Comparative study of renal cell carcinoma by CGH, multicolor-FISH and conventional cytogenic banding analysis

Sanjmyatav, Jimsgene; Schubert, Jöerg; Junker, Kerstin

doi:10.3892/or.14.5.1183

Cited by 17 publications

(25 citation statements)

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“…In our knowledge, this is the first study applying the Affymetrix SNP array technology to assess at genome-wide level both CNAs and LOH in ccRCC primary cultures. Globally, our cultures confirmed the typical ccRCC genomic signature [13,23,30]. These cultures typically showed alterations on at most 4 or 5 chromosomes.…”

Section: Discussionsupporting

confidence: 78%

“…A comparison of the genomic profile between primary cultures and parental tissues has been reported only by Sanjmyatav et al by using traditional CGH [23]. Their DNA profiling showed a poor overlap of CNAs between ccRCC primary cultures and parental tumor tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Till now, the comparison of DNA profile between tumor primary cultures and parental tissues has been reported, with discordant results, in melanoma [20], neuroblastoma [21] and glioblastoma [22], using either SNP array or array-CGH techniques, and in RCC [23] only using traditional CGH on metaphase spreads and short-term primary cultures not extensively characterized.…”

Section: Introductionmentioning

confidence: 99%

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Renal cell carcinoma primary cultures maintain genomic and phenotypic profile of parental tumor tissues

et al. 2011

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BackgroundClear cell renal cell carcinoma (ccRCC) is characterized by recurrent copy number alterations (CNAs) and loss of heterozygosity (LOH), which may have potential diagnostic and prognostic applications. Here, we explored whether ccRCC primary cultures, established from surgical tumor specimens, maintain the DNA profile of parental tumor tissues allowing a more confident CNAs and LOH discrimination with respect to the original tissues.MethodsWe established a collection of 9 phenotypically well-characterized ccRCC primary cell cultures. Using the Affymetrix SNP array technology, we performed the genome-wide copy number (CN) profiling of both cultures and corresponding tumor tissues. Global concordance for each culture/tissue pair was assayed evaluating the correlations between whole-genome CN profiles and SNP allelic calls. CN analysis was performed using the two CNAG v3.0 and Partek software, and comparing results returned by two different algorithms (Hidden Markov Model and Genomic Segmentation).ResultsA very good overlap between the CNAs of each culture and corresponding tissue was observed. The finding, reinforced by high whole-genome CN correlations and SNP call concordances, provided evidence that each culture was derived from its corresponding tissue and maintained the genomic alterations of parental tumor. In addition, primary culture DNA profile remained stable for at least 3 weeks, till to third passage. These cultures showed a greater cell homogeneity and enrichment in tumor component than original tissues, thus enabling a better discrimination of CNAs and LOH. Especially for hemizygous deletions, primary cultures presented more evident CN losses, typically accompanied by LOH; differently, in original tissues the intensity of these deletions was weaken by normal cell contamination and LOH calls were missed.ConclusionsccRCC primary cultures are a reliable in vitro model, well-reproducing original tumor genetics and phenotype, potentially useful for future functional approaches aimed to study genes or pathways involved in ccRCC etiopathogenesis and to identify novel clinical markers or therapeutic targets. Moreover, SNP array technology proved to be a powerful tool to better define the cell composition and homogeneity of RCC primary cultures.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Renal cell carcinoma primary cultures maintain genomic and phenotypic profile of parental tumor tissues

et al. 2011

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“…Other genetic alterations in papillary renal cell carcinoma include gains of chromosome 8, 12q, 16q, and 20q and loss of chromosomes 1p, 4q, 6q, 9p, 11p, 13q, 14q, 18, 21q, and X [74,[84][85][86]. Chromosome 20q is believed to contain genes involved in the development of papillary renal cell carcinoma [83,87].…”

Section: Papillary Renal Cell Carcinomamentioning

confidence: 99%

Molecular and cytogenetic insights into the pathogenesis, classification, differential diagnosis, and prognosis of renal epithelial neoplasms

et al. 2009

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“…29 This chromosomal region is also found to be lost in many clear-cell RCC. 30,31 The important role of SFTPC in host defense mechanisms in the lung might contribute to the inhibition of tumour cell proliferation and therefore, retard the growth of Mets. However, surfactant proteins are expressed in the normal lung tissue.…”

Section: Molecular Patterns Distinguish Late and Early Metsmentioning

confidence: 99%

Gene signatures of pulmonary metastases of renal cell carcinoma reflect the disease‐free interval and the number of metastases per patient

Wuttig

Baier²,

Fuessel

et al. 2009

Intl Journal of Cancer

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Our understanding of metastatic spread is limited and molecular mechanisms causing particular characteristics of metastasis are largely unknown. Herein, transcriptome-wide expression profiles of a unique cohort of 20 laser-resected pulmonary metastases (Mets) of 18 patients with clear-cell renal cell carcinoma (RCC) were analyzed to identify expression patterns associated with two important prognostic factors in RCC: the disease-free interval (DFI) after nephrectomy and the number of Mets per patient. Differentially expressed genes were identified by comparing early (DFI 9 months) and late (DFI 5 years) Mets, and Mets derived from patients with few ( 8) and multiple ( 16) Mets. Early and late Mets could be separated by the expression of genes involved in metastasis-associated processes, such as angiogenesis, cell migration and adhesion (e.g., PECAM1, KDR). Samples from patients with multiple Mets showed an elevated expression of genes associated with cell division and cell cycle (e.g., PBK, BIRC5, PTTG1) which indicates that a high number of Mets might result from an increased growth potential. Minimal sets of genes for the prediction of the DFI and the number of Mets per patient were identified. Microarray results were confirmed by quantitative PCR by including nine further pulmonary Mets of RCC. In summary, we showed that subgroups of Mets are distinguishable based on their expression profiles, which reflect the DFI and the number of Mets of a patient. To what extent the identified molecular factors contribute to the development of these characteristics of metastatic spread needs to be analyzed in further studies. ' UICC Key words: kidney cancer; lung metastases; oligonucleotide microarraysIn numerous tumour types, the development of metastases (Mets) causes the patients' death. The median survival of renal cell carcinoma (RCC) patients amounts to merely 6 to 12 months after Mets have been diagnosed. 1 RCC is the urological cancer with the highest percentage of tumour-related deaths 2 because metastasis occurs in about 60% of the patients. 3 The preferential localization of RCC Mets is the lung. 1 In contrast to the emerging development of molecular-based therapies for RCC in the last few years, 3 molecular prognostic markers are still missing. Despite the knowledge of several molecular factors involved in metastatic spread like angiogenesis, cell adhesion, invasion or migration, 4,5 little is known about specific characteristics of this complex process. These are, for example, primary-dependent site-specific metastasis, 6 varying dormancy periods of Mets originating from the same primary tumour entity causing disease-free intervals (DFI) ranging from several months to many years, or the differing number of Mets in patients with the same primary tumour. Knowing the molecular fundamentals of these phenomena would support the prognosis of patients' outcome and facilitate the decision for an appropriate therapy regime, particularly in RCC where the DFI and the number of Mets are important predictors of clinical...

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Comparative study of renal cell carcinoma by CGH, multicolor-FISH and conventional cytogenic banding analysis

Cited by 17 publications

References 0 publications

Renal cell carcinoma primary cultures maintain genomic and phenotypic profile of parental tumor tissues

Renal cell carcinoma primary cultures maintain genomic and phenotypic profile of parental tumor tissues

Molecular and cytogenetic insights into the pathogenesis, classification, differential diagnosis, and prognosis of renal epithelial neoplasms

Gene signatures of pulmonary metastases of renal cell carcinoma reflect the disease‐free interval and the number of metastases per patient

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