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Nathan Goodyear

Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities - PMC - 0 views

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    Melatonin has broad anti-cancer properties.
Nathan Goodyear

Antitumor Activity of Plant Cannabinoids with Emphasis on the Effect of Cannabidiol on Human Breast Carcinoma | Journal of Pharmacology and Experimental Therapeutics - 0 views

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    CBD tops CBG and CBC in anti-breast cancer effects.
Nathan Goodyear

The Anti-aromatase Effect of Progesterone and of its Natural Metabolites 20α- and 5α-Dihydroprogesterone in the MCF-7aro Breast Cancer Cell Line - 0 views

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    The progesterone metabolite, 20alpha-dihydroprogesterone, is found to have anti-aromatase activity.  20alphaDHP via the enzyme 20alpha-HSO is a 4-pregnene.
Nathan Goodyear

Antineoplastic Mechanisms of Niclosamide in Acute Myelogenous Leukemia Stem Cells: Inactivation of the NF-κB Pathway and Generation of Reactive Oxygen Species | Cancer Research - 0 views

  • Here, we report on niclosamide as an antileukemic agent with two independent antineoplastic mechanisms: NF-κB pathway inactivation and ROS generation
  • In this report, we validated the inhibitory action of niclosamide against tumor necrosis factor (TNF)–induced NF-κB activation in AML cells and identified its mechanism, together with generation of reactive oxygen species (ROS), as being responsible for induced apoptosis of AML cells
  • NF-κB plays a critical role in inflammation, antiapoptotic responses, and carcinogenesis
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  • pharmacologic inhibition of NF-κB was effective in killing AML cells
  • High NF-κB expression is found in primitive human AML blast cells
  • niclosamide inhibited the TNF-induced NF-κB reporter activity in a dose- and time-dependent manner
  • niclosamide inhibiting TNF-induced IKK phosphorylation (Fig. 2A), niclosamide may exert its inhibitory effect at the TAK1 step
  • Pretreatment with niclosamide completely blocked the time- and dose-dependent TNFα-induced alteration of the NF-κB–DNA complex
  • niclosamide inhibited constitutively active NF-κB binding to DNA in U266 cells
  • niclosamide completely abolished the TNFα-induced phosphorylation of IKKα/β and IκBα
  • Accordingly, the TNFα-induced degradation of IκBα was abrogated by niclosamide
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    Old anti-parasitic medication, niclosamide, found to have anti-leukemic acitivty through inactivation of NF-kappaB and increase in ROS production in in Vitro and in Vivo study.
Nathan Goodyear

Mechanisms of the anti-cancer and... [Annu Rev Pharmacol Toxicol. 2011] - PubMed - NCBI - 0 views

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    Vitamin D inhibits inflammatory signaling and thus useful in cancer therapies.
Nathan Goodyear

Classification of mitocans, anti-cancer drugs acting on mitochondria - 0 views

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    Good review of therapies directed at mitochondria in cancer.
Nathan Goodyear

Recent developments in mushrooms as anti-cancer therapeutics: a review - 0 views

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    mushrooms and cancer
Nathan Goodyear

Antidepressant Medication Use and Breast Cancer Risk - Am J Epidemiol - 0 views

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    Patients on paxil have a 7 fold increase breast cancer risk
Nathan Goodyear

PLoS ONE: Antidepressants and Breast and Ovarian Cancer Risk: A Review of the Literature and Researchers' Financial Associations with Industry - 0 views

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    Antidepressants shown to increase Breast and Ovarian Cancer risk in review of 61 articles. Clear relationship found, but exact risk still needs further research.  Interestingly, the pharmaceutical industry's research, showed no risk.
Nathan Goodyear

High Progesterone Receptor Expression in Prostate Cancer Is Associated with Clinical Failure - 0 views

  • Currently, there is a general agreement of PGR presence in the stromal cells of PCa
  • expressed in both stromal and tumor cells of the PCa tissue
  • In univariate analysis, a high density level of PGR in both TE and TS was associated with CF
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  • High density level of PGR in the TE was an independent prognostic factor for CF.
  • Our large-sized study demonstrates a wide distribution of PGR in stromal and epithelial cells of both benign and malignant prostate tissue
  • there seems to be a general agreement of PGR presence in the stromal cells of PCa
  • In line with our findings, several have also reported a high PGR expression in TE of PCa [9,10,23,25]. In contrast, others have demonstrated a total lack of PGR expression in TE
  • the actions of progesterone are tissue specific
  • In our work univariate analysis demonstrated a high PGR expression in TS to be associated with clinical failure in PCa patients. So far we have not yet demonstrated the mechanism underlying this association
  • Several non-genomic proliferative actions of progesterone have been proposed in tumor cells of other organs, including breast [35–37], astrocytoma [38] and osteosarcoma [39] cell lines. However, such results are contradicted by suggestions of anti-proliferative actions of progesterone in endometrial cancer
  • Yu et al. found PGR to be negatively regulating stromal cell proliferation in vitro
  • high PGR density level in TE was associated with CF in patients with Gleason score ≥ 7
  • Bonkhoff et al. have suggested progressive emergence of PGR during PCa progression and metastasis
  • Latil and co-workers found a decreased PGR expression in clinically localized tumors and increased PGR expression in hormone-refractory tumors, when compared with normal prostate tissue
  • Our findings provide further support to these findings, indicating that PGR plays a role in the pathogenesis of PCa
  • Ki67 and PGR in TE were correlated with CF (S3 Text), indicating an association between PGR and proliferative activity
  • The mechanism behind the PGR up-regulation in PCa has not yet been elucidated
  • The PGR is, like the glucocorticoid receptor, similar to androgen receptor with 88% sequence homology in the ligand-binding domain
  • progesterone induced expression of androgen receptor-regulated genes could be a potential mechanism contributing to the development of castrate resistant PCa
  • A possibility of different roles by the two PGR isoforms in normal prostate tissue and PCa, as is suggested for the estrogen receptors [13], must also be taken into account
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    STudy finds that increased Progesterone receptor expression on epithelial and stromal cells is associated with increased clinical failure of therapy.  Several proposed mechanisms: 88% homologous with androgen receptor suggesting cross-stimulation and via progesterone induced increased androgen receptor gene stimulation i.e. epigenetics.
Nathan Goodyear

Anti-angiogenic peptides for cancer therapeutics - 0 views

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    Peptides to block angiogenesis in the treatment of cancer
Nathan Goodyear

Turning Tumor-Promoting Copper into an Anti-Cancer Weapon via High-Throughput Chemistry - 0 views

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    Cu and cancer and means to lower
Nathan Goodyear

Anti-cancer peptides from ras-p21 and p53 proteins - PubMed - 0 views

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    PNC-27 and 28, contain HDM-2-protein-binding domain sequences from the tumor suppressor p53 to induce pore formation in the membranes of a wide range of cancer cells but not any normal cells tested
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