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Analysis of chromosome 10 aberrations in rat endometrial cancer-evidence for a tumor suppressor locus distal to Tp53.

Artikel i vetenskaplig tidskrift
Författare Carola Nordlander
Sandra Karlsson
Åsa Karlsson
Åsa Sjöling
Marta Winnes
Karin Klinga-Levan
Afrouz Behboudi
Publicerad i International journal of cancer. Journal international du cancer
Volym 120
Nummer/häfte 7
Sidor 1472-81
ISSN 0020-7136
Publiceringsår 2007
Publicerad vid Institutionen för cell- och molekylärbiologi
Institutionen för biomedicin, avdelningen för medicinsk genetik och klinisk genetik
Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Sidor 1472-81
Språk en
Länkar dx.doi.org/10.1002/ijc.22533
Ämnesord Adenocarcinoma, genetics, Allelic Imbalance, genetics, Animals, Blotting, Northern, Chromosome Aberrations, Chromosome Painting, Chromosomes, Mammalian, genetics, Endometrial Neoplasms, genetics, Female, Humans, In Situ Hybridization, Fluorescence, Loss of Heterozygosity, Microsatellite Repeats, Rats, Rats, Inbred Strains, Tumor Suppressor Protein p53, genetics
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

We have recently shown in the BDII rat model of human endometrial adenocarcinoma (EAC), rat chromosome 10 (RNO10) is frequently involved in chromosomal aberrations. In the present study, we investigated the association between RNO10 deletions, allelic imbalance (AI) at RNO10q24 and Tp53 mutation in 27 rat EAC tumors. We detected chromosomal breakage accompanied by loss of proximal and/or gain of distal parts of RNO10 in approximately 2/3 of the tumors. This finding is suggestive of a tumor suppressor activity encoded from the proximal RNO10. Given the fact that Tp53 is located at RNO10q24-q25, we then performed Tp53 mutation analysis. However, we could not find a strong correlation between AI/deletions at RNO10q24 and Tp53 mutation. Instead, the observed patterns for AI, chromosomal breaks and deletions suggest that major selection was directed against a region located close to, but distal of Tp53. In different human malignancies a similar situation of AI at chromosome band 17p13.3 (HSA17p13.3) unassociated with TP53 mutation has been observed. Although RNO10 is largely homologous to HSA17, the conservation with respect to gene order among them is not extensive. We utilized publicly available draft DNA sequences to study intrachromosomal rearrangement during the divergence between HSA17 and RNO10. By using reciprocal comparison of rat and human genome data, we could substantially narrow down the candidate tumor suppressor region in rat from 3 Mb to a chromosomal segment of about 0.5 Mb in size. These results provide scientific groundwork for identification of the putative tumor suppressor gene(s) at 17p13.3 in human tumors.

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