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Nathan Goodyear

Curcumin decreases malignant characteristics of glioblastoma stem cells via induction o... - 0 views

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    Curcumin increases ROS in glioblastoma.
Nathan Goodyear

Radiation-induced reprograming of breast cancer cells - 0 views

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    Radiation induces CSCs.
Nathan Goodyear

Salinomycin: A Novel Anti-Cancer Agent with Known Anti-Coccidial Activities - 0 views

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    To be read
Nathan Goodyear

Metronomic Chemotherapy: A Systematic Review of the Literature and Clinical Experience - 0 views

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    Awesome article on how metronomic, low-dose chemotherapy reduces angiogenesis via decrease in HIF-1alpha and VEGF. Many other effects.
Nathan Goodyear

Function of oncogenes in cancer development: a changing paradigm - 0 views

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    to be read
Nathan Goodyear

Redox regulation in cancer - 0 views

  • Mitochondrial electron-transport chain and other oxidizing agents are the prime pathways that generate excess ROS in vivo
  • Permanent modification of genetic material resulting from the oxidative damage is one of the vital steps involved in mutagenesis that leads to carcinogenesi
  • The most frequent DNA mutations caused during oxidative stress, initiated by ionizing radiation and other environmental carcinogens are 7,8-dihydro-8-oxoguanine (8-Oxo-G) and Thymine Glycol (TG)
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  • catalase and SOD, GPx, GST
  • insulin like growth factor I, or fibroblast growth factor 2 generates ROS
  • Depletion of GSH increases the sensitivity of cells to ROS
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    The redox reaction in cancer: great read!
Nathan Goodyear

TGF-β1 secreted by M2 phenotype macrophages enhances the stemness and migrati... - 0 views

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    T-regulator cells secrete TGF-beta to promote M2 polarization in the TME to promote tumor progression and spread.
Nathan Goodyear

Endothelial Induced EMT in Breast Epithelial Cells with Stem Cell Properties - 0 views

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    Endothelial cells play role in EMT, which plays key role in metastasis.
Nathan Goodyear

The effect of N-acetyl-l-cysteine (NAC) on liver toxicity and clinical outcome after he... - 0 views

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    NAC lowers evidence of liver toxicity.
Nathan Goodyear

Repurposing Drugs in Oncology (ReDO)-chloroquine and hydroxychloroquine as anti-cancer ... - 0 views

  • HCQ, doses for long-term use range between 200 and 400 mg per day.
  • Short-term administration of CQ or HCQ rarely causes severe side effects
  • Short-term administration of CQ or HCQ rarely causes severe side effects
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  • bone marrow suppression
  • cardiomyopathy
  • irreversible retinal toxicity
  • hypoglycaemia
  • daily doses up to 400 mg of HCQ or 250 mg CQ for several years are considered to carry an acceptable risk for CQ-induced retinopathies, with the exception of individuals of short stature
  • chronic CQ or HCQ therapy be monitored through regular ophthalmic examinations (3–6 month intervals), full blood counts and blood glucose level checks
  • long-term HCQ exposure, skeletal muscle function and tendon reflexes should be monitored for weakness
  • both CQ and HCQ, specific caution is advised in patients suffering from impaired hepatic function (especially when associated with cirrhosis), porphyria, renal disease, epilepsy, psoriasis, glucose-6-phosphate dehydrogenase deficiency and known hypersensitivity to 4-aminoquinoline compounds
  • CQ and HCQ can effectively increase the efficacy of various anti-cancer drugs
  • CQ can prevent the entrapment of protonated chemotherapeutic drugs by buffering the extracellular tumour environment and intracellular acidic spaces
  • This study recommends an adjuvant HCQ dose of 600 mg, twice daily.
  • HCQ addition was shown to produce metabolic stress in the tumours
  • HCQ (400 mg/day)
  • important effects of CQ and HCQ on the tumour microenvironment
  • The main and most studied anti-cancer effect of CQ and HCQ is the inhibition of autophagy
  • the expression levels of TLR9 are higher in hepatocellular carcinoma, oesophageal, lung, breast, gastric and prostate cancer cells as compared with adjacent noncancerous cells, and high expression is often linked with poor prognosis
  • TLR9-mediated activation of the NF-κB signalling pathway and the associated enhanced expression of matrix metalloproteinase-2 (MMP-2), MMP-7 and cyclo-oxygenase 2 mRNA
  • HCQ can activate caspase-3 and modulate the Bcl-2/Bax ratio inducing apoptosis in CLL, B-cell CLL and glioblastoma cells
  • In triple-negative breast cancer, CQ was shown to eliminate cancer stem cells through reduction of the expression of Janus-activated kinase 2 and DNA methyl transferase 1 [106] or through induction of mitochondrial dysfunction, subsequently causing oxidative DNA damage and impaired repair of double-stranded DNA breaks
  • CQ or HCQ would be considered for use in combination with immunomodulation anti-cancer therapies
  • Therapies used in combination with CQ or HCQ include chemotherapeutic drugs, tyrosine kinase inhibitors, various monoclonal antibodies, hormone therapies and radiotherapy
  • Most studies hypothesise that CQ and HCQ could increase the efficacy of other anti-cancer drugs by blocking pro-survival autophagy.
  • daily doses between 400 and 1200 mg for HCQ are safe and well tolerated, but two studies identified 600-mg HCQ daily as the MTD
  • HCQ is often administered twice daily to limit plasma fluctuations and toxicity
Nathan Goodyear

Anti-Cancer Activity of Cannabis sativa Phytocannabinoids: Molecular Mechanisms and Pot... - 0 views

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    Review of the targeted effects of CBDA CBD and THC in cancer treatment
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