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Renal Cell Carcinoma (RCC) tumorgrafts exhibit similar DNA copy number alterations to corresponding primary tumors

ABSTRACT: Primary tumors of Renal Cell Carcinoma (RCC) were implanted orthotopically into mice and their DNA copy number abnormalities were compared to their corresponding tumors using Affymetrix SNP arrays 6.0

ORGANISM(S): Homo sapiens

SUBMITTER: Samuel Pena-Llopis

PROVIDER: E-MTAB-1051 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A validated tumorgraft model reveals activity of dovitinib against renal cell carcinoma.

Sivanand Sharanya S Peña-Llopis Samuel S Zhao Hong H Kucejova Blanka B Spence Patrick P Pavia-Jimenez Andrea A Yamasaki Toshinari T McBride David J DJ Gillen Jessica J Wolff Nicholas C NC Morlock Lorraine L Lotan Yair Y Raj Ganesh V GV Sagalowsky Arthur A Margulis Vitaly V Cadeddu Jeffrey A JA Ross Mark T MT Bentley David R DR Kabbani Wareef W Xie Xian-Jin XJ Kapur Payal P Williams Noelle S NS Brugarolas James J

Science translational medicine 20120601 137

Most anticancer drugs entering clinical trials fail to achieve approval from the U.S. Food and Drug Administration. Drug development is hampered by the lack of preclinical models with therapeutic predictive value. Herein, we report the development and validation of a tumorgraft model of renal cell carcinoma (RCC) and its application to the evaluation of an experimental drug. Tumor samples from 94 patients were implanted in the kidneys of mice without additives or disaggregation. Tumors from 35 o ...[more]

PMID: 22674553

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Renal Cell Carcinoma (RCC) tumorgrafts exhibit similar gene expression profiling to corresponding primary tumors

Project description:Primary tumors of Renal Cell Carcinoma (RCC) were implanted orthotopically into mice and their gene expression profiling was compared to their corresponding tumors using Affymetrix Human Genome U133 Plus 2.0 arrays.

2012-06-05 | E-MTAB-1050 | biostudies-arrayexpress

DNA Copy-Number Alterations in clear-cell Renal Cell Carcinoma (ccRCC) Tumors and Tumorgrafts for samples deficient in BAP1 or PBRM1

Project description:Renal cell carcinoma (RCC) exhibits some unusual features and genes commonly mutated in cancer are rarely mutated in clear-cell RCC (ccRCC), the most common type. The most prevalent genetic alteration in ccRCC is the inactivation of the tumor suppressor gene VHL. Using whole-genome and exome sequencing we discovered BAP1 as a novel tumor suppressor in ccRCC that shows little overlap with mutations in PBRM1, another recent tumor suppressor. Whereas VHL was mutated in 81% of the patients (142/176), PBRM1 was lost in 58% and BAP1 in 15% of the patients analyzed. All these tumor suppressor genes are located in chromosome 3p, which is partially or completely lost in most ccRCC patients. However, BAP1 but not PBRM1 loss was associated with higher Fuhrman grade and, therefore, poorer outcome. Xenograft tumors (tumorgrafts) implanted orthotopically in mice retained >92% of mutations and exhibited similar DNA copy number alterations to corresponding primary tumors. Thus, after inactivation of VHL, the acquisition of a mutation in BAP1 or PBRM1 defines a different program that might alter the fate of the patient. Our results establish the foundation for an integrated pathological and molecular genetic classification of about 70% of ccRCC patients, paving the way for subtype-specific treatments exploiting genetic vulnerabilities. The genomic DNA of clear-cell renal cell carcinoma (ccRCC) primary tumors, tumors growing in immunodeficient mice (tumorgrafts), and normal samples were labeled and hybridized to Affymetrix SNP arrays 6.0.

2012-06-09 | E-GEOD-25540 | biostudies-arrayexpress

Molecular Genetic Classification of clear-cell Renal Cell Carcinoma (ccRCC) based on the Gene Expression Profiling of Tumors and Tumorgrafts deficient for BAP1 or PBRM1

Project description:Renal cell carcinoma (RCC) exhibits some unusual features and genes commonly mutated in cancer are rarely mutated in clear-cell RCC (ccRCC), the most common type. The most prevalent genetic alteration in ccRCC is the inactivation of the tumor suppressor gene VHL. Using whole-genome and exome sequencing we discovered BAP1 as a novel tumor suppressor in ccRCC that shows little overlap with mutations in PBRM1, another recent tumor suppressor. Whereas VHL was mutated in 81% of the patients (142/176), PBRM1 was lost in 58% and BAP1 in 15% of the patients analyzed. All these tumor suppressor genes are located in chromosome 3p, which is partially or completely lost in most ccRCC patients. However, BAP1 but not PBRM1 loss was associated with higher Fuhrman grade and, therefore, poorer outcome. Xenograft tumors (tumorgrafts) implanted orthotopically in mice exhibited similar gene expression profiling to corresponding primary tumors. Gene expression profiling of tumors and tumorgrafts displayed different signatures for BAP1- and PBRM1-deficient samples. Thus, after inactivation of VHL, the acquisition of a mutation in BAP1 or PBRM1 defines a different program that might alter the fate of the patient. Our results establish the foundation for an integrated pathological and molecular genetic classification of about 70% of ccRCC patients, paving the way for subtype-specific treatments exploiting genetic vulnerabilities. The RNA of clear-cell renal cell carcinoma (ccRCC) primary tumors, tumors growing in immunodeficient mice (tumorgrafts), and normal kidney cortices were labeled and hybridized to Affymetrix Human Genome U133 Plus 2.0 arrays.

2012-06-09 | E-GEOD-36895 | biostudies-arrayexpress

Microarray expression profiling of dysregulated long non-coding RNAs between RCC tumor tissues and corresponding adjacent tissues

Project description:During the past decade, increasing evidence has shown that lncRNAs play important roles in oncogenesis and tumor suppression; however, the roles of lncRNAs in RCC are poorly understood. To address this issue, we used Agilent human lncRNA microarray chips and bioinformatics tools to assess lncRNA expression in 5 pairs of RCC tissues. A dysregulated lncRNA expression profile was identified by microarray and verified by qRT-PCR in 60 pairs of renal cell carcinoma.

2017-06-10 | GSE88811 | GEO

Gene expression analysis of TGF-beta signaling-disrupting gastric cancer cell line 2MLN

Project description:Diffuse-type gastric carcinoma is a poor-prognostic cancer with high expression of transforming growth factor (TGF)-β and thick stromal fibrosis. However, detailed investigations on the roles of TGF-β signaling in diffuse-type gastric carcinoma have not been performed. We generated two diffuse-type gastric carcinoma cell lines, dominant-negative TGF-β type II receptor expressing cells (2MLN-dnTβRII) and GFP-expressing cells (2MLN-GFP). Cells were subcutaneously or orthotopically injected into nude mice. Although dnTβRII did not affect the growth of OCUM-2MLN in vitro, it accelerated the growth of subcutaneously or orthotopically transplanted tumors in vivo. By microarray analysis, we found gene expression of TSP-1, an angiogenic inhibitor, was down-regulated in dnTβRII tumors. This results suggested disruption of TGF-β signaling in diffuse-type gastric carcinoma cells leads to alteration of tumor microenvironment and acceleration of tumor growth. We generated two OCUM-2MLN-derived gastric carcinoma cell lines; 2MLN-dnTβRII, which expresses dominant negative form of TβRII, and control 2MLN-GFP, which expresses GFP. The transplanted tumors of these cell lines were subjected to gene expression analysis with Affymetrix U133 plus2 arrays.

2011-12-30 | E-GEOD-12336 | biostudies-arrayexpress