estrogen administration has been found to increase tryptophan hydroxylase
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shared by Nathan Goodyear on 11 Jul 17
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Sex hormones affect neurotransmitters and shape the adult female brain during hormonal ... - 0 views
www.ncbi.nlm.nih.gov/...PMC4335177
hormones neurotransmitters serotonin GABA dopamine estradiol progesterone glutamate
shared by Nathan Goodyear on 11 Jul 17
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5-HT2A mRNA levels in brain areas relevant for the control of mood, mental state and cognition (Sumner and Fink, 1998) and 5-HTT mRNA when administered for a longer period
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n the other hand, estrogen treatment has also been observed to decrease mRNA related to serotonergic neurotransmission
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Furthermore, acute estrogen administration decreases 5-HTT mRNA levels (Pecins-Thompson et al., 1998) and 5-HT1A mRNA levels and binding
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assigning the effects of estrogen on serotonin to a homogenous functional class of stimulation or inhibition seems not to be feasible
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Progesterone has been suggested to increase serotonergic neurotransmission via the regulation of the expression of serotonin-related genes and proteins
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menopausal women gain less benefit from antidepressant treatments compared to women during their reproductive years
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good review of the relationship of the sex hormones and neurotransmitters.
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Medical education in pharmacogenomics-results from a survey on pharmacogenetic knowledg... - 0 views
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Of participants, 84.3% found pharmacogenomics relevant to their current practice
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More than two-thirds (65.7%) did not order nor recommend a pharmacogenomic test in the past year
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pharmacogenomic testing was understood mainly for assessment of the variability of genes affecting drug disposition, metabolism and drug transport leading to individual responses to drugs
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Pre-emptive, prospective, genotyping to make individualised drug therapy feasible is seen to contribute to personalised medicine
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assumed to improve drug efficacy and safety
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Potential benefits of pharmacogenomics (PGx) have been defined such as predicting intended response to medication by more accurate dosing, avoiding adverse drug reactions and therefore enhancing drug safety and reducing health care cost
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survey among Dutch pharmacists revealed 14.7% recent users of PGx diagnostics [27], whereas in our cohort, the percentage was with 34.3% higher.
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Doctors and pharmacists are slow to integrate pharmacogenetics. Good working definition of pharmacogenetics as well.
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Promising role for Gc-MAF in cancer immunotherapy: from bench to bedside - 0 views
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MAF precursor activity has also been lost or reduced after Gc-globulin treatment in some cancer cell lines
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This appears to result from the deglycosylated ɑ-N-acetylgalactosaminidase (nagalase) secreted from cancerous cells
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Nagalase has been detected in many cancer patients, but not in healthy individuals
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Studies have shown that the production of nagalase has a mutual relationship with Gc-MAF level and immunosuppression
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It has been demonstrated that serum levels of nagalase are good prognosticators of some types of cancer
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The nagalase level in serum correlates with tumor burden and it has been shown that Gc-MAF therapy progresses, nagalase activity decreases
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It has been shown that Gc-MAF can inhibit the angiogenesis induced by pro-inflammatory prostaglandin E1
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The effect of Gc-MAF on chemotaxis or activation of tumoricidal macrophages is likely the main mechanism against angiogenesis.
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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.”
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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
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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.”
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Yamamoto et al. showed that the administration of Gc-MAF to 16 patients with prostate cancer led to improvements in all patients without recurrence
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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
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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).
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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
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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
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weekly administration of 100 ng Gc-MAF to cancer at different stages and types showed curative effects at different follow-up times
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this treatment has been suggested for non-anemic patients
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Studies have shown that weekly administration of 100 ng Gc-MAF to cancer patients had curative effects on a variety of cancers
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Because the half-life of the activated macrophages is approximately one week, it must be administered weekly
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In vivo weekly intramuscular administration of Gc-MAF (100 ng) for 16-22 weeks was used to treat patients with breast cancer
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individuals harboring different VDR genotypes had different responses to Gc-MAF and that some genotypes were more responsive than others
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Administration of Gc-MAF for cancer patients exclusively activates macrophages as an important cell in adaptive immunity
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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
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There is also evidence that confirms the tumoricidal role of Gc-MAF via Fc-receptor mediation
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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
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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
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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
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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).
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Activating or modifying natural killer cells, dendritic cells, DC, CTL, INF and IL-2 have all been recommended for cancer immunotherapy
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It has been reported that nagalase cannot deglycosylate Gc-MAF as it has specificity for Gc globulin alone
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inflammation-derived macrophage activation with the participation of B and T lymphocytes is the main mechanism
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macrophages highly-activated by the addition of Gc-MAF can show tumoricidal activity
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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
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great review on Gc-MAF in cancer. An increase in nagalase blocks Gc-protein to Gc-MAF activity leaving the host immune system compromised.
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Curcumin Down-Regulates DNA Methyltransferase 1 and Plays an Anti-Leukemic Role in Acut... - 0 views
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In a variety of solid tumors and blood cancers, aberrant hypermethylation of CpG-rich regions (>55% CG content, 0.5-4 kb in length, the so-called “CpG islands”) in the promoters of tumor suppressor genes (TSGs) results in their transcriptional silencing
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These agents have been reported to suppress tumor growth by reversing aberrantly hypermethylation in the promoters of inactivated TSGs (e.g. p15INK4B), allowing re-expression of TSGs, thereby restoring normal cell cycle regulation, proliferation, apoptosis, and differentiation
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groups have reported that curcumin acts as a scavenger of free radicals [13], an inhibitor of NF-κB nuclear translocation [14], and a modulator of histone deacetylase (HDAC) and histone acetyltransferase (HAT)
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In this study, we found that curcumin down-regulated DNMT1 expression in AML cells. This occurred, at least in part, through down-modulation of two positive regulators of DNMT1: Sp1 and the NF-κB component, p65. We also found that curcumin-mediated down-regulation of DNMT1 was associated with reactivation of TSGs and tumor suppression, both in vivo and in vitro.
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curcumin may selectively downregulate DNMT1 expression in tumor cells, but not in normal cells
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DNMT1 expression is positively regulated by Sp1 and the NF-κB signaling component
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indicating that curcumin may have significant anti-tumor activity in AML
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We found that, compared to the vehicle control, curcumin treatment reduced tumor weight by 70%
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Surprisingly, although curcumin significantly inhibited tumor growth in these mice, we were unable to find any obvious toxicity associated with curcumin treatment
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Consistent with our observations regarding curcumin’s ability to inhibit tumor growth in vivo (Figure 4) and down-regulate DNMT1 expression in vitro and ex vivo (Figure 1), we found that decreased levels of DNMT1 protein and mRNA were expressed by tumor cells isolated from curcumin-treated mice
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we identified curcumin as a substance which acts as an inhibitor of DNA methyltransferase enzymatic activity and induces significant global DNA hypomethylation in AML cells
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In this study, we first demonstrated that curcumin decreases DNMT1 mRNA and protein expression levels, most likely through inhibiting expression of positive regulators of DNMT1, such as Sp1 and the p65 component of NF-κB component, and/or altering their ability to bind to the promoter region of DNMT1
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Vitamin C increases viral mimicry induced by 5-aza-2′-deoxycytidine | PNAS - 0 views
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Vitamin C alone at concentrations up to 57 μM had little effect on cell growth but was toxic at 228 μM (SI Appendix, Fig. S1B), in line with recent studies of high vitamin C concentrations (125–2,000 μM)
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In our combination approach, vitamin C increased the effects of low doses of 5-aza-CdR, with 57 μM vitamin C almost doubling the growth inhibition
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Using the Chou–Talalay method (28), we found that the two compounds indeed acted synergistically, rather than additively, to inhibit cancer cell growth over the physiological ranges of vitamin C in healthy individuals (26–84 μM)
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These results show that targeting the cancer DNA methylome by combining low-dose 5-aza-CdR and vitamin C stimulates the expression of ERVs, the induction of a cell-autonomous immune activation response, and increased apoptosis of cancer cells
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The addition of vitamin C to treatment protocols therefore may be a straightforward way to increase the clinical efficacy of such drugs in MDS and leukemia patients
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Vitamin C deficiency has been seen previously in patients with multiple types of cancer, including hematological malignancies (35⇓–37). We predict that these patients might receive the most benefits from the combination treatment.
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induction of an innate immune response
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We therefore measured plasma concentrations of vitamin C in a small number of patients with miscellaneous hematologic malignancies. Strikingly, 58% of patients with hematological neoplasia who were not taking vitamin C supplements had severe vitamin C deficiency (serum concentration <11.4 μM, at which clinical features of scurvy may be manifested) (34), and 33% had vitamin C levels below the normal range
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it is possible that vitamin C was oxidized to DHA before it was transported into the cells
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Oral administration of vitamin C should be sufficient for the therapeutic strategy, because the concentrations reported in this study would not require i.v. administration.
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This statement lacks a basic understanding of vitamin C pharmacokinetics.
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Vitamin C is an essential nutrient for humans and has been reported to increase IFN levels in human cells upon virus infection
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daily treatment with vitamin C alone at physiological concentrations enhanced the expression of viral-defense genes relative to untreated cells
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When combined with low-dose 5-aza-CdR, physiological concentrations of vitamin C synergistically inhibited cancer-cell growth and induced apoptosis. Such synergy was associated with increased ERV expression and dsRNA in treated cells. The mechanism of action differs from that of vitamin C at higher doses, which involves its pro-oxidant activity, including GSH inhibition, to generate reactive oxygen species
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This activity has been shown to induce DNA damage and to enhance the sensitivities of myeloid malignancies, multiple myeloma, and cutaneous T-cell lymphoma to arsenic trioxide (41⇓⇓–44). It also can increase chemosensitivity of ovarian cancer cells (27) and selectively kill KRAS or BRAF mutant colorectal cancer cells by inhibiting GAPDH
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reactive oxygen species
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91% of patients with hematologic malignancies have vitamin C levels that are either low or severly deficient. This study found that vitamin C plus low dose DNA methyltransferase inhibitors have synergistic inhibition of cancer cell proliferation and increased apoptosis. Unfortunately, the authors claimed that oral vitamin C would be sufficient which indicates an incredible lack of understanding of vitamin C pharmacokinetics.
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Immune responses to malignancies - 0 views
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increased densities of T-cell infiltrates with a high proportion of CD8+ T cells within primary colorectal carcinomas were associated with a significant protection against tumor recurrence
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coexpression of genes mediating cytotoxicity and TH1 adaptive immune responses accurately predicted survival in patients with colorectal carcinoma independently of the metastatic status.
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tumor-specific cytolytic T lymphocytes (CTLs)
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tumor-associated antigens (TAs)
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Proinflammatory cytokines secreted by inflammatory cells can contribute to tumor progression, and soluble factors produced by the tumor in response to nonspecific or tumor-specific signals, such as prostaglandin E2 (PGE2), adenosine, or TGF-β, downregulate functions of immune cells
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they are largely ineffective in arresting tumor growth, although they can proliferate and mediate antitumor cytotoxicity on their removal from the tumor bed and ex vivo IL-2 activation.42
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DCs (HLA-DR+CD86+CD80+CD14−) are nature’s best APCs
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They are a common component of tumor immune infiltrates and are responsible for the uptake, processing, and cross-presentation of TAs to naive or memory T cells, thus playing a crucial role in the generation of tumor-specific effector T cells
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DCs control the induction of Treg cells. In patients with cancer, cellular interactions between antigen-presenting DCs and T cells lead to expansion and accumulation of Treg cells at the tumor site and in the periphery
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NK cells (CD3−CD56+CD16+), which mediate innate immunity and contain both perforin-rich and granzyme-rich granules, are well equipped to mediate lysis of tumor cells
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B cells (CD19+, CD20+) are also rare in most human tumors, with the exception of breast cancer and melanoma
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The initial acute inflammation involving the recruitment and influx of antitumor effector cells is replaced by chronic inflammation in later stages of tumor progression
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Tissue hypoxia plays a major role in shaping the nature of immune infiltrates in tumors
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Another great review of the immune system during different stages of carcinogenesis; how the cancer manipulates the immue system to cloak itself from the immune system.
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Curcumin-Mediated Reversal of p15 Gene Promoter Methylation: Implication in Anti-Neopla... - 0 views
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How is the Immune System Suppressed by Cancer - 1 views
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nitric oxide (NO) released by tumor cells
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Excellent work by Prof de Groot of Essen, indicated by adding exogenous xanthine oxidase ( XO) in hepatoma cells, hydrogen peroxide was produced to destroy the hepatoma cells
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NO from eNOS in cancer cells can travel through membranes and over long distances in the body
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NO also is co linked to VEGF which in turn increases the antiapoptotic gene bcl-2
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The other important influence of NO is in its inhibition of the proapoptoic caspases cascade. This in turn protects the cells from intracellular preprogrammed death.
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nitric oxide in immune suppression in relation to oxygen radicals is its inhibitory effect on the binding of leukocytes (PMN) at the endothelial surface
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Inhibition of inducible Nitric Oxide Synthase (iNOS)
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NO from the tumor cells actually suppresses the iNOS, and in addition it reduces oxygen radicals to stop the formation of peroxynitrite in these cells. But NO is not the only inhibitor of iNOS in cancer.
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Spermine and spermidine, from the rate limiting enzyme for DNA synthases, ODC, also inhibit iNOS
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tolerance in the immune system that decreases the immune response to antigens on the tumors
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Freund’s adjuvant
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increase in kinases in these cells which phosphorylate serine, and tyrosine
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responsible for activation of many growth factors and enzymes
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phosphorylated amino acids suppress iNOS activity
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Hexokinase II
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Prostaglandin E2, released from tumor cells is also an inhibitor of iNOS, as well as suppressing the immune system
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Th-1 subset of T-cells. These cells are responsible for anti-viral and anti-cancer activities, via their cytokine production including Interleukin-2, (IL-2), and Interleukin-12 which stimulates T-killer cell replication and further activation and release of tumor fighting cytokines.
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Th1 cells stimulate NK and other tumor fighting macrophages via IL-2 and IL-12; In contrast, Th2, which is stimulated in allergies and parasitic infections, produce IL-4 and IL-10. IL-4 and IL-10 inhibit TH-1 activation and the histamine released from mast cell degranulation upregulates T suppressor cells to further immune suppression.
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Th-2 subset of lymphocytes, on the other hand are activated in allergies and parasitic infections to release Interleukin-4 and Interleukin-10
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These have respectively inhibitory effects on iNOS and lymphocyte Th-1 activation
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Mast cells contain histamine which when released increases the T suppressor cells, to lower the immune system and also acts directly on many tumor Histamine receptors to stimulate tumor growth
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Tumor cells release IL-10, and this is thought to be one of the important areas of Th-1 suppression in cancer patients
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IL-10 is also increased in cancer causing viral diseases such as HIV, HBV, HCV, and EBV
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IL-10 is also a central regulator of cyclooxygenase-2 expression and prostaglandin production in tumor cells stimulating their angiogenesis and NO production
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nitric oxide in tumor cells even prevents the activation of caspases responsible for apoptosis
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NO produced by cancer cells inhibits proapoptotic pathways such as the caspases.
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early stages of carcinogenesis, which we call tumor promotion, one needs a strong immune system, and fewer oxygen radicals to prevent mutations but still enough to destroy the tumor cells should they develop
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later stages of cancer development, the oxygen radicals are decreased around the tumors and in the tumor cells themselves, and the entire cancer fighting Th-1 cell replication and movement are suppressed. The results are a decrease in direct toxicity and apoptosis, which is prevented by NO, a suppression of the macrophage and leukocyte toxicity and finally, a suppression of the T-cell induced tumor toxicity
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cGMP is increased by NO
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NO in cancer is its ability to increase platelet-tumor cell aggregates, which enhances metastases
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the greater the malignancies and the greater the metastatic potential of these tumors
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The greater the NO production in many types of tumors,
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gynecological
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elevated lactic acid which neutralizes the toxicity and activity of Lymphocyte immune response and mobility
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The lactic acid is also feeding fungi around tumors and that leads to elevated histamine which increases T-suppressor cells. Histamine alone stimulates many tumor cells.
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The warburg effect in cancer cells results in the increase in local lactic acid production which suppresses lymphocyte activity and toxicity as well as stimulates histamine production with further stimulates tumor cell growth.
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T-regulatory cells (formerly,T suppressor cells) down regulate the activity of Natural killer cells
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last but not least, the Lactic acid from tumor cells and acidic diets shifts the lymphocyte activity to reduce its efficacy against cancer cells and pathogens in addition to altering the bacteria of the intestinal tract.
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intestinal tract bacteria in cancer cells release sterols that suppress the immune system and down regulate anticancer activity from lymphocytes.
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In addition to the lactic acid, adenosine is also released from tumors. Through IL-10, adenosine and other molecules secreted by regulatory T cells, the CD8+ cells can be inactivated to an anergic state
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Adenosine up regulates the PD1 receptor in T-1 Lymphocytes and inhibits their activity
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Adenosine is a purine nucleoside found within the interstitial fluid of solid tumors at concentrations that are able to inhibit cell-mediated immune responses to tumor cells
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Adenosine appears to up-regulate the PD1 receptor in T-1 Lymphocytes and inhibits the immune system further
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Mast cells with their release of histamine lower the immune system and also stimulate tumor growth and activate the metalloproteinases involved in angiogenesis and metastases
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COX 2 inhibitors or all trans-retinoic acid
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Cimetidine, an antihistamine has been actually shown to increase in apoptosis in MDSC via a separate mechanism than the antihistamine effect
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interleukin-8 (IL-8), a chemokine related to invasion and angiogenesis
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In vitro analyses revealed a striking induction of IL-8 expression in CAFs and LFs by tumor necrosis factor-alpha (TNF-alpha)
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these data raise the possibility that the majority of CAFs in CLM originate from resident LFs. TNF-alpha-induced up-regulation of IL-8 via nuclear factor-kappaB in CAFs is an inflammatory pathway, potentially permissive for cancer invasion that may represent a novel therapeutic target
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Great review of the immunosuppression in cancer driven by the likes of NO.
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shared by Nathan Goodyear on 18 May 17
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Hyperbaric oxygen therapy promotes neurogenesis: where do we stand? - 0 views
www.ncbi.nlm.nih.gov/...PMC3231808
hbot hyperbaric therapy hyperbaric brain TBI stroke neurogenesis neuorplasticity
shared by Nathan Goodyear on 18 May 17
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Numerous in vivo and in vitro studies confirm that HBOT induces neurogenesis
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HIF-1α is the principal mediator of cellular hypoxia adaptations
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activated by hypoxia, HIF-1α causes the transcription of its regulated downstream genes, including erythropoietin (EPO) and VEGF which are known to promote neurogenesis
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The safety of HBOT was also evaluated and it was pointed out that, if given at proper paradigms, like 1.5 ATA for 60 minutes, HBOT will not cause oxygen toxicity
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Rockswold et al., on the other hand, found that HBOT might be potentially beneficial for severe TBI patients
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McDonagh et al., concluded that there was insufficient evidence to establish the effectiveness of HBOT in the treatment of TBI
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The first multicenter, randomized, double-blind, controlled trial in 2009 found that 40-hour HBOT of 24% oxygen at 1.3 ATM produced significant improvement in children's overall functioning, receptive language, social interaction, eye contact, and sensory/cognitive awareness compared to those received slightly pressurized room air
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Another study in 2010 on 16 autism patients, adopting a similar treatment paradigm, showed no effect on a wide array of behavioral evaluations
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To date, there is little evidence that HBOT causes malignant growth or metastasis. A history of malignancy should therefore not be considered as a contraindication for HBOT
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HBOT enhances the production of reactive oxygen species (ROS) and causes oxidative stress in body tissues
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Excessive accumulation of oxidative stress may contribute to neurodegenerative processes and cell death in the brain, as seen in diseases like Alzheimer's disease (AD) and Parkinson's disease (PD)
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Hormesis
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process that results in a functional improvement of cellular stress resistance, survival, and longevity in response to sub-lethal levels of stress
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Striatal H3K27 Acetylation Linked to Glutamatergic Gene Dysregulation in Human Heroin A... - 0 views
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Heroin use, and yes prescription opiate use, alters glutamate pathways. Opiates change the brain.
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Effects of short-term high-fat overfeeding on genome-wide DNA methylation in the skelet... - 0 views
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short-term HFO introduces DNA methylation changes on a genome-wide scale in human skeletal muscle
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These changes were only partly reversed after 6–8 weeks
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The induction of DNA methylation changes after 5 days of HFO supports the growing awareness of DNA methylation as a dynamic signal that is possibly relevant to short-term day-to-day metabolic adaptations, including acute exercise
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Diverging DNA methylation levels between elderly, but not young, genetically identical twins indicate that environmental exposures throughout life may permanently influence DNA methylation, suggesting some preservation of de novo DNA methylation in adults
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our finding of a slow reversibility rate indicates the demethylation process may be somewhat impeded compared with the induction of methylation changes by diet, which could have implications for the preservation or build-up of CpG methylation over time
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A slow reversibility of DNA methylation induced by carcinogenic agents has likewise been observed due to ingestion of high-fat diets in rodents
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the relationship between DNA methylation and gene expression is not always straightforward
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Study finds variability of methylation and some genetic expression alteration with high fat diet. Restated, what you eat interacts with your DNA to alter genetic expression. This has implications on initiation of therapy as well as response to therapy.
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Cross-kingdom inhibition of breast cancer growth by plant miR159 - 0 views
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MicroRNAs (miRNAs), a major family of small RNAs, are ∼23 nt-long single strands of RNA that bind to mRNA transcripts to inhibit their translation
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A recent study by Zhang et al. reported that plant-derived miRNAs can be found in human serum.
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The group demonstrates that the plant miRNA miR168 may be taken up through dietary intake to inhibit the expression of its target low-density lipoprotein receptor 1 in the liver21, providing the first evidence that miRNA in food may influence gene expression in mammalian organs.
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A more recent finding by the same group shows that a plant miRNA from honeysuckle is able to inhibit Influenza A replication22, indicating that plant miRNAs may be useful for treating human diseases.
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We found that plant miR159 could be detected in human sera and its levels were inversely correlated with BC incidence and progression.
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We further identified TCF7 as a mammalian target for miR159 and showed the anti-proliferative function of miR159 in BC cells using in vitro and in vivo models, demonstrating for the first time that a plant miRNA is able to influence BC cell growth.
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certain dietary miRNAs from plants and other species may serve as highly affordable and powerful means of treatment with minimal inconvenience to patients.
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miR159 which (using a synthetic mimic) targets TCF7 to inhibit the proliferation of cells whose growth is dependent on TCF7 such as the BC cells MDA-MB-231
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our study using a BC model clearly indicates the anti-tumor effect of orally administered synthetic miR159 in its naturally existing form with the plant-specific 2'-O-methylation, suggesting the feasibility of using synthetic forms of plant miRNAs as dietary supplements in the treatment of human cancers, including those outside of the GI track
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Plant microRNA found to exist in human serum from gut absorption to then alter genetic expression in in-vitro and in vivo studies.
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shared by Nathan Goodyear on 11 Mar 21
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Mechanisms of Estrogen Receptor Signaling: Convergence of Genomic and Nongenomic Action... - 0 views
academic.oup.com/...2741274
cancer breast cancer ER-alpha ER alpha non-genomic signaling ERE estrogen response elements genomic signaling
shared by Nathan Goodyear on 11 Mar 21
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The thyroid hormone-αvβ3 integrin axis in ovarian cancer: regulation of gene ... - 0 views
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Cancer Cell Gene Expression Modulated from Plasma Membrane Integrin αvβ3 by T... - 0 views
Actions of L-thyroxine (T4) and Tetraiodothyroacetic Acid (Tetrac) on Gene Expression i... - 0 views
Astrocyte Elevated Gene-1 (AEG-1) Contributes to Non-thyroidal Illness Syndrome (NTIS) ... - 0 views
www.ncbi.nlm.nih.gov/...PMC4505468
T4 cancer non-thyroidal illness syndrome rT3 hepatocellular cancer T3 hepatocellular carcinoma euthyroid sick syndrome
shared by Nathan Goodyear on 15 Mar 21
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TERT gene: its function and dysregulation in cancer | Journal of Clinical Pathology - 0 views