[Cytomics and receptor interaction].
The system of erbB-receptor-tyrosine-kinases (RTKs) appears considerable complex because four erbB-receptors crossactivate each other via homo- and heterointeraction upon ligand binding. This complexicity is additionally elevated by scores of corresponding growth factors with unique binding- and activation-specificity. The total receptor-ligand system provides the basis for intracellular signal- diversity and -specificity. Significant oncological importance is attributed to the family of erbB-RTKs, which are known to cause and contribute to carcinogenesis, tumor progression, invasion, metastasis, e. g. based on uncontrolled cell growth and cell proliferation. The detection of erbB-receptor gene amplification or corresponding protein overexpression is well established in tumor diagnosis and an essential element for therapy decision. However, the assessment of the coexpression profile of erbB-receptors and the presence or absence of growth factors has not been implemented into pathological diagnosis so far. Cytomics represents a novel discipline in systems-biology. It is dedicated to understand and resolve biocomplexicity of cells, cellular components, and cell-systems. Understanding the function of the integrated erbB-receptor-system on a cytomic level will facilitate to more precisely follow-up the course of disease and thereby to elevate prognosis to the level of individual prediction. A system biological approach should involve the analysis of molecular function and dynamics on a single cell level and thereby is expected to characterize the disease in terms of a given molecular equivalent. Additionally, new and highly specific drug targets are likely to be identified. The comprehensive analysis of the complex molecular erbB-receptor system will enable to stratify tumor patients more precisely and simultaneously to specify erbB-receptor based therapeutic strategies in terms of individualized medicine.
Brockhoff
Gero
G
Institut für Pathologie, Universität Regensburg.
D001695:Biology / Q000379:methods; D002455:Cell Division; D004789:Enzyme Activation; D066246:ErbB Receptors / Q000235:genetics / Q000378:metabolism*; D005784:Gene Amplification; D006801:Humans; D008024:Ligands; D008954:Models, Biological; D009369:Neoplasms / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D020239:Receptor Cross-Talk; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism
D008024:Ligands; D066246:ErbB Receptors; D020794:Receptor Protein-Tyrosine Kinases