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Nathan Goodyear

Metformin as an anti-cancer agent: actions and mechanisms targeting cancer stem cells |... - 0 views

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    Great review on the multi-prong effect of metformin on cancer cells. Of particular to this article, is the effects on CSCs.
fnfdoc

Symptoms Of Aplastic Anemia | Your Health Our Priority - 0 views

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    Aplastic Anemia is a rare but serious disease of the blood cells. It is diagnosed by the inability of the bone marrow to synthesize RBCs, WBCs and platelets. The spongy bone marrow contains stem cells that are actively involved in Hematopoiesis.
Nathan Goodyear

Cellular toxicity driven by high-dose vitamin C on normal and cancer stem cells - PubMed - 0 views

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    High dose vitamin C preferentially targets CSC but not differentiated cells.
Nathan Goodyear

Ivermectin as an inhibitor of cancer stem‑like cells - PubMed - 0 views

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    Cell and computational study, so limited to take; however, it did showed that ivermectin inhibited CSC.
Nathan Goodyear

Bisphenol A Promotes Human Prostate Stem-Proge... [Endocrinology. 2014] - PubMed - NCBI - 0 views

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    Another strike against BPA.  This time, BPA exposure during development increased hormone-dependent cancer risk in the prostate through its interaction with prostate stem-progenitor cells.  Again, we are being altered prior to birth.
Nathan Goodyear

NADH autofluorescence, a new metabolic biomarker for cancer stem cells: Identification ... - 0 views

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    Vitamin C effective agains CSC.
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

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

Radiation treatment generates therapy‐resistant cancer stem cells from less a... - 0 views

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    Radiation induces CSC radiation resistance.
Nathan Goodyear

Induction of metastasis, cancer stem cell phenotype, and oncogenic metabolism in cancer... - 0 views

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    This study focuses on the molecular mechanisms of IR-induced EMT, CSCs, oncogenic metabolism, alterations in the TME, and treatment resistance.
Nathan Goodyear

In Vitro Anticancer Activity of Plant-Derived Cannabidiol on Prostate Cancer Cell Lines - 0 views

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    High CBD downregulates prostate CBD1, CBD2, chemosensitizes CSCs, suppressed cancer cell formation, down regulated IL-6 and IL-8, decreased PSA, and VEGF.
Nathan Goodyear

Huperzine A promotes hippocampal neurogenesis in vitro and in vivo - 0 views

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    Huperzine A increases hippocampal neural stem cell proliferation--neurogenesis.  This study an animal study.
Nathan Goodyear

Sulforaphane, a Dietary Component of Broccoli/Broccoli Sprouts, Inhibits Breast Cancer ... - 0 views

  • sulforaphane, a natural compound derived from broccoli/broccoli sprouts
  • Sulforaphane inhibits breast CSCs
  • These findings support the use of sulforaphane for the chemoprevention of breast cancer stem cells
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    Sulforaphane, naturally found in broccoli  inhibits breast CSCs
Nathan Goodyear

Environmental Estrogen Exposure During Fetal Life: A Time Bomb for Prostate Cancer: End... - 0 views

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    environmental toxins that have estrogenic activity, i.e. BPA alter the prostate stem cells.  These and other xenoestrogens, as they are collectively called, increase the sensitivity of the prostate to estrogen.  This increases the risk of prostate Ca.  This just sets the pattern of signal interpretation and sensitivity.  Add in the continued estrogenic environment, add in the excess weight, the increased aromatase activity and resultant estrogen production and one has all the ingredients for prostate cancer.
Nathan Goodyear

Imp2 controls oxidative phosphorylation and is crucial for preserving glioblastoma canc... - 0 views

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    Glioblastoma's CSCs found to rely on oxidative phosphorylation metabolism and not aerobic glycolysis.
Nathan Goodyear

Substantial contribution of extrinsic risk factors to cancer development - 0 views

  • Here we provide evidence that intrinsic risk factors contribute only modestly (<10~30%) to cancer development
  • we conclude that cancer risk is heavily influenced by extrinsic factors. These results carry immense consequences for strategizing cancer prevention
  • cancers are proposed to originate from the malignant transformation of normal tissue progenitor and stem cells
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  • “Intrinsic processes” include those that result in mutations due to random errors in DNA replication whereas “extrinsic factors” are environmental factors that affect mutagenesis rates (such as UV radiation, ionizing radiation, and carcinogens
  • intrinsic factors do not play a major causal role.
  • intrinsic cancer risk should be determined by the cancer incidence for those cancers with the least risk in the entire group controlling for total stem cell divisions
  • if one or more cancers would feature a much higher cancer incidence, for example, lung cancer among smokers vs. non-smokers, then this most likely reflects additional (and probably extrinsic) risk factors (smoking in this case)
  • Particularly, for breast and prostate cancers, it has long been observed that large international geographical variations exist in their incidences (5-fold for breast cancer, 25-fold for prostate cancer)14, and immigrants moving from countries with lower cancer incidence to countries with higher cancer rates soon acquire the higher risk of their new country
  • Colorectal cancer is another high-incidence cancer that is widely considered to be an environmental disease17, with an estimated 75% or more colorectal cancer risk attributable to diet
  • melanoma, its risk ascribed to sun exposure is around 65–86%
  • non-melanoma basal and squamous skin cancers, ~90% is attributable to UV
  • 75% of esophageal cancer, or head and neck cancer are caused by tobacco and alcohol
  • HPV may cause ~90% cases in cervical cancer23, ~90% cases in anal cancer24, and ~70% in oropharyngeal cancer
  • HBV and HCV may account for ~80% cases of hepatocellular carcinoma
  • H pylori may be responsible for 65–80% of gastric cancer
  • While a few cancers have relatively large proportions of intrinsic mutations (>50%), the majority of cancers have large proportions of extrinsic mutations, for example, ~100% for Myeloma, Lung and Thyroid cancers and ~80–90% for Bladder, Colorectal and Uterine cancers, indicating substantial contributions of carcinogen exposures in the development of most cancers
  • onsistent estimate of contribution of extrinsic factors of >70–90% in most common cancer types. This concordance lends significant credibility to the overall conclusion on the role of extrinsic factors in cancer development
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    Really great read.  Cancer is a majority lifestyle disease.
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