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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Samuel Pena-Llopis

PROVIDER: E-MTAB-1050 | 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 DNA copy number alterations to corresponding primary tumors

Project description: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

2012-06-05 | E-MTAB-1051 | 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.

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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.

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