Analysis of ovarian borderline tumors using comparative genomic hybridization and fluorescence in situ hybridization

Wolf, Nancy G.; Abdul‐Karim, Fadi W.; Farver, Carol; Schröck, Evelin; Manoir, Stanislas du; Schwartz, Stuart

doi:10.1002/(sici)1098-2264(199908)25:4<307::aid-gcc1>3.0.co;2-1

Cited by 38 publications

(17 citation statements)

References 34 publications

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“…Because chromosomes 3 and 8 have been previously shown to be subject to rearrangement and copy number change (12)(13)(14) and were found to be commonly involved in rearrangements by SKY and/or CGH, we performed a more detailed expression evaluation of cDNA mapping to these chromosomes. We identified a contiguous distribution of reduced expression of seven genes mapping to 3p25.5-3p21.3 interval and increased expression of four genes from 3q13.33-3q28 that were consistent with loss of 3p and gain of 3q in this and other CGH studies of ovarian cancer (17)(18)(19)(20)(21)(22)(23)(24)(25). Within the 3q13.33-3q28 interval, it is noteworthy that there was elevated expression of the calcium-sensing receptor (55) that has been previously shown to induce human ovarian surface epithelial cells to modulate extracellular calcium and induce proliferation.…”

Section: Discussionsupporting

confidence: 81%

“…Previous CGH studies (17)(18)(19)(20)(21)(22)(23)(24) have identified a similar pattern of genomic change, and attempts have been made to correlate these data with clinical endpoints (53). Studies by Yonescu et al (54) and Jenkins et al (11) show that structural and numerical changes predominantly occur on chromosome 11 endometrioid tumors.…”

Section: Discussionmentioning

confidence: 99%

“…To date, CGH has been widely used (17)(18)(19)(20)(21)(22)(23)(24)(25) in studying ovarian carcinomas and has identified increased copy numbers at 1q32, 3q26, 8q24.1-q24.2, 20q13.2-qter and frequent chromosomal losses identified at 5q21, 9q, 17p, 17q12-q21, 4q26-q31, 16q, and 22q. Sites of amplification have been identified at 7q36, 8q24.1-q24.2, 3q26.3, 17q25, 19q13.1-q13.2, and 20q13.2-qter by CGH.…”

Section: Introductionmentioning

confidence: 99%

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Expression Microarrays

2006

Introduction to Genomic Signal Processing With Control

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Analysis of ovarian carcinomas has shown that karyotypes are often highly abnormal and cannot be identified with certainty by conventional cytogenetic methods. In this study, 17 tumors derived from 13 patients were analyzed by a combination of spectral karyotyping (SKY), comparative genomic hybridization (CGH), and expression microarrays. Within the study group, a total of 396 chromosomal rearrangements could be identified by SKY and CGH analysis. When the distribution of aberrations was normalized with respect to relative genomic length, chromo-

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Expression Microarrays

2006

Introduction to Genomic Signal Processing With Control

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“…There are different opinions concerning the histogenesis of serous ovarian tumors, some supporting a progression from SBT to SAC [8,10] and others favoring a dualistic model [5,[11][12][13][14]. We studied this issue using high-resolution DNA ploidy image analysis in different subgroups of SBT and grades of SAC in a large and well-characterized retrospective material.…”

Section: Discussionmentioning

confidence: 99%

Gross genomic alterations differ between serous borderline tumors and serous adenocarcinomas—an image cytometric DNA ploidy analysis of 307 cases with histogenetic implications

et al. 2009

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Our objective was to study the gross genomic alterations in serous borderline tumors and serous adenocarcinomas of the ovary. A retrospective analysis of 245 serous borderline tumors and 62 serous adenocarcinomas from 249 patients was performed using high-resolution image cytometric DNA ploidy analysis. DNA ploidy status, S-phase fraction, and DNA index were evaluated. The majority of serous borderline tumors were diploid (225/245 cases, 92%). The remaining 8% showed an aneuploid peak predominantly with DNA index of less than 1.4. Grades 2 and 3 serous adenocarcinomas were more often (80%) nondiploid, mostly with DNA index exceeding 1.4. Grade 1 serous adenocarcinomas were an intermediate group, more similar to serous borderline tumors. The S-phase fraction increased from serous borderline tumors (mean = 0.6%) through grade 1 serous adenocarcinomas (mean = 2.8%), being highest in grades 2 and 3 adenocarcinomas (mean = 6.8%). Our findings support the hypothesis that serous borderline tumors and grades 2 and 3 serous adenocarcinomas are genomically different lesions, with grade 1 serous adenocarcinomas being an intermediate group more close to borderline tumors.

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“…Summarizing the cytogenetic reports, we found chromosomal abnormalities in 37% (Table 1) [23,30,49,55,62,90,104,124,125,135,140]. Compared to data obtained by DNA cytometry (see Part 1) describing a rate of aneuploidy of around 10%, the above mentioned percentage is surprisingly high.…”

Section: Genetic Alterations Associated With Slmp Tumorsmentioning

confidence: 58%

Serous tumors of low malignant potential of the ovary-molecular pathology: part 2

Hauptmann

Dietel

2001

Virchows Arch

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A progressive development from serous tumors of low malignant potential (SLMP) to bluntly invasive serous carcinoma has been suggested in parallel to the concept of adenoma-carcinoma sequence in colorectal carcinomas. However, recent genetic data enforces a reassessment of the concept that SLMP tumors represent precursor lesions to invasive serous carcinoma. Despite the benign nature of the majority of these tumors, some will behave worse. The identification of those SLMP tumors with an aggressive clinical behavior remains difficult, regardless of a growing body of molecular pathologic investigations. Expression of p53, c-erbB2, as well as the presence of ras mutations are not helpful in this respect. Immunostaining of both MMP-2 and basement membrane components such as collagen type IV, as well as the disintegration of collagen type I at the tumor-host interface, may be helpful for the diagnosis of a microinvasive SLMP, but it remains questionable whether this is important for prognosis. The differential diagnosis to frankly invasive carcinoma depends on the detection of destructive stromal invasion. In questionable cases, the loss of N-cadherin would argue for the presence of a carcinoma whereas the coexpression of p21 and MDM2 is rather characteristic for SLMP tumors.

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Analysis of ovarian borderline tumors using comparative genomic hybridization and fluorescence in situ hybridization

Cited by 38 publications

References 34 publications

Expression Microarrays

Expression Microarrays

Gross genomic alterations differ between serous borderline tumors and serous adenocarcinomas—an image cytometric DNA ploidy analysis of 307 cases with histogenetic implications

Serous tumors of low malignant potential of the ovary-molecular pathology: part 2

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