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No p16 INK4A /CDKN2/MTS1 mutations independent of p53 status in soft tissue sarcomas
Author(s) -
Meye Axel,
Würl Peter,
Hinze Raoul,
Berger Dieter,
Bache Matthias,
Schmidt Hannelore,
Rath FriedrichWilhelm,
Taubert Helge
Publication year - 1998
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/(sici)1096-9896(199801)184:1<14::aid-path957>3.0.co;2-k
Subject(s) - biology , immunohistochemistry , cancer research , gene , cyclin d1 , cyclin dependent kinase , single strand conformation polymorphism , tumor suppressor gene , mutation , microbiology and biotechnology , cell cycle , carcinogenesis , genetics , immunology
The p16 INK4A /CDKN2/MTS1 gene encodes a specific inhibitor of cyclin‐dependent kinases (CDKs) 4 and 6. This study investigates p16 INK4A gene status and expression in mesenchymal tumours, in particular soft tissue sarcomas (STSs). Employing non‐radioactive polymerase chain reaction–single strand conformational polymorphism (PCR–SSCP) sequencing, no p16 INK4A mutation was found in 86 samples taken from 74 mesodermal tumours with known p53 gene status. This suggests that p16 INK4A gene alterations, in contrast to p53, are not involved in the progression of STS. This finding is supported by the reports of a low frequency of deletions and intragenic mutations in STS. Furthermore, by immunohistochemistry (IHC), an inverse correlation was established between p16 INK4A and RB positivity for 62 per cent of the frozen tumour samples investigated. However, alterations in other components of the pRb/p16 INK4A /CDK4/cyclin D1/E2F pathway have been proven crucial for tumourigenesis in human sarcomas. © 1998 John Wiley & Sons, Ltd.