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ACGH profiling of prostate tumors

ABSTRACT: This experiment was an aCGH study on 86 prostate tumors samples. The samples were profiled on Agilent Human Genome 44karrays to identify recurrent regions of deletion and amplification, thus revealing potential new tumor suppressor genes and/or oncogenes involved in prostate cancer. The CGH profile on the 44k arrays revealed a deletion at 5q21 in 17% of samples. CGH analysis of 86 prostate tumor samples.

ORGANISM(S): Homo sapiens

SUBMITTER: Stephanie Huang

PROVIDER: E-GEOD-29227 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Recurrent deletion of CHD1 in prostate cancer with relevance to cell invasiveness.

Huang S S Gulzar Z G ZG Salari K K Lapointe J J Brooks J D JD Pollack J R JR

Oncogene 20111219 37

Though prostate cancer is often indolent, it is nonetheless a leading cause of cancer death. Defining the underlying molecular genetic alterations may lead to new strategies for prevention or treatment. Towards this goal, we performed array-based comparative genomic hybridization (CGH) on 86 primary prostate tumors. Among the most frequent alterations not associated with a known cancer gene, we identified focal deletions within 5q21 in 15 out of 86 (17%) cases. By high-resolution tiling array CG ...[more]

PMID: 22179824

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5q21 tiling array on prostate tumors

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aCGH profiling of prostate tumors

Project description:This experiment was an aCGH study on 86 prostate tumors samples. The samples were profiled on Agilent Human Genome 44karrays to identify recurrent regions of deletion and amplification, thus revealing potential new tumor suppressor genes and/or oncogenes involved in prostate cancer. The CGH profile on the 44k arrays revealed a deletion at 5q21 in 17% of samples.

2011-12-19 | GSE29227 | GEO

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Chromosomes 6 and 18 Induce Neoplastic Suppression in Epithelial Ovarian Cancer Cells

Project description:Metaphase comparative genomic hybridisation (CGH) studies indicate that chromosomes 4, 5, 6, 13, 14, 15 and 18 are frequently deleted in primary ovarian cancers (OC). Therefore, we used microcell-mediated chromosome transfer (MMCT) to establish the functional effects of transferring normal copies of these chromosomes into two epithelial OC cell lines. The in vitro neoplastic phenotype (measured as anchorage dependent and independent growth and invasion) was compared between recipient OC cell lines and multiple MMCT hybrids. Chromosomes 6 and 18 showed strong evidence of functional, neoplastic suppression for multiple hybrids in both cell lines. We also found evidence in one cancer cell line suggesting that chromosomes 4, 13 and 14 may also cause functional suppression. Array CGH and microsatellite analyses were used to characterise the extent of genomic transfer in chromosome 6 and 18 hybrids. A 35Mb deletion on chromosome 6 in two hybrids from one cell line mapped the candidate region proximal to 6q15 and distal to 6q22.2; and an approximate 10Mb candidate region spanning the centromere on chromosome 18 was identified in another two hybrids from the other cell line. These data confirm reported functional effects of chromosome 6 in OC cell lines; but to our knowledge, this is the first time that functional suppression for chromosome18 has been reported. This suggests that these chromosomes may harbour genes that behave as tumour suppressors. The future identification of these genes may have a significant impact on the understanding and treatment of the disease and the identification of novel therapeutic targets. Four clones from chr 6 and chr 18 hybrids that were transferred by MMCT successfully were mapped by CGH microarray to identified transferred regions that induced neoplastic suppression in epithelial ovarian cancer cell lines (TOV21G and TOV112D).

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