[Mutations of the gene coding for the receptor tyrosine kinase FLT3 in acute myeloid leukemia. Significance as the disease-specific molecular marker for diagnosis, prognosis and innovative therapy approaches]

Dtsch Med Wochenschr. 2005 Apr 22;130(16):1020-5. doi: 10.1055/s-2005-866780.
[Article in German]
No abstract available

Publication types

  • Review

MeSH terms

  • Biomarkers, Tumor / genetics*
  • Biomarkers, Tumor / metabolism
  • Biomarkers, Tumor / physiology
  • Enzyme Inhibitors / therapeutic use
  • Gene Expression Regulation, Neoplastic
  • Hematopoiesis / genetics
  • Hematopoiesis / physiology
  • Humans
  • Leukemia, Myeloid, Acute / diagnosis
  • Leukemia, Myeloid, Acute / genetics*
  • Leukemia, Myeloid, Acute / therapy
  • Mutation*
  • Proto-Oncogene Proteins / antagonists & inhibitors
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins / physiology
  • Receptor Protein-Tyrosine Kinases / antagonists & inhibitors
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Receptor Protein-Tyrosine Kinases / metabolism
  • Receptor Protein-Tyrosine Kinases / physiology
  • fms-Like Tyrosine Kinase 3

Substances

  • Biomarkers, Tumor
  • Enzyme Inhibitors
  • Proto-Oncogene Proteins
  • FLT3 protein, human
  • Receptor Protein-Tyrosine Kinases
  • fms-Like Tyrosine Kinase 3