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© Fabrice Chrétien with Ultrapole, colorized by Jean-Marc Panaud
Cellule souche (en jaune) de muscle squelettique partiellement recouverte par la membrane basale, migrant sur une fibre musculaire (en bleu).
Publication : Cancer genetics and cytogenetics

Chromosome mechanisms and INI1 inactivation in human and mouse rhabdoid tumors

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Cancer genetics and cytogenetics - 01 Mar 2005

Rousseau-Merck MF, Fiette L, Klochendler-Yeivin A, Delattre O, Aurias A

Link to Pubmed [PMID] – 15721633

Cancer Genet. Cytogenet. 2005 Mar;157(2):127-33

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.

http://www.ncbi.nlm.nih.gov/pubmed/15721633