[<< wikibooks] Radiation Oncology/Radiobiology/Growth Factors
Growth Factors


== ErbB ==
Family of 4 receptor tyrosine kinases
ErbB-1 (EGFR)
ErbB-2 (her2)
ErbB-3
ErbB-4
Transmembrane proteins, existing as monomers at surface
When a ligand binds, dimerisation arm becomes untethered, and the proteins dimerize
Tyrosine kinase activity


== EGFR ==

Ligands:
Epidermal growth factor (EGF): produced by platelets, macrophages, salivary glands, kidneys
Transforming growth factor alpha (TGF-α): produced by macrophages, brain cells, keratinocytes
HB-EGF, Amphiregulin, betacellulin, epigen, epiregulin: produced by various cells around the bodyReview: PMID 15142631, Herbst R, IJROBP 2004


== EGFR Pathways ==
EGFR -> Ras -> Raf -> MEK -> MAPK -> myc -> transcription
EGFR -> Ras -> Raf -> MEK -> MAPK -> RSK -> S6 -> transcription
EGFR -> PI3K -> AKT -> mTOR


== PTEN ==
PTEN gene encodes a phosphatase, which uses PIP-3, which is also produced by PI3K above. Loss of PTEN therefore increases PIP-3 levels, leading to inappropriate AKT activity, and subsequent protection of cancer cells from apoptosis
PTEN is a tumor suppressor
PTEN loss confers resistance to EGFR inhibitors
Please see PTEN Hamartoma Tumor Syndrome