TY - JOUR
T1 - Chromosome mechanisms and INI1 inactivation in human and mouse rhabdoid tumors
AU - Rousseau-Merck, Marie Françoise
AU - Fiette, Laurence
AU - Klochendler-Yeivin, Agnès
AU - Delattre, Olivier
AU - Aurias, Alain
N1 - Funding Information:
Supported in part by grants from INSERM, Institut Curie, and La Ligue Nationale Contre le Cancer.
PY - 2005/3
Y1 - 2005/3
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=13844299029&partnerID=8YFLogxK
U2 - 10.1016/j.cancergencyto.2004.06.006
DO - 10.1016/j.cancergencyto.2004.06.006
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C2 - 15721633
AN - SCOPUS:13844299029
SN - 0165-4608
VL - 157
SP - 127
EP - 133
JO - Cancer Genetics and Cytogenetics
JF - Cancer Genetics and Cytogenetics
IS - 2
ER -
