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Prevalence and prognostic influence of genomic changes of EGFR pathway markers in synovial sarcoma
Author(s) -
Teng HaoWei,
Wang HseiWei,
Chen WeiMing,
Chao TaChung,
Hsieh YaoYu,
Hsih ChiHsiu,
Tzeng ChengHwai,
Chen Paul ChihHsueh,
Yen ChuehChuan
Publication year - 2011
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21852
Subject(s) - pten , tensin , exon , synovial sarcoma , kras , cancer research , point mutation , viral oncogene , epidermal growth factor receptor , medicine , mutation , oncogene , sarcoma , biology , pi3k/akt/mtor pathway , pathology , cancer , gene , colorectal cancer , genetics , signal transduction , cell cycle
Background We aimed to study the prevalence and prognostic influence of epidermal growth factor receptor (EGFR) and its downstream effectors in synovial sarcoma (SS). Objectives and Methods The tissue blocks from 30 patients were obtained. Expression of EGFR and phosphatase and tensin homolog (PTEN) were examined by immunohistochemistry, and mutation status of v‐Ki‐ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) exon 2, V‐raf murine sarcoma viral oncogene homolog B1 (BRAF) exon 15, phosphoinositide‐3‐kinase, catalytic, alpha polypeptide (PI3KCA) exons 9, 20, and PTEN exons 5–9 were analyzed by direct sequencing. Results: EGFR overexpression and PTEN deletion were found in 63.3% and 46.7% of patients. Sequence analysis failed to demonstrate mutations of KRAS and BRAF. However, an E545A point mutation in exon 9 of PI3KCA was found in 2 of the 30 (6.7%) cases and 4 point mutations in exon 5 (E99K, D106N), intro 6 to exon 7 (AATA(G)), and exon 9 (A359T) of PTEN were found in 2 of the 30 (6.7%) cases. PTEN loss was significantly more frequent in cases of trunk tumors, and the overexpression of EGFR was significantly more prevalent in patients who were 35 or older. Conclusions: PTEN deletion was associated with poor survival. J. Surg. Oncol. 2011;103:773–781. © 2011 Wiley‐Liss, Inc.