Association of 20q13.2 copy number changes with the advanced stage of ovarian cancer—tissue microarray analysis

Dimova, Ivanka; Yosifova, Aleksandra; Zaharieva, Boriana; Raitcheva, S.; Doganov, N; Toncheva, Draga

doi:10.1016/j.ejogrb.2004.06.007

Cited by 7 publications

(6 citation statements)

References 23 publications

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“…Gains of chromosome 20 have been reported in 20% in GBMs (Mohapatra et al, 1998), although relatively little is known about its contribution to gliomagenesis. It has been suggested that gains in chromosome 20 represent a negative prognostic marker in breast carcinoma (Nakopoulou et al, 2002), but most reports focus on the negative impacts of amplifications in 20q13 in ovarian cancers (Dimova et al, 2005) and sporadic colorectal cancers (Aust et al, 2004), implicating the possible involvement of putative oncogene STK15/Aurora-A.…”

Section: Discussionmentioning

confidence: 99%

Candidate glioblastoma development gene identification using concordance between copy number abnormalities and gene expression level changes

Rossi

LaDuca

et al. 2007

Genes Chromosomes & Cancer

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Copy number abnormalities (CNAs) in tumor cells are presumed to affect expression levels of genes located in region of abnormality. To investigate this relationship we have surveyed the losses, gains and amplifications in 30 glioblastomas using array comparative genome hybridization and compared these data with gene expression changes in the same tumors using the Affymetrix U133Plus2.0 oligonucleotide arrays. The two datasets were overlaid using our in-house overlay tool which highlights concordance between CNAs and expression level changes for the same tumors. In this survey we have highlighted genes frequently overexpressed in amplified regions on chromosomes 1, 4, 11, and 12 and have identified novel amplicons on these chromosomes. Deletions of specific regions on chromosomes 9, 10, 11, 14, and 15 have also been correlated with reduced gene expression in the regions of minimal overlap. In addition we describe a novel approach for comparing gene expression levels between tumors based on the presence or absence of chromosome CNAs. This genome wide screen provides an efficient and comprehensive survey of genes which potentially serve as the drivers for the CNAs in GBM.

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Section: Discussionmentioning

confidence: 99%

Candidate glioblastoma development gene identification using concordance between copy number abnormalities and gene expression level changes

Rossi

LaDuca

et al. 2007

Genes Chromosomes & Cancer

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“…Chromosomal region 20q13 has been identified as one region that is amplified in several tumour types, including breast, ovarian and colon cancers . In addition, amplification of this chromosomal region has been associated with carcinogenesis, metastatic progression and poor clinical prognosis , , .…”

Section: Discussionmentioning

confidence: 99%

“…The involvement of chromosome 20 in human cancers is well documented. In particular, the 20q13 region is frequently amplified in solid tumours and contains several putative oncogenes . The cellular apoptosis susceptibility (chromosome segregation 1‐like, CSE1L ) gene, maps to 20q13 .…”

Section: Introductionmentioning

confidence: 99%

Cellular apoptosis susceptibility (chromosome segregation 1‐like, CSE1L) gene is a key regulator of apoptosis, migration and invasion in colorectal cancer

Alnabulsi

Agouni

Mitra

et al. 2012

The Journal of Pathology

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Cellular apoptosis susceptibility (chromosome segregation 1-like, CSE1L) gene maps to chromosomal region 20q13.13, a region frequently amplified in solid tumours. In this study, we investigated the roles played by CSE1L in colorectal cancer by examining CSE1L expression and clinico-pathological parameters in colorectal cancer and investigating the effect of CSE1L on the viability, adhesion and migration of colorectal cancer cells. RT-PCR showed that CSE1L mRNA was over-expressed in colorectal cancer. CSE1L depletion by knock-down with CSE1L-specific siRNA significantly reduced viability in HCT116 cells (p = 0.004) and SW480 cells (p = 0.003) whilst significantly increasing the proportion of apoptotic HCT116 cells (p < 0.001) and SW480 cells (p < 0.001). Furthermore, CSE1L depletion significantly reduced the adhesive capacity of HCT116 (p = 0.003) and SW480 cells (p = 0.004). Analysis by qRT-PCR following CSE1L siRNA treatment of HCT116 and SW480 cells showed significant modulation of key apoptotic (p53, p73 and BAK) and adhesive (E-cadherin, Ep-CAM and ICAM-1) molecules. Immunohistochemistry of a colorectal cancer tissue microarray showed that CSE1L had a significantly increased level in colorectal cancer compared to normal colorectal epithelium (p < 0.001). There were significant decreases in both nuclear (p = 0.006) and cytoplasmic (p = 0.003) staining of CSE1L in tumours with lymph node metastasis (stage 3 tumours) compared with lymph node-negative tumours (stage 1 and 2 tumours). In lymph node-negative patients, poor survival was associated with increased CSE1L cytoplasmic expression (p = 0.042). These results indicate that CSE1L is associated with viability and apoptosis, cellular adhesion and invasion, thus implicating CSE1L in the progression of colorectal cancer.

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“…In vitro studies have shown that 20q gain plays an important role in tumor cell proliferation, apoptosis, immortalization, and acquisition of drug resistance [6,7]. Moreover, regional 20q gain has been associated with advanced tumor stage [8,9], distant metastasis [10][11][12][13][14], and poor patient survival [15][16][17][18][19][20][21][22], with conflicted results for colorectal and esophageal cancer [23,24]. In HCC, gain of 20q as one of the most common CNAs [25][26][27] has been detected more frequently in advanced stages and in larger tumors [28], but its prognostic significance and target genes thereof are still unexplored.…”

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confidence: 98%

Multiple genes identified as targets for 20q13.12–13.33 gain contributing to unfavorable clinical outcomes in patients with hepatocellular carcinoma

et al. 2015

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Association of 20q13.2 copy number changes with the advanced stage of ovarian cancer—tissue microarray analysis

Cited by 7 publications

References 23 publications

Candidate glioblastoma development gene identification using concordance between copy number abnormalities and gene expression level changes

Candidate glioblastoma development gene identification using concordance between copy number abnormalities and gene expression level changes

Cellular apoptosis susceptibility (chromosome segregation 1‐like, CSE1L) gene is a key regulator of apoptosis, migration and invasion in colorectal cancer

Multiple genes identified as targets for 20q13.12–13.33 gain contributing to unfavorable clinical outcomes in patients with hepatocellular carcinoma

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