Dysfunction of the RET receptor in human cancer.
RET is the receptor for glial-derived neurotrophic factor growth factors. It is a paradigm of a single gene that causes different types of human cancer when targeted by different genetic alterations. Like other receptor tyrosine kinases, once activated, RET recruits a variety of signaling molecules that mediate biological responses. Here we review data on the signaling pathways that lead to RET-mediated cell transformation and recent evidence that manipulation of RET holds promise for thyroid cancer treatment.
Santoro
M
M
Dipartimento di Biologia e Patologia Cellulare e Molecolare, University Federico II, via S. Pansini 5, 80131 Naples, Italy. masantor@unina.it
Carlomagno
F
F
Melillo
R M
RM
Fusco
A
A
D002291:Carcinoma, Papillary / Q000378:metabolism; D002471:Cell Transformation, Neoplastic; D006801:Humans; D008024:Ligands; D008954:Models, Biological; D008957:Models, Genetic; D009369:Neoplasms / Q000378:metabolism*; D010766:Phosphorylation; D017434:Protein Structure, Tertiary; D011518:Proto-Oncogene Proteins / Q000502:physiology*; D051096:Proto-Oncogene Proteins c-ret; D020794:Receptor Protein-Tyrosine Kinases / Q000502:physiology*; D015398:Signal Transduction; D013964:Thyroid Neoplasms / Q000378:metabolism
D008024:Ligands; D011518:Proto-Oncogene Proteins; D051096:Proto-Oncogene Proteins c-ret; D020794:Receptor Protein-Tyrosine Kinases