, including freshly recovered human AML blasts
  • histamine improves the effects of IL-2 on T cell activation
  • ...3 more annotations...
  • principal action of histamine is to protect cytotoxic lymphocytes from myeloid-cell-induced inactivation, thus improving the efficiency of the T and NK cell stimulation achieved by IL-2
  • random-ized Phase II study of patients with renal cell carcinoma further support the suggestion that the combination of HDC and IL-2 improves lymphocyte functions
  • HDC improves the effectiveness of IL-2-induced T and NK cell activation in cancer patients, as predicted in preclinical models
  • Nathan Goodyear on 31 May 18
     
    histamine dihydrochloride enhances immune effects of NK cells in IL02 therapy; specifically in this analysis in AML, the histamin prevented inactivation of the IL-2 activated NK cells.
Nathan Goodyear

Metronomic capecitabine as an immune modulator in glioblastoma patients reduces myeloid... - 0 views

pubmed.ncbi.nlm.nih.gov/31600167

myeloid-derived suppressor cells glioblastoma multiforme metronomic chemotherapy low-dose chemotherapy MDSC glioblastoma

shared by Nathan Goodyear on 08 Nov 20 - No Cached
  • Nathan Goodyear on 08 Nov 20
     
    Low-dose, metronomic chemotherapy induces suppression of MDSCs in the TME in glioblastoma.
Nathan Goodyear

Metronomic capecitabine as an immune modulator in glioblastoma patients reduces myeloid... - 0 views

www.ncbi.nlm.nih.gov/...PMC6948860

myeloid-derived suppressor cells metronomic chemotherapy low-dose chemotherapy MDSC

shared by Nathan Goodyear on 15 Nov 20 - No Cached
  • Nathan Goodyear on 15 Nov 20
     
    Metronomic chemotherapy reduces MDSCs recruitment.
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

Immunosuppressive Myeloid Cells Induced by Chemotherapy Attenuate Antitumor CD4+ T-Cell... - 0 views

cancerres.aacrjournals.org/...3441

MDSC chemotherapy myeloid-derived suppressor cells

shared by Nathan Goodyear on 15 Nov 20 - No Cached
  • Nathan Goodyear on 15 Nov 20
     
    This study points to the increase in immunosuppression as a result of chemotherapy induced increase in MDSCs and T reg. This effect is dose dependent.
Nathan Goodyear

Thymosin alpha-1 blocks the accumulation of myeloid suppressor cells in NSCLC by inhibi... - 0 views

pubmed.ncbi.nlm.nih.gov/32942159

MDSC TME TA-1 VEGF tumor microenvironment myeloid-derived suppressor cells thymosin alpha-1

shared by Nathan Goodyear on 16 Aug 21 - No Cached
  • Nathan Goodyear on 16 Aug 21
     
    TA-1 alters tumor microenvironment via VEGF induced decrease in MDSC.
Nathan Goodyear

Promising role for Gc-MAF in cancer immunotherapy: from bench to bedside - 0 views

www.ncbi.nlm.nih.gov/...PMC5686300

nagalase Gc-MAF cancer

shared by Nathan Goodyear on 29 Jan 18 - No Cached
  • MAF precursor activity has also been lost or reduced after Gc-globulin treatment in some cancer cell lines
  • This appears to result from the deglycosylated ɑ-N-acetylgalactosaminidase (nagalase) secreted from cancerous cells
  • Nagalase has been detected in many cancer patients, but not in healthy individuals
  • ...31 more annotations...
  • Studies have shown that the production of nagalase has a mutual relationship with Gc-MAF level and immunosuppression
  • It has been demonstrated that serum levels of nagalase are good prognosticators of some types of cancer
  • The nagalase level in serum correlates with tumor burden and it has been shown that Gc-MAF therapy progresses, nagalase activity decreases
  • It has been shown that Gc-MAF can inhibit the angiogenesis induced by pro-inflammatory prostaglandin E1
  • The effect of Gc-MAF on chemotaxis or activation of tumoricidal macrophages is likely the main mechanism against angiogenesis.
  • Administration of Gc-MAF stimulates immune-cell progenitors for extensive mitogenesis, activates macrophages and produces antibodies. “This indicates that Gc-MAF is a powerful adjuvant for immunization.”
  • Cancer cell lines do not develop into tumor genes in mouse models after Gc-MAF-primed immunization (29-31) and the effect of Gc-MAF has been approved for macrophage stimulation for angiogenesis, proliferation, migration and metastatic inhibition on tumors induced by MCF-7 human breast cancer cell line
  • The protocol included: "a high dose of second-generation Gc-MAF (0.5 ml) administered twice a week intramuscularly for a total of 21 injections.”
  • Yamamoto et al. showed that the administration of Gc-MAF to 16 patients with prostate cancer led to improvements in all patients without recurrence
  • Inui et al. reported that a 74-year-old man diagnosed with prostate cancer with multiple bone metastases was in complete remission nine months after initiation of GcMAF therapy simultaneously with hyper T/NK cell, high-dose vitamin C and alpha lipoic acid therapy
  • It has also been approved for non-neoplastic diseases such as autism (41), multiple sclerosis (42, 43), chronic fatigue syndrome (CFS) (40), juvenile osteoporosis (44) and systemic lupus erythematous (45).
  • Gc-MAF has been verified for use in colon, thyroid (38), lung (39), liver, thymus (36), pancreatic (40), bladder and ovarian cancer and tongue squamous carcinoma
  • Prostate, breast, colon, liver, stomach, lung (including mesothelioma), kidney, bladder, uterus, ovarian, head/neck and brain cancers, fibrosarcomas and melanomas are the types of cancer tested thus far
  • weekly administration of 100 ng Gc-MAF to cancer at different stages and types showed curative effects at different follow-up times
  • this treatment has been suggested for non-anemic patients
  • Studies have shown that weekly administration of 100 ng Gc-MAF to cancer patients had curative effects on a variety of cancers
  • Because the half-life of the activated macrophages is approximately one week, it must be administered weekly
  • In vivo weekly intramuscular administration of Gc-MAF (100 ng) for 16-22 weeks was used to treat patients with breast cancer
  • individuals harboring different VDR genotypes had different responses to Gc-MAF and that some genotypes were more responsive than others
  • Administration of Gc-MAF for cancer patients exclusively activates macrophages as an important cell in adaptive immunity
  • Gc-MAF supports humoral immunity by producing, developing and releasing large quantities of antibodies against cancer. Clinical evidence from a human model of breast cancer patients supports this hypothesis
  • There is also evidence that confirms the tumoricidal role of Gc-MAF via Fc-receptor mediation
  • It is likely that the best therapeutic responses will be observed when the nutritional and inflammatory aspects are taken together with stimulation of the immune system
  • it should be noted that no harmful side effects of Gc-MAF treatment have been reported, even when it was successfully administered to autistic children
  • The natural activation mechanism of macrophages by Gc-MAF is so natural and it should not have any side effects on humans or animal models even in cell culture
  • Besides the Gc-MAF efficacy on macrophage activity, it can be a potential anti-angiogenic agent (28) and an inhibitor of the migration of cancerous cells in the absence of macrophages (47).
  • Activating or modifying natural killer cells, dendritic cells, DC, CTL, INF and IL-2 have all been recommended for cancer immunotherapy
  • It has been reported that nagalase cannot deglycosylate Gc-MAF as it has specificity for Gc globulin alone
  • inflammation-derived macrophage activation with the participation of B and T lymphocytes is the main mechanism
  • macrophages highly-activated by the addition of Gc-MAF can show tumoricidal activity
  • Previous clinical investigations have confirmed the efficacy of Gc-MAF. In addition to activating existing macrophages, Gc-MAF is a potent mitogenic factor that can stimulate the myeloid progenitor cells to increase systemic macrophage cell counts by 40-fold in four days
  • Nathan Goodyear on 29 Jan 18
     
    great review on Gc-MAF in cancer.  An increase in nagalase blocks Gc-protein to Gc-MAF activity leaving the host immune system compromised.
Nathan Goodyear

Curcumin inhibits the growth of liver cancer by impairing myeloid-derived suppressor ce... - 0 views

www.ncbi.nlm.nih.gov/...PMC7905673

NF-kappaB MDSC curcumin TLR4 COX2 COX-2 IL-1 angiogenesis cancer LOX IL-6

shared by Nathan Goodyear on 14 May 21 - No Cached
  • Nathan Goodyear on 14 May 21
     
    Curcumin inhibit MDSC
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