Chromosome mechanisms and INI1 inactivation in human and mouse rhabdoid tumors

Marie Françoise Rousseau-Merck*, Laurence Fiette, Agnès Klochendler-Yeivin, Olivier Delattre, Alain Aurias

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

The human rhabdoid tumorigenesis orchestrated by INI1 inactivation is associated with specific rearrangements of chromosome 22 that correlate with preferential anatomic tumor locations. A literature review revealed significant correlations between an apparently normal karyotype and kidney tumors, monosomy 22 and cerebral tumors, and chromosome 22 translocations and tumors at other anatomic sites. In the mouse rhabdoid tumor model, specifically in the four tumors that we tested for loss of heterozygosity, neither partial deletion nor monosomy of chromosome 10 could be detected. In contrast to the human data, the only chromosome mechanism involved in the 18 mouse tumors studied appears to be a mitotic recombination or a nondisjunction-duplication. Additionally, and despite mouse tumor incidence across a variety of sites, no rhabdoid tumor could be observed in the mouse kidney. These data suggest that the chromosome mechanisms for INI1 inactivation and the selective cell survival pressure differ in human and mouse.

Original languageAmerican English
Pages (from-to)127-133
Number of pages7
JournalCancer Genetics and Cytogenetics
Volume157
Issue number2
DOIs
StatePublished - Mar 2005

Bibliographical note

Funding Information:
Supported in part by grants from INSERM, Institut Curie, and La Ligue Nationale Contre le Cancer.

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