Frequent loss of 9p21 (p16(INK4A)) and other genomic imbalances in human malignant fibrous histiocytoma

Annet Simons, Marga Schepens, Judith Jeuken, Sandra Sprenger, Guillaume Van De Zande, Bodil Bjerkehagen, Anne Forus, Vines Weibolt, Ineke Molenaar, Eva Van Den Berg, Ola Myklebost, Julia Bridge, Ad Geurts Van Kessel, Ron Suijkerbuijk

Research output: Contribution to journalArticlepeer-review

63 Scopus citations


To search for new recurrent genetic aberrations in malignant fibrous histiocytoma (MFH), a combination of conventional cytogenetic, comparative genomic hybridization (CGH), and Southern blot analyses was applied to a series of 34 tumors. Cytogenetic analysis revealed the presence of multiple structural and numerical aberrations, including marker chromosomes, telomeric associations, double minutes, and ring chromosomes. The most frequent genomic imbalances in this series of neoplasms as detected by CGH were gains of 1q21-q22 (69%), 17q23-qter (41%), and 20q (66%), and losses of 9p21-pter (55%), 10q (48%), 11q23-qter (55%), and 13q10-q31 (55%). Southern blot analyses with p16(INK4A) (CDKN2A; 9p21) and RB1 (13q14) probes provided clear indications for frequent deletions of these tumor suppressor genes, and as such, substantiated the CGH results. Additionally, examination of the TP53 and MDM2 genes showed frequent loss and amplification, respectively. These data indicate that genes involved in the RB1- and TP53-associated cell cycle regulatory pathways may play prominent roles in the development of human MFH. Copyright (C) 2000 Elsevier Science Inc.

Original languageEnglish (US)
Pages (from-to)89-98
Number of pages10
JournalCancer genetics and cytogenetics
Issue number2
StatePublished - Apr 15 2000

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


Dive into the research topics of 'Frequent loss of 9p21 (p16(INK4A)) and other genomic imbalances in human malignant fibrous histiocytoma'. Together they form a unique fingerprint.

Cite this