Patterns of expression of chromosome 17 genes in primary cultures of normal ovarian surface epithelia and epithelial ovarian cancer cell lines

Presneau, Nadège; Mes-Masson, Anne-Marie; Ge, Bing; Provencher, Diane; Hudson, Thomas J.; Tonin, Patricia N.

doi:10.1038/sj.onc.1206219

Cited by 26 publications

(53 citation statements)

References 35 publications

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“…Cytogenetic changes in ovarian cancer are similar to those observed in breast cancer and affect genes located on chromosome 17, in particular those located on 17q12-21 [62]. Recently, oligonucleotide microarray analyses of ovarian cancer cell lines were used to specifically identify genetic changes of chromosome 17 genes [63]. Future data mining of such in vitro gene expression array data may provide further insight into the role of PKC-α in tumorigenesis of ovarian cancer.…”

Section: Epidemiological and Genetic Considerations For Developing Inmentioning

confidence: 99%

Protein Kinase C Alpha Expression in Breast and Ovarian Cancer

Lahn¹,

Köhler

Sundell³

et al. 2004

Oncology

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In recent years research has focused on the development of specific, targeted drugs to treat cancer. One approach has been to block intracellular signaling proteins, such as protein kinase C alpha (PKC-α). To help support the rationale for clinical studies of a PKC-α-targeted therapy in breast and ovarian cancers, we reviewed publications studying PKC-α expression in these tumors. Since these investigations were mostly performed in cell lines, we supplemented this review with some preliminary findings from studies examining PKC-α expression in tumor tissue biopsies obtained from patients with breast and ovarian cancer. Based on the reviewed publications using representative cell lines and our preliminary findings on tumor tissue of patients with breast cancer, we infer that PKC-α levels may especially be increased in breast cancer patients with low or negative estrogen receptor (ER) levels. Thus, clinical studies determining efficacy of selective or specific inhibitors of PKC-α should include determination of ER status in order to help answer whether blocking PKC-α in patients with low or absent ER can result in clinical benefit.

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Section: Epidemiological and Genetic Considerations For Developing Inmentioning

confidence: 99%

Protein Kinase C Alpha Expression in Breast and Ovarian Cancer

Lahn¹,

Köhler

Sundell³

et al. 2004

Oncology

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show abstract

“…DNA was extracted from clinical specimens, peripheral blood lymphocytes, and EOC cell lines, as described previously (31,33). Total RNA was extracted with TRIzol™ reagent (Gibco/BRL, Life Technologies Inc., Grand Island, NY) from the primary cultures of NOSE samples, and the EOC cell lines, grown to 80% confluency in 100 mm Petri dishes, and from frozen ovarian tumour samples as described previously (31,38). RNA quality was assessed by gel electrophoresis and 2100 Bioanalyzer analysis using the Agilent RNA 6000 Nano kit.…”

Section: Eoc Cell Linesmentioning

confidence: 99%

Chromosome 17q25 genes, RHBDF2 and CYGB, in ovarian cancer

et al. 2012

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Abstract. It has been proposed that the frequent loss of heterozygosity (LOH) of an entire chromosome 17 contig in epithelial ovarian cancers (EOC) is the consequence of the inactivation of multiple tumour suppressor genes on this chromosome. We report the characterization of a 453 Kb 17q25 locus shown previously to exhibit a high frequency of LOH in EOC samples. LOH analysis further defined the minimal region of deletion to a 65 Kb interval flanked by D17S2239 and D17S2244, which contains RHBDF2, CYGB and PRCD as tumour suppressor gene candidates. Tissue specific expression excluded PRCD as a candidate. RHBDF2 was expressed at low levels in the majority of benign and low malignant potential (LMP) tumours, and in a subset of malignant ovarian tumour samples, as compared with primary cultures of normal ovarian surface epithelial cell (NOSE) samples. CYGB was expressed at low levels in the majority of LMP and malignant samples compared with benign and NOSE samples. In contrast to CYGB expression, RHBDF2 was expressed at low or undetectable levels in EOC cell lines exhibiting tumourigenic characteristics and up-regulated in a genetically modified EOC cell line rendered non-tumourigenic. DNA sequence analysis identified variants but no apparent deleterious mutations in either gene. Methylation-specific PCR analysis suggested that promoter methylation of CYGB but not RHBDF2 occurred in 6 of 31 malignant samples. The results combined suggest that RHBDF2 and CYGB may play distinctive roles in ovarian cancer and could be added to the growing roster of chromosome 17 genes implicated in this disease.

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“…Detailed protocols are available at www.genomequebec.mcgill.ca. Gene expression levels were calculated for each probe set from the scanned image by Affymetrix s GeneChip (MAS5) and prepared as previously described (Novak et al, 2002;Presneau et al, 2003). As reproducibility of expression values is highly variable at low values of expression (Arcand et al, 2004), all normalized values below five were reassigned a threshold value of five based on the mean expression value of the lowest reliability scores (A calls).…”

Section: Microarray Analysis Of Expression Profilesmentioning

confidence: 99%

“…GAPDH was used as a control and primer sequences have been reported elsewhere (Presneau et al, 2003).…”

Section: Rt-pcr Analysismentioning

confidence: 99%

“…Probe sets that represented genes or ESTs on chromosome 3 were extracted from the main expression data file with Extractor & 2001 Lypny and Tonin (Presneau et al, 2003), using UniGene Homo sapiens database, May 2005 based on UniGene Build 184 retrieved from the National Center for Biotechnology Information (www.ncbi.nlm.nih.gov/ UniGene). Additional mapping information (physical distances and cytoband positions) of all chromosome 3 probe sets was retrieved from the University of California Santa Cruz (UCSC) Human Genome Browser database May 2004 (hg 17) assembly (genome.ucsc.edu).…”

Section: Microarray Analysis Of Expression Profilesmentioning

confidence: 99%

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Transfer of chromosome 3 fragments suppresses tumorigenicity of an ovarian cancer cell line monoallelic for chromosome 3p

et al. 2006

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Multiple chromosome 3p tumor suppressor genes (TSG) have been proposed in the pathogenesis of ovarian cancer based on complex patterns of 3p loss. To attain functional evidence in support of TSGs and identify candidate regions, we applied a chromosome transfer method involving cell fusions of the tumorigenic OV90 human ovarian cancer cell line, monoallelic for 3p and an irradiated mouse cell line containing a human chromosome 3 in order to derive OV90 hybrids containing normal 3p fragments. The resulting hybrids showed complete or incomplete suppression of tumorigenicity in nude mouse xenograft assays, and varied in their ability to form colonies in soft agarose and three-dimensional spheroids in a manner consistent with alteration of their in vivo tumorigenic phenotypes. Expression microarray analysis identified a set of common differentially expressed genes, such as SPARC, DAB2 and VEGF, some of which have been shown implicated in ovarian cancer. Genotyping assays revealed that they harbored normal 3p fragments, some of which overlapped candidate TSG regions (3p25-p26, 3p24 and 3p14-pcen) identified previously in loss of heterozygosity analyses of ovarian cancers. However, only the 3p12-pcen region was acquired in common by all hybrids where expression microarray analysis identified differentially expressed genes. The correlation of 3p12-pcen transfer and tumor suppression with a concerted reprogramming of the cellular transcriptome suggest that the putative TSG may have affected key underlying events in ovarian cancer.

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Patterns of expression of chromosome 17 genes in primary cultures of normal ovarian surface epithelia and epithelial ovarian cancer cell lines

Cited by 26 publications

References 35 publications

Protein Kinase C Alpha Expression in Breast and Ovarian Cancer

Protein Kinase C Alpha Expression in Breast and Ovarian Cancer

Chromosome 17q25 genes, RHBDF2 and CYGB, in ovarian cancer

Transfer of chromosome 3 fragments suppresses tumorigenicity of an ovarian cancer cell line monoallelic for chromosome 3p

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