Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of human enosynovial giant-cell tumor (TGCT) and pigmented villonodular synovitis (PVNS) samples

ABSTRACT: Tenosynovial giant-cell tumor (TGCT) and pigmented villonodular synovitis (PVNS) are related conditions with features of both reactive inflammatory disorders and clonal neoplastic proliferations. Chromosomal translocations involving chromosome 1p13 have been reported in both TGCT and PVNS. We confirm that translocations involving 1p13 are present in a majority of cases of TGCT and PVNS and show that CSF1 is the gene at the chromosome 1p13 breakpoint. In some cases of both TGCT and PVNS, CSF1 is fused to COL6A3 (2q35). The CSF1 translocations result in overexpression of CSF1. In cases of TGCT and PVNS carrying this translocation, it is present in a minority of the intratumoral cells, leading to CSF1 expression only in these cells, whereas the majority of cells express CSF1R but not CSF1, suggesting a tumor-landscaping effect with aberrant CSF1 expression in the neoplastic cells, leading to the abnormal accumulation of nonneoplastic cells that form a tumorous mass.

ORGANISM(S): Homo sapiens

SUBMITTER: Janos Demeter

PROVIDER: E-SMDB-3598 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

A landscape effect in tenosynovial giant-cell tumor from activation of CSF1 expression by a translocation in a minority of tumor cells.

West Robert B RB Rubin Brian P BP Miller Melinda A MA Subramanian Subbaya S Kaygusuz Gulsah G Montgomery Kelli K Zhu Shirley S Marinelli Robert J RJ De Luca Alessandro A Downs-Kelly Erinn E Goldblum John R JR Corless Christopher L CL Brown Patrick O PO Gilks C Blake CB Nielsen Torsten O TO Huntsman David D van de Rijn Matt M

Proceedings of the National Academy of Sciences of the United States of America 20060106 3

Tenosynovial giant-cell tumor (TGCT) and pigmented villonodular synovitis (PVNS) are related conditions with features of both reactive inflammatory disorders and clonal neoplastic proliferations. Chromosomal translocations involving chromosome 1p13 have been reported in both TGCT and PVNS. We confirm that translocations involving 1p13 are present in a majority of cases of TGCT and PVNS and show that CSF1 is the gene at the chromosome 1p13 breakpoint. In some cases of both TGCT and PVNS, CSF1 is ...[more]

PMID: 16407111

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Project description:The development of chemo-resistance has dramatically limited the clinical efficiency of platinum-based therapy. Although many resistant mechanisms have been demonstrated, genetic/molecular alterations responsible for drug resistance in the majority of clinical cases has not been identified. We analyzed three pairs of testicular germ cell tumor (TGCT) cell lines using Affymetrix expression microarrays to identify differential expressed genes. Then the expression of CCND1/CyclinD1, selected from the microarray analysis, was determined in cisplatin sensitive and resistance cancer samples including TGCTs, ovarian and prostate cancers by quantitative reverse transcription PCR analysis (qRT-PCR). Finally, we determined the gene knocked-down effect of CyclinD1. Expression microarray study revealed a limited number of differentially expressed genes across all three cell lines when comparing the parental and resistant cells. Among them, CyclinD1 was the most significantly differentially expressed gene. Importantly, we found that, in clinical TGCT samples, the overall expression level of cyclinD1 is higher in resistant cases compared to those sensitive samples (9/12 in the resistant group and only 3/8 in the sensitive group). We also found that cyclinD1 expressed dozens of fold higher in the resistant than in the sensitive ovarian cancer cell lines and dramatically overexpressed in prostate cancer. We re-sensitized the resistant cells by knocking-down cyclinD1. We demonstrated that deregulation of cyclinD1 is the major cause of TGCT cisplatin resistance and it may also be commonly involved in other human cancers. Combined cyclinD1 inhibition and cisplatin chemotherapy may be used clinically to treat the large number of cyclinD1 deregulated resistant tumors. RNA from three paired parental and cisplatin-resistant TGCT cell lines was extracted and analysed by Affymetrix gene expression microarray profiling (Human Genome U133 plus 2.0 arrays). Expression changes associated with the resistant phenotype were identified by comparing the three cisplatin-resistant derivatives to their parental counterparts.

Dataset Information

Transcription profiling of human enosynovial giant-cell tumor (TGCT) and pigmented villonodular synovitis (PVNS) samples

Publications

A landscape effect in tenosynovial giant-cell tumor from activation of CSF1 expression by a translocation in a minority of tumor cells.

Similar Datasets

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