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Are there any more ovarian tumor suppressor genes? A new perspective using ultra high-resolution copy number and loss of heterozygosity analysis
Genes chromosomes & cancer, 2009-10, Vol.48 (10), p.931-942
Gorringe, Kylie L.
Ramakrishna, Manasa
Williams, Louise H.
Sridhar, Anita
Boyle, Samantha E.
Bearfoot, Jennifer L.
Li, Jason
Anglesio, Michael S.
Campbell, Ian G.
2009
Details
Autor(en) / Beteiligte
Gorringe, Kylie L.
Ramakrishna, Manasa
Williams, Louise H.
Sridhar, Anita
Boyle, Samantha E.
Bearfoot, Jennifer L.
Li, Jason
Anglesio, Michael S.
Campbell, Ian G.
Titel
Are there any more ovarian tumor suppressor genes? A new perspective using ultra high-resolution copy number and loss of heterozygosity analysis
Ist Teil von
Genes chromosomes & cancer, 2009-10, Vol.48 (10), p.931-942
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2009
Link zum Volltext
Quelle
Wiley Online Library - AutoHoldings Journals
Beschreibungen/Notizen
Ovarian cancer is characterized by complex genetic alterations, including copy number loss and copy number‐neutral loss of heterozygosity (LOH). These alterations are assumed to represent the “second hit” of the underlying tumor suppressor gene (TSG), however, relative to the number of LOH hotspots reported, few ovarian TSGs have been identified. We conducted a high‐resolution LOH analysis using SNP arrays (500K and SNP6.0) of 106 primary ovarian tumors of various histological subtypes together with matching normal DNA. LOH was detected in at least 35% of samples on chromosomes 17, 19p, 22q, Xp, 13q, 8p, 6q, 4q, 5q, 1p, 16q, and 9q with a median minimal region of overlap of only 300 kb. Subtype‐specific differences in LOH frequency were noted, particularly for mucinous cases. We also identified 192 somatic homozygous deletions (HDs). Recurrent HDs targeted known TSGs such as CDKN2A (eight samples), RB1 (five samples), and PTEN (three samples). Additional recurrent HDs targeted 16 candidate TSGs near minimal regions of LOH on chromosomes 17, 13, 8p, 5q, and X. Given the importance of HDs in inactivating known genes, these candidates are highly likely to be ovarian TSGs. Our data suggest that the poor success of previous LOH studies was due to the inability of previous technology to resolve complex genomic alterations and distinguish true LOH from allelic imbalance. This study shows that recurrent regions of LOH and HD frequently align with known TSGs suggesting that LOH analysis remains a valid approach to discovering new candidates. © 2009 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 1045-2257
eISSN: 1098-2264
DOI: 10.1002/gcc.20694
Titel-ID: cdi_proquest_miscellaneous_744622139
Format
–
Schlagworte
Chromosomes, Human, Pair 15
,
Chromosomes, Human, Pair 8
,
Computational Biology - methods
,
Female
,
Gene Deletion
,
Gene Dosage
,
Gene Expression Profiling
,
Genes, Tumor Suppressor
,
Humans
,
Loss of Heterozygosity
,
Oligonucleotide Array Sequence Analysis
,
Ovarian Neoplasms - classification
,
Ovarian Neoplasms - genetics
,
Polymorphism, Single Nucleotide
,
Statistics, Nonparametric
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