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Sarcomas: genetics, signalling, and cellular origins. Part 2: TET‐independent fusion proteins and receptor tyrosine kinase mutations
Author(s) -
Suvà ML,
Cironi L,
Riggi N,
Stamenkovic I
Publication year - 2007
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.2208
Subject(s) - receptor tyrosine kinase , biology , tyrosine kinase , genetics , gene , fusion gene , sarcoma , cancer research , kinase , signal transduction , computational biology , medicine , pathology
Although the mechanisms that underlie sarcoma development are still poorly understood, the identification of non‐random chromosomal translocations and receptor tyrosine kinase mutations associated with defined sarcoma types has provided new insight into the pathogenesis of these tumours. In Part 1 of the review ( J Pathol 2007; 213: 4–20), we addressed sarcomas that express fusion genes containing TET gene family products. Part 2 of the review summarizes our current understanding of the implications of fusion genes that do not contain TET family members in sarcoma development, as well as that of specific mutations in genes encoding receptor tyrosine kinases (RTKs). The final section will serve as a summary of both reviews and will attempt to provide a synthesis of some of the emerging principles of sarcomagenesis. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.