Genomic profiling of invasive melanoma cell lines by array comparative genomic hybridization

2016 ◽  
Vol 26 (2) ◽  
pp. 100-107 ◽  
Author(s):  
Viktória Koroknai ◽  
Szilvia Ecsedi ◽  
Laura Vízkeleti ◽  
Tímea Kiss ◽  
István Szász ◽  
...  
Keyword(s):  
Comparative Genomic Hybridization ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Array Comparative Genomic Hybridization ◽  
Comparative Genomic ◽  
Genomic Profiling ◽  
Genomic Hybridization ◽  
Melanoma Cell Lines

scholarly journals Genomic Profiling by Array Comparative Genomic Hybridization Reveals Novel DNA Copy Number Changes in Breast Phyllodes Tumours

2009 ◽  
Vol 31 (1) ◽  
pp. 31-39
Author(s):  
Arno Kuijper ◽  
Antoine M. Snijders ◽  
Els M. J. J. Berns ◽  
Vibeke Kuenen-Boumeester ◽  
Elsken van der Wall ◽  
...  
Keyword(s):  
Comparative Genomic Hybridization ◽  
Copy Number ◽  
Array Comparative Genomic Hybridization ◽  
Copy Number Change ◽  
Genetic Alterations ◽  
Comparative Genomic ◽  
Genomic Profiling ◽  
Genomic Hybridization ◽  
Dna Copy Number ◽  
Copy Number Changes

Breast phyllodes tumour (PT) is a rare fibroepithelial tumour. The genetic alterations contributing to its tumorigenesis are largely unknown. To identify genomic regions involved in pathogenesis and progression of PTs we obtained genome-wide copy number profiles by array comparative genomic hybridization (CGH).DNA was isolated from fresh-frozen tissue samples. 11 PTs and 3 fibroadenomas, a frequently occurring fibroepithelial breast tumour, were analyzed. Arrays composed of 2464 genomic clones were used, providing a resolution of ~1.4 Mb across the genome. Each clone contains at least one STS for linkage to the human genome sequence.No copy number changes were detected in fibroadenomas. On the other hand, 10 of 11 PT (91%) showed DNA copy number alterations. The mean number of chromosomal events in PT was 5.5 (range 0–16) per case. A mean of 2.0 gains (range 0–10) and 3.0 losses (range 0–9) was seen per case of PT. Three cases showed amplifications. DNA copy number change was not related to PT grade. We observed recurrent loss on chromosome 1q, 4p, 10, 13q, 15q, 16, 17p, 19 and X. Recurrent copy number gain was seen on 1q, 2p, 3q, 7p, 8q, 16q, 20.In this study we used array CGH for genomic profiling of fibroepithelial breast tumours. Whereas most PT showed chromosomal instability, fibroadenomas lacked copy number changes. Some copy number aberrations had not previously been associated with PT. Several well-known cancer related genes, such as TP53 and members of the Cadherin, reside within the recurrent regions of copy number alteration. Since copy number change was found in all benign PT, genomic instability may be an early event in PT genesis.

Genomic profiling of myeloid sarcoma by array comparative genomic hybridization

2005 ◽  
Vol 44 (4) ◽  
pp. 373-383 ◽  
Author(s):  
George Deeb ◽  
Maria R. Baer ◽  
Daniel P. Gaile ◽  
Sheila N. Jani Sait ◽  
Maurice Barcos ◽  
...  
Keyword(s):  
Comparative Genomic Hybridization ◽  
Array Comparative Genomic Hybridization ◽  
Myeloid Sarcoma ◽  
Comparative Genomic ◽  
Genomic Profiling ◽  
Genomic Hybridization

scholarly journals Molecular features and vulnerabilities of recurrent chordomas

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Carolin Seeling ◽  
André Lechel ◽  
Michael Svinarenko ◽  
Peter Möller ◽  
Thomas F. E. Barth ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Culture ◽  
Comparative Genomic Hybridization ◽  
Cell Lines ◽  
Array Comparative Genomic Hybridization ◽  
Expression Patterns ◽  
Comparative Genomic ◽  
Genomic Hybridization ◽  
Culture Models ◽  
Cell Culture Models

Abstract Background Tumor recurrence is one of the major challenges in clinical management of chordoma. Despite R0-resection, approximately 50% of chordomas recur within ten years after initial surgery. The underlying molecular processes are poorly understood resulting in the lack of associated therapeutic options. This is not least due to the absence of appropriate cell culture models of this orphan disease. Methods The intra-personal progression model cell lines U-CH11 and U-CH11R were compared using array comparative genomic hybridization, expression arrays, RNA-seq, and immunocytochemistry. Cell line origin was confirmed by short tandem repeat analysis. Inter-personal cell culture models (n = 6) were examined to validate whether the new model is representative. Cell viability after HOX/PBX complex inhibition with small peptides was determined by MTS assays. Results Using whole genome microarray analyses, striking differences in gene expression between primary and recurrent chordomas were identified. These expression differences were confirmed in the world’s first intra-personal model of chordoma relapse consisting of cell lines established from a primary (U-CH11) and the corresponding recurrent tumor (U-CH11R). Array comparative genomic hybridization and RNA-sequencing analyses revealed profound genetic similarities between both cell lines pointing to transcriptomic reprogramming as a key mechanism of chordoma progression. Network analysis of the recurrence specific genes highlighted HOX/PBX signaling as a common dysregulated event. Hence, HOX/PBX complexes were used as so far unknown therapeutic targets in recurrent chordomas. Treating chordoma cell lines with the complex formation inhibiting peptide HXR9 induced cFOS mediated apoptosis in all chordoma cell lines tested. This effect was significantly stronger in cell lines established from chordoma relapses. Conclusion Clearly differing gene expression patterns and vulnerabilities to HOX/PBX complex inhibition in highly therapy resistant chordoma relapses were identified using the first intra-personal loco-regional and further inter-personal chordoma progression models. For the first time, HOX/PBX interference was used to induce cell death in chordoma and might serve as the basic concept of an upcoming targeted therapy for chordomas of all progression stages.

Sign in / Sign up

Export Citation Format

Share Document