Unknown,Transcriptomics,Genomics,Proteomics

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Genomic profiling of oral squamous cell carcinoma by array-based comparative genomic hybridization

ABSTRACT: In this study, we investigated CNAs of 40 tumor samples from 25 patients, including 15 metastatic primary tumor (MPT), paired neck lymph-node metastasis (LNM) and 10 non-metastatic primary tumor (NMPT), by 44k oligonucleotide-based array comparative genomic hybridization (array CGH). 15 MPT vs 15 LNM, 10 NMPT vs 15 LNM

ORGANISM(S): Homo sapiens

SUBMITTER: shunichi yoshioka

PROVIDER: E-GEOD-36942 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Background & Aims. Resection of hepatocellular carcinoma (HCC) tumors by partial hepatectomy (PHx) is associated with promoting hepatocarcinogenesis. We have previously reported that PHx promotes hepatocarcinogenesis in the Mdr2-knockout (Mdr2-KO) mouse, a model for inflammation-mediated HCC. Now, we explored the molecular mechanisms underlying the tumor-promoting effect of PHx in these mice. Methods. Using microarrays-based techniques, we compared genomic and transcriptomic profiles of HCC tumors developing in the Mdr2-KO mice either spontaneously or following PHx. Results. PHx accelerated HCC development in these mice by four months. PHx-induced tumors had only amplifications affecting multiple chromosomes and locating mainly near the acrocentric centromeres of murine chromosomes. Four different chromosomal regions were amplified each in at least three tumors. All tumors of untreated mice had chromosomal aberrations, including both deletions and amplifications. Comparison of gene expression profiles revealed a significantly enriched expression of oncogenes, chromosomal instability markers and E2F1 targets in the post-PHx compared to spontaneous tumors. Both tumor groups shared the same frequent amplification at chromosome 18. Here, we demonstrated that one of the regulatory genes encoded by this amplified region, Crem, was over-expressed in the nuclei of murine and human HCC cells in vivo, and that it stimulated proliferation of human HCC cells in vitro. Conclusions: PHx of a chronically inflamed liver directed tumor development to a discrete pathway characterized by amplification of specific chromosomal regions and expression of specific tumor-promoting genes. Crem is a new candidate HCC oncogene frequently amplified in this model and frequently over-expressed in human HCC. To explore the mechanisms of the accelerated HCC development by PHx, we compared liver tumors and their matched non-tumor liver tissues between 9-month-old hepatectomized and 13-14-month-old untreated Mdr2-KO mice.

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Genomic profiling of oral squamous cell carcinoma by array-based comparative genomic hybridization

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