Loss of heterozygosity at the FHIT gene in different solid human tumours and its association with survival in colorectal cancer patients.

2.50
Hdl Handle:
http://hdl.handle.net/2336/31293
Title:
Loss of heterozygosity at the FHIT gene in different solid human tumours and its association with survival in colorectal cancer patients.
Authors:
Petursdottir, Thorgunnur Eyfjord; Hafsteinsdottir, Sigridur H; Jonasson, Jon G; Moller, Pall H; Thorsteinsdottir, Unnur; Huiping, Chen; Egilsson, Valgardur; Ingvarsson, Sigurdur
Citation:
Anticancer Res. 2002, 22(6A):3205-12
Issue Date:
1-Nov-2002
Abstract:
BACKGROUND: Genomic alterations and abnormal expression of the FHIT gene have been reported for a number of cancers. FHIT encompasses FRA3B, the most common fragile site in the human genome, and is suggested to be a candidate tumour suppressor gene. MATERIALS AND METHODS: We analysed and compared the loss of heterozygosity (LOH) pattern in 397 solid human tumours from 9 different locations, using four polymorphic microsatellite markers within the gene (D3S1234, D3S1300, D3S2757 and D3S4260), and two markers (D3S1313 and D3S1600) flanking the gene. In addition, we tested whether there was an association between FHIT LOH and overall patient survival in colorectal cancer. RESULTS: LOH at the FHIT gene affecting at least one of the investigated markers was detected in 166 out of 332 informative tumours, or 50%. The highest detected LOH was in lung tumours (66%) while the lowest was in thyroid and endometrium tumours, (30% and 31%, respectively). Breakpoints were found inside the gene in all tumour types in 12-80% of the tumours with FHIT LOH depending on tumour type, and up to 41% could additionally be located adjacent to the 3' or 5' end of the FHIT gene. Thus we were able to locate breakpoints within or in the vicinity of the FHIT gene in 25-100% of different tumours with LOH. Although not statistically significant, we observed a trend towards a poorer survival of patients with FHIT LOH versus those with retention of heterozygosity. CONCLUSION: Based on our results, LOH of the FHIT gene is a common event in all tumour types analysed with a possible association with poorer survival in colorectal cancer patients. LOH at all markers analysed was, in most of the tumour types, a more common pattern of alterations than breakpoints.

Full metadata record

DC FieldValue Language
dc.contributor.authorPetursdottir, Thorgunnur Eyfjord-
dc.contributor.authorHafsteinsdottir, Sigridur H-
dc.contributor.authorJonasson, Jon G-
dc.contributor.authorMoller, Pall H-
dc.contributor.authorThorsteinsdottir, Unnur-
dc.contributor.authorHuiping, Chen-
dc.contributor.authorEgilsson, Valgardur-
dc.contributor.authorIngvarsson, Sigurdur-
dc.date.accessioned2008-07-08T13:36:24Z-
dc.date.available2008-07-08T13:36:24Z-
dc.date.issued2002-11-01-
dc.date.submitted2008-07-08-
dc.identifier.citationAnticancer Res. 2002, 22(6A):3205-12en
dc.identifier.issn0250-7005-
dc.identifier.pmid12530066-
dc.identifier.urihttp://hdl.handle.net/2336/31293-
dc.description.abstractBACKGROUND: Genomic alterations and abnormal expression of the FHIT gene have been reported for a number of cancers. FHIT encompasses FRA3B, the most common fragile site in the human genome, and is suggested to be a candidate tumour suppressor gene. MATERIALS AND METHODS: We analysed and compared the loss of heterozygosity (LOH) pattern in 397 solid human tumours from 9 different locations, using four polymorphic microsatellite markers within the gene (D3S1234, D3S1300, D3S2757 and D3S4260), and two markers (D3S1313 and D3S1600) flanking the gene. In addition, we tested whether there was an association between FHIT LOH and overall patient survival in colorectal cancer. RESULTS: LOH at the FHIT gene affecting at least one of the investigated markers was detected in 166 out of 332 informative tumours, or 50%. The highest detected LOH was in lung tumours (66%) while the lowest was in thyroid and endometrium tumours, (30% and 31%, respectively). Breakpoints were found inside the gene in all tumour types in 12-80% of the tumours with FHIT LOH depending on tumour type, and up to 41% could additionally be located adjacent to the 3' or 5' end of the FHIT gene. Thus we were able to locate breakpoints within or in the vicinity of the FHIT gene in 25-100% of different tumours with LOH. Although not statistically significant, we observed a trend towards a poorer survival of patients with FHIT LOH versus those with retention of heterozygosity. CONCLUSION: Based on our results, LOH of the FHIT gene is a common event in all tumour types analysed with a possible association with poorer survival in colorectal cancer patients. LOH at all markers analysed was, in most of the tumour types, a more common pattern of alterations than breakpoints.en
dc.language.isoenen
dc.publisherJ.G. Delinassios, Anticancer Researchen
dc.subject.meshAcid Anhydride Hydrolasesen
dc.subject.meshColorectal Neoplasmsen
dc.subject.meshFemaleen
dc.subject.meshGenetic Markersen
dc.subject.meshHumansen
dc.subject.meshLoss of Heterozygosityen
dc.subject.meshMaleen
dc.subject.meshNeoplasm Proteinsen
dc.subject.meshNeoplasmsen
dc.subject.meshSurvival Rateen
dc.titleLoss of heterozygosity at the FHIT gene in different solid human tumours and its association with survival in colorectal cancer patients.en
dc.typeArticleen
dc.contributor.departmentDepartment of Pathology, National University Hospital, P.O. Box 1465, IS-121 Reykjavik, Iceland.en
dc.identifier.journalAnticancer researchen

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