• Corpus ID: 85920289

Targeting the cancer metabolic phenotype using high dose vitamin B1 therapy

  title={Targeting the cancer metabolic phenotype using high dose vitamin B1 therapy},
  author={Bradley S. Hanberry},



Membrane transport of folates.

Biochemical pathways: an atlas of biochemistry and molecular biology

  • Br J Cancer
  • 2013

Site Specificity of Four Pyruvate Dehydrogenase Kinase Isoenzymes toward the Three Phosphorylation Sites of Human Pyruvate Dehydrogenase*

Site specificity for phosphorylation of four PDKs with unique tissue distribution could contribute to the tissue-specific regulation of the pyruvate dehydrogenase complex in normal and pathophysiological states.

Hypoxia, HIF1 and glucose metabolism in the solid tumour

  • N. Denko
  • Biology
    Nature Reviews Cancer
  • 2008
New data suggests that this metabolic switch within the solid tumour may provide a benefit to the tumour not by increasing glycolysis but by decreasing mitochondrial activity.

Some properties of the thiamine uptake system in isolated rat hepatocytes.

  • K. Yoshioka
  • Biology, Chemistry
    Biochimica et biophysica acta
  • 1984

Expression of oncogenes depends on biotin in human small cell lung cancer cells NCI-H69.

  • Sarah B. ScheergerJ. Zempleni
  • Biology, Chemistry
    International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vitaminologie et de nutrition
  • 2003
Biotin concentrations in culture media correlated negatively with biotin transport rates, suggesting that cells responded to marginal biotin supply with increased expression of biotin transporters, consistent with a role for biotin in oncogene-dependent metabolic pathways.

Brick by brick: metabolism and tumor cell growth.

Induction of hypoxia-inducible factor-1, erythropoietin, vascular endothelial growth factor, and glucose transporter-1 by hypoxia: evidence against a regulatory role for Src kinase.

Results indicate that src is not critical for the hypoxic induction of HIF-1, erythropoietin, VEGF, or Glut-1 and that the expression of these genes in src- or c-src kinase-deficient cells did not differ from wild-type cells at either 1% oxygen or more severe hypoxia.

prognosis." Pancreas

  • 1976