Comparative genomic hybridization detects frequent overrepresentation of chromosomal material from 3q26, 8q24, and 20q13 in human ovarian carcinomas

Sonoda, Gonosuke; Palazzo, Juan; Manoir, Stanislas du; Godwin, Andrew K.; Feder, Madelyn; Yakushiji, M; Testa, Joseph R.

doi:10.1002/(sici)1098-2264(199712)20:4<320::aid-gcc2>3.0.co;2-3

Cited by 171 publications

(52 citation statements)

References 28 publications

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“…Comparative genomic hybridization (CGH) studies have also demonstrated differences between low-and high-grade serous carcinomas in that high-grade serous carcinomas showed significantly higher CNA frequencies than low-grade tumors. [79][80][81] Differences between low-and highgrade tumors were also demonstrated genetically. High-grade carcinomas showed under-representation of 11p and 13q, and over-representation of 8q and 7p, while 12p under-representation and 18p over-representation were present significantly more frequently in well and moderately differentiated tumors.…”

Section: Molecular Genetic Datamentioning

confidence: 99%

Origins and molecular pathology of ovarian cancer

2005

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Epithelial ovarian cancer comprises the majority of malignant ovarian tumors in adult women. These neoplasms are classified into distinct morphologic categories based on the appearance of the epithelium into tumors of serous, mucinous, endometrioid, clear cell, transitional, squamous, mixed and undifferentiated type. Current data indicate that each of these histologic subtypes is associated with distinct morphologic and molecular genetic alterations: high-grade serous and possibly endometrioid carcinomas most probably arise from surface epithelial inclusion glands with TP53 mutations and dysfunction of BRCA1 and/or BRCA2; low-grade serous carcinomas probably arise in a stepwise fashion in an adenoma-borderline tumor-carcinoma sequence from typical to micropapillary borderline tumors to low-grade invasive serous carcinoma via activation of the RAS-RAF signaling pathway secondary to mutations in KRAS and BRAF; mucinous carcinomas arise via an adenoma-borderline tumor-carcinoma sequence with mutations in KRAS; low-grade endometrioid carcinomas arise from endometriosis via mutations in CTNNB1 (the gene encoding b-catenin) and PTEN. Although the morphologic data strongly support an origin of clear cell carcinoma from endometriosis, there is limited data on the genetic alterations in these uncommon tumors. Thus it is likely that most low-grade, relatively indolent ovarian carcinomas of serous, mucinous and endometrioid type arise from pre-existing cystadenomas or endometriosis whereas most high-grade serous carcinomas arise without an easily identifiable precursor lesion. Modern Pathology (2005) 18, S19-S32. doi:10.1038/modpathol.3800306Keywords: ovarian cancer; ovarian borderline tumors; histogenesis; molecular pathology Epithelial ovarian cancer comprises the majority of malignant ovarian tumors in adult women. These neoplasms are classified into distinct morphologic categories based on the appearance of the epithelium into tumors of serous, mucinous, endometrioid, clear cell, transitional, squamous, mixed and undifferentiated type. 1,2 Two types of ovarian surface epithelial lesions have been described as possible precursors of these carcinomas: lesions that appear in situ in surface epithelium or surface epithelial inclusion glands (SEIG); and preexisting benign epithelial ovarian tumors and endometriosis. The morphologic and genetic data implicating each as a precursor lesion of the major histologic subtypes of ovarian carcinoma are discussed. Surface epithelium and surface epithelial inclusion glands as precursor lesions Morphologic DataTwo types of morphologic data are available regarding the malignant potential of ovarian surface epithelium and inclusion glands, alterations in these structures and studies on microscopic ovarian carcinoma.Surface epithelium and surface epithelial inclusion glands Despite the widespread acceptance of the origin of surface epithelial cancers from the ovarian surface epithelium and its inclusion glands, only rarely have putative precursor lesions been described at these sites. Two...

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Section: Molecular Genetic Datamentioning

confidence: 99%

Origins and molecular pathology of ovarian cancer

2005

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“…Evi1 activation has been implicated in hematopoietic malignancies in humans (Bartholomew and Ihle, 1991;Ogawa et al, 1996), and the oncogenic role of Evi1 has been studied extensively in myeloid and lymphoid leukemia. Evi1 is located on human chromosome 3q26, and the 3q25-27 region is amplified in cancer of the cervix (Sugita et al, 2000), ovary (Sonoda et al, 1997), lung (Brass et al, 1996;Racz et al, 1999;Imoto et al, 2001), head and neck (Bergamo et al, 2000), and prostate (Sattler et al, 2000). The relationship between 3q26 amplification and Evi1 expression has not been systematically studied, although it is known that Evi1 is overexpressed in some ovarian cancers (Brooks et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Evi1 is a survival factor which conveys resistance to both TGFβ- and taxol-mediated cell death via PI3K/AKT

Liu

Chen

et al. 2006

Oncogene

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“…This gene belongs to the family of cell adhesion molecules of which E-cadherin is a well-recognised tumour suppressor gene in gastric cancer (Becker et al, 1994). Copy number increases of chromosome 3q in ovarian carcinomas have previously been reported (Arnold et al, 1996;Sonoda et al, 1997) Figure 2 Chromosome 9 LOH marker results with chromosome 9 ideogram. Loss of heterozygosity was performed on a total of 27 cases.…”

Section: Discussionmentioning

confidence: 84%

“…Furthermore, upregulation of this gene has been seen in 36% of malignant, mostly serous, high-grade ovarian carcinomas (Sonoda et al, 1997). PIK3CA encodes a subunit of a phosphatidylinositol 3-kinase involved in kinase-mediated cell signalling (Rodriguez-Viciana et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…Comparative genomic hybridisation analysis has revealed numerous cytogenetic changes in epithelial ovarian cancers (Sonoda et al, 1997) with common sites of amplification, in order of frequency, at 8q, 20q, 3q, 1q, 20p, 9p and 12p along with deletions at 5q, 9q, 17p, 4q, 16q and 22q. Comparative genomic hybridisation has detected aberrations that correlate with ovarian tumour grade including deletions at chromosome 11p and 13q, and amplifications at 8q and 7p in poorly differentiated tumours as compared with 12p deletions and 18p amplifications in well-and moderately differentiated tumours (Kiechle et al, 2001).…”

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Cytogenetic alterations in ovarian clear cell carcinoma detected by comparative genomic hybridisation

et al. 2003

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Ovarian clear cell carcinoma (OCCC) accounts for a small but significant proportion of all ovarian cancers and is a distinct clinical and pathological entity. It tends to be associated with poorer response rates to chemotherapy and with a worse prognosis. Little is known about possible underlying genetic changes. DNA extracted from paraffin-embedded samples of 18 pure OCCC cases was analysed for genetic imbalances using comparative genomic hybridisation (CGH). All of the 18 cases showed genomic alterations. The mean number of alterations detected by CGH was 6 (range 1 -15) indicating a moderate level of genetic instability. Chromosome deletions were more common than amplifications. The most prominent change involved chromosome 9 deletions in 10 cases (55%). This correlates with changes seen in other epithelial ovarian cancers. This deletion was confirmed using microsatellite markers to assess loss of heterozygosity (LOH) at four separate loci on chromosome 9. The most distinct region of loss detected was around the IFNA marker at 9p21 with 41% (11 out of 27cases) LOH. Other frequent deletions involved 1p (five out of 18; 28%); 11q (four out of 18; 22%) and 16 (five out of 18; 28%). Amplification was most common at chromosome 3 (six out of 18; 33%); 13q (four out of 18; 22%) and 15 (three out of 18; 17%). No high-level amplifications were identified. These features may serve as useful prognostic indicators in the management of OCCC.

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Comparative genomic hybridization detects frequent overrepresentation of chromosomal material from 3q26, 8q24, and 20q13 in human ovarian carcinomas

Cited by 171 publications

References 28 publications

Origins and molecular pathology of ovarian cancer

Origins and molecular pathology of ovarian cancer

Evi1 is a survival factor which conveys resistance to both TGFβ- and taxol-mediated cell death via PI3K/AKT

Cytogenetic alterations in ovarian clear cell carcinoma detected by comparative genomic hybridisation

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