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Numerous observations suggest that chromosome instability is caused by mitotic abnormalities such as errors in the partitioning of chromosomes. Chfr was recently defined as a central

component of a new mitotic checkpoint that delays chromosome condensation in response to mitotic stress. Chfr was shown to be frequently inactivated in several human neoplasms, including

colon, lung and esophageal cancers. To test whether Chfr inactivation may lead or participate to chromosomal instability (CIN), we analysed the genetic and epigenetic status of the gene in a

large panel of primary colon and breast cancers, as well as in colon and breast cancer cell lines displaying either a microsatellite instability or a CIN. Our results confirm that Chfr is

frequently inactivated in colon cancers, through a mechanism of hypermethylation of the promoter sequences. In contrast, the loss of Chfr expression appears to be a rare event in breast

cancers. Furthermore, our data demonstrate that Chfr inactivation is not associated with CIN in these frequent types of human cancers.

We thank T Halazonetis for Chfr constructs. This work was supported by grants from the Comité Départemental du Rhône and the Comité Départemental de l'Ain de la Ligue de Lutte contre le

Cancer, and from the Association pour la Recherche sur le Cancer.

Unité d'Oncologie Moléculaire, INSERM U590, Centre Léon Bérard, 28 rue Laënnec, Lyon, Cedex 08, 69373, France

Jacques Bertholon, Qing Wang, Nicole Falette, Carole Verny, Jessie Auclair, Christelle Chassot, Claudine Navarro & Alain Puisieux

Faculté de Pharmacie, 8 avenue Rockefeller, Lyon, Cedex 08, 69373, France

Fédération de Spécialités Digestives, Hôpital Edouard Herriot, Place d'Arsonval, Lyon, Cedex 03, 69437, France

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