Open AccessThe RET proto‐oncogene: A molecular therapeutic target in thyroid cancer
Author(s) -
Kodama Yoshinori,
Asai Naoya,
Kawai Kumi,
Jijiwa Mayumi,
Murakumo Yoshiki,
Ichihara Masatoshi,
Takahashi Masahide
Publication year - 2005
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2005.00023.x
Subject(s) - ret proto oncogene , cancer research , proto oncogene proteins c ret , multiple endocrine neoplasia type 2 , thyroid carcinoma , thyroid cancer , tyrosine kinase , cancer , germline , medullary thyroid cancer , point mutation , medicine , oncogene , receptor tyrosine kinase , papillary thyroid cancer , biology , germline mutation , mutation , gene , kinase , thyroid , genetics , signal transduction , receptor , glial cell line derived neurotrophic factor , neurotrophic factors , cell cycle
The RET proto‐oncogene is responsible for the development of several human inherited and non‐inherited diseases. Germline point mutations were identified in multiple endocrine neoplasia types 2A and 2B, and familial medullary thyroid carcinoma. More than 10 rearranged forms of RET , referred to as RET/PTC 1–9, ELKS/RET and RFP/RET, have been cloned from sporadic and radiation‐associated papillary thyroid carcinomas. These mutations induced oncogenic activation of RET tyrosine kinase by different mechanisms. To date, various kinds of therapeutic approaches have been developed for the treatment of RET‐associated cancers, including tyrosine kinase inhibitors, gene therapy with dominant negative RET mutants, and RNA interference to abrogate oncogenic mutant RET expression. RET and some signaling molecules that function downstream of RET could be potential targets for the development of selective cancer therapeutics. ( Cancer Sci 2005; 96: 143–148)