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Gene expression profile of tumor cells from primary tumors, ascites and metastases of low grade serous ovarian cancer patients

ABSTRACT: Differ from the aggressive nature of HGSOC (high grade serous ovarian cancer), LGSOC (low grade serous ovarian cancer) is characterized by an early age of disease onset, slow growth pattern, and poor response to chemotherapy. To understand more specifically the underlying gene profiling discrepancy that contributes to their behavior distinction, we performed parallel gene expression profiling in 9 magnetic sorted tumor cells samples from matched primary tumors, ascites and metastases of 3 LGSOC patients as in HGSOC. By comparing the expression data among primary tumor cells, ascitic tumor cells and metastasis tumor cells, we identified a set of differential expressed genes along LGSOC progression. Further study revealed that the gene phenotype perturbance along LGSOC progression was quite different from that of HGSOC patients. We used microarrays to profile the expression of 9 matched tumor cells samples in order to identify molecular alteration between primary tumor cells, ascitic tumor cells and metastatic tumor cells in low grade serous ovarian cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE73091 | GEO | 2017/12/19

SECONDARY ACCESSION(S): PRJNA296123

REPOSITORIES: GEO

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Project description:Intra-individual tumoral heterogeneity (ITH) is a hallmark of solid tumors and impedes accurate genomic diagnosis and selection of proper therapy. The purpose of this study was to identify ITH of ovarian serous adenocarcinomas (OSAs) and to determine the utility of ascitic cancer cells as a resource for mutation profiling in spite of ITH. We performed whole-exome sequencing, copy number profiling, and DNA methylation profiling of four OSA genomes using multiregional biopsies from 13 intraovarian lesions, 12 extraovarian tumor lesions (omentum/peritoneum), and ascitic cells. We observed substantial levels of heterogeneity in mutations and copy number alterations (CNAs) of the OSAs. We categorized the mutations into 'common', 'shared' and 'private' according to the regional distribution. Six common, 8 shared, and 24 private mutations were observed in known cancer-related genes,. but common mutations had a higher mutant allele frequency and included TP53 mutations in all four OSAs. Region-specific chromosomal amplifications and deletions involving BRCA1, PIK3CA, and RB1 were also identified. Of note, the mutations detected in ascitic cancer cells represented 92.3-100% of overall somatic mutations in the given case. Phylogenetic analyses of ascitic genomes predicted a polyseeding origin of somatic mutations in ascitic cells. Our results demonstrate that despite ITH, somatic mutations, CNAs, and DNA methylations in both âcommonâ category and cancer-related genes were highly conserved in ascitic cells of OSAs, highlighting the clinical relevance of genome analysis of ascitic cells. Ascitic tumor cells may serve as a potential resource to discover somatic mutations of primary OSA with diagnostic and therapeutic relevance. The purpose of this study was to identify intra-individual tumor heterogenety of ovarian serous adenocarcinomas Four to nine different ovarian cancer areas from intraovarian and extra-ovarian lesions that were at least 1cm apart as well as 50 ml ascites were collected from the four OSA patients. Genomic DNA from tumor and matched normal samples were simultaneously hybridized onto the array. Total 29 array experiments were conducted.

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Gene expression profile of tumor cells from primary tumors, ascites and metastases of low grade serous ovarian cancer patients

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