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Profile of differentially expressed genes after transfer of chromosome 17 into the breast cancer cell line CAl51

Item Type:Article
Title:Profile of differentially expressed genes after transfer of chromosome 17 into the breast cancer cell line CAl51
Creators Name:Klebig, C., Seitz, S., Korsching, E., Kristiansen, G., Gustavus, D., Scherneck, S. and Petersen, I.
Abstract:Previous studies have shown that transfer of chromosome 17 suppresses the tumorigenic phenotype of the breast cancer cell line CAL51, suggesting the presence of putative tumor suppressor genes on this chromosome. Suppression subtractive hybridization and oligonucleotide microarray analyses were performed to identify differentially expressed genes in nontumorigenic microcell hybrids, CAL/17-1 and CAL/17-3, when compared with CAL51 cells. In total, 263 differentially expressed transcripts were associated with these phenotypes. Of these, a high percentage is involved in various biological processes associated with tumorigenesis, including DNA-dependent regulation of transcription, regulation of cell cycle, signal transduction, and cell proliferation. Microarray analysis of selected chromosome 17 genes in a series of 25 human primary breast tumors showed associations with clinicopathologic parameters of the tumors. Of these genes, TOB1 (transducer of ERBB2) was selected for further expression analysis. Using RT-PCR and immunohistochemical staining of tissue microarrays, we could reveal a differential mRNA and protein expression of TOBI in the majority of breast tumors and lymph node metastases compared with normal breast tissues, indicating a potential role of this protein in breast tumorigenesis.
Keywords:Biological Tumor Markers, Breast, Breast Neoplasms, Cultured Tumor Cells, Gene Expression Profiling, Human Pair 17 Chromosomes, Intracellular Signaling Peptides and Proteins, Neoplasm RNA, Oligonucleotide Array Sequence Analysis, Reverse Transcriptase Polymerase Chain Reaction, Tissue Array Analysis, Tumor Suppressor Proteins
Source:Genes Chromosomes & Cancer
ISSN:1045-2257
Publisher:Wiley
Volume:44
Number:3
Page Range:233-246
Date:27 July 2005
Official Publication:https://doi.org/10.1002/gcc.20240
PubMed:View item in PubMed

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