BIOM20001 Lecture 67: 66-67 Neoplasia C
Document Summary
The binding of a ligand to receptor triggers series of events by which extracellular signals are transduced, resulting in changes in gene expression. Receptors lacking intrinsic tyrosine kinase activity transmit extracellular signals by activating members of the jak (janus kinase) family of proteins. Jak link the receptors with and activate cytoplasmic transcription factors (stats) which directly shuttle into the nucleus and activate gene transcription. Binding of the growth factor (ligand) induces: receptor dimerisation tyrosine residue autophosphorylation activation of the receptor tyrosine kinase active kinase then phosphorylates and activates downstream effector molecules. Growth factors include: egf, tgf-a, hgf, pdgf, vegf, fgf and insulin. Inactivation of growth-inhibiting genes - tumour suppressor genes e. g. p53, apc, cyclin(cdk) inhibitors p53 is a checkpoint protein that checks for dna damage. Mutation in p53 allows cell to divide despite dna damage/instability. 70% to 80% of nonfamilial colorectal carcinomas and sporadic adenomas also show homozygous loss of the apc gene.
