Cytogenetic and molecular genetic characterization of immortalized human ovarian surface epithelial cell lines: consistent loss of chromosome 13 and amplification of chromosome 20

Jin, Yuesheng; Zhang, Hao; Tsao, Sai Wah; Jin, Charlotte; Lv, Mei; Strömbeck, Bodil; Wiegant, J.; Wan, T. S. K.; Yuen, Po Wing; Kwong, Yok–Lam

doi:10.1016/j.ygyno.2003.09.007

Cited by 24 publications

(22 citation statements)

References 23 publications

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“…Several recurring deviations are apparent. These include previously described cell line-specific gains of 20q12-13.33 and losses of 13q22 (13,14) as well as newly identified cell line-specific gains of 5q35.1-35.3 and losses of 18q12.2-23. A homozygous loss of the tumor suppressor locus CDKN2A and amplification of the MYC oncogene seem to be more frequent in cell lines in several histologies, indicating that the dysregulation of these genes may be acquired as part of cell immortalization or their occurrence is selected when tumors are chosen for transformation.…”

Section: Discussionmentioning

confidence: 92%

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Cancer Cell Lines as Genetic Models of Their Parent Histology: Analyses Based on Array Comparative Genomic Hybridization

et al. 2007

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Tumor-derived cell lines are used as in vitro cancer models, but their ability to accurately reflect the phenotype and genotype of the parental histology remains questionable, given the prevalence of documented cell line-specific cytogenetic changes. We have addressed the issue of whether copy number alterations seen in tumor-derived cell lines reflect those observed in studies of fresh tissue by carrying out a meta-analysis of array-based comparative genomic hybridization data that considers both copy number alteration frequencies and the occurrence of cancer gene amplifications and homozygous deletions. Pairwise correlation comparisons between the data sets of seven diagnosisspecific matched tumor and cell line groups indicate that the trends in aberration frequencies are highly correlated between tumors and cell line sets of matched cancer histology relative to unmatched pairings. Despite their similarities, cell lines showed uniformly higher locus-specific alteration frequencies (P = 0.004) and several recurring cell linespecific alterations emerged. These include the previously documented losses of 13q and 9p and gains of 20q, as well as additional undescribed cell line-specific gains of 5p, 7p, and 17q and losses of 18q and 4q. These results indicate that, on average, cell lines preserve in vitro the genetic aberrations that are unique to the parent histology from which they were derived while acquiring additional locus-specific alterations. These data may enable a more predictive understanding of individual cell lines as in vitro models of cancer biology and therapy. [Cancer Res 2007;67(8):3594-600]

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Section: Discussionmentioning

confidence: 92%

“…This is likely a result of a number of factors. Most notably, the cell line immortalization process has been implicated as a source of cytogenetic changes (13,14). In addition, multiple growth passages, to which commercially available cell lines are routinely subjected, have been shown to be associated with random genomic instability (15).…”

Section: Introductionmentioning

confidence: 99%

Cancer Cell Lines as Genetic Models of Their Parent Histology: Analyses Based on Array Comparative Genomic Hybridization

et al. 2007

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“…This is one of the first reports on the cytotoxicity of autologous CIK cells against fresh cancer cells harvested from ovarian cancer patients. Although established cell lines can provide useful information to study ovarian cancer, cell lines undergo many manipulations during their development and propagation that may result in changes that no longer accurately represent the original tumor (16). Thus, results obtained from primary tumor cultures rather than established cell lines may be more readily translated into the clinical setting.…”

Section: Discussionmentioning

confidence: 99%

“…Although established cell lines can provide useful information to study ovarian cancer, these cells typically undergo many manipulations during their development and propagation that can result in nonrandom genomic aberrations (16). Given that cell lines may not accurately represent the original tumors, we performed experiments using fresh ovarian cancer cells and believe that these results may be more readily translated into the clinical setting.…”

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confidence: 99%

Enhanced Killing of Primary Ovarian Cancer by Retargeting Autologous Cytokine-Induced Killer Cells with Bispecific Antibodies: A Preclinical Study

Chan¹,

Hamilton²,

Cheung³

et al. 2006

Clinical Cancer Research

112

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Cr release assay of fresh ovarian cancer cells exposed to autologous CIK cells increased from 21.7 F 0.3% to 89.4 F 2.1% at an E:Tratio of100:1 (P < 0.001). Anti-NKG2D antibodies attenuated the CIK activity by 56.8% on primary cells (P < 0.001). In a xenograft severe combined immunodeficient mouse model, real-time tumor regression and progression was visualized using a noninvasive in vivo bioluminescence imaging system. Four hours after CIK cell injection, we were able to visualize CD8 + NKG2D + CIK cells infiltrating Her2-expressing cancer cells on fluorescence microscopy. Mice that underwent adoptive transfer of CIK cells redirected with BSAbxCA125 and BSAbxHer2 had significant reduction in tumor burden (P < 0.001and P < 0.001) and improvement in survival (P = 0.05 and P = 0.006) versus those treated with CIK cells alone. Bispecific antibodies significantly enhanced the cytotoxicity of CIK cells in primary ovarian cancer cells and in our in vivo mouse model. The mechanism of cytolysis seems to be mediated in part by the NKG2D receptor.

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“…AIB1 is located on chromosome 20q, a region commonly amplified in ovarian cancers (21)(22)(23). In a cohort of 24 sporadic malignant ovarian tumors, amplification of the 20q12 region (containing AIB1) was identified in 25%, and correlated with poor survival (6).…”

Section: Discussionmentioning

confidence: 99%

AIB1 Polymorphisms Predict Aggressive Ovarian Cancer Phenotype

Lerner

Gapuzan

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Purpose: The androgen receptor (AR) harbors a polymorphic CAG repeat sequence in exon 1, coding for a polyglutamine tract whose length inversely correlates with AR transactivation function. AIB1, an AR coactivator, expresses a similar polymorphic glutamine sequence within the carboxyl-terminal coding region. We hypothesized that genotypic variations in the androgen-signaling pathway promote aggressive epithelial ovarian cancer biology, and sought to examine the effect of AIB1 genotype on clinical outcome. Experimental Design: Genotype analysis of the AIB1 CAG repeat region was done on 89 patients with epithelial ovarian cancer. Medical records were reviewed for clinicopathologic factors and survival. Data were examined using the C 2 test and Kaplan-Meier survival and Cox regression analyses.Results: We identified four AIB1 genotypes, with glutamine codon lengths of 26, 28, 29, and 30. Patients with a short AIB1 genotype (with V28 CAG repeats) showed statistically shorter time to disease recurrence compared to those with a long genotype (z29 CAG repeats; 15.0 versus 30.0 months; P = 0.01). Patients with short AIB1 also showed decreased overall survival (57.0 months) compared to those with a long genotype (median survival not yet reached; P = 0.02). When controlling for established prognostic factors, multivariate analysis identified the presence of a short AIB1 genotype as an independent poor prognostic factor for overall survival (P = 0.05).

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Cytogenetic and molecular genetic characterization of immortalized human ovarian surface epithelial cell lines: consistent loss of chromosome 13 and amplification of chromosome 20

Cited by 24 publications

References 23 publications

Cancer Cell Lines as Genetic Models of Their Parent Histology: Analyses Based on Array Comparative Genomic Hybridization

Cancer Cell Lines as Genetic Models of Their Parent Histology: Analyses Based on Array Comparative Genomic Hybridization

Enhanced Killing of Primary Ovarian Cancer by Retargeting Autologous Cytokine-Induced Killer Cells with Bispecific Antibodies: A Preclinical Study

AIB1 Polymorphisms Predict Aggressive Ovarian Cancer Phenotype

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