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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Melanoma brain metastases and matched extracranial metastases

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Guo Chen

PROVIDER: E-GEOD-50496 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Molecular profiling of patient-matched brain and extracranial melanoma metastases implicates the PI3K pathway as a therapeutic target.

Chen Guo G Chakravarti Nitin N Aardalen Kimberly K Lazar Alexander J AJ Tetzlaff Michael T MT Wubbenhorst Bradley B Kim Sang-Bae SB Kopetz Scott S Ledoux Alicia A AA Gopal Y N Vashisht YN Pereira Cristiano Goncalves CG Deng Wanleng W Lee Ju-Seog JS Nathanson Katherine L KL Aldape Kenneth D KD Prieto Victor G VG Stuart Darrin D Davies Michael A MA

Clinical cancer research : an official journal of the American Association for Cancer Research 20140506 21

<h4>Purpose</h4>An improved understanding of the molecular pathogenesis of brain metastases, one of the most common and devastating complications of advanced melanoma, may identify and prioritize rational therapeutic approaches for this disease. In particular, the identification of molecular differences between brain and extracranial metastases would support the need for the development of organ-specific therapeutic approaches.<h4>Experimental design</h4>Hotspot mutations, copy number variations ...[more]

PMID: 24803579

Similar Datasets

Gene expression profiling of melanoma brain metastases and matched extracranial metastases

Project description:An improved understanding of the molecular pathogenesis of brain metastases, one of the most common and devastating complications of advanced melanoma, may identify and prioritize rational therapeutic approaches for this disease. In particular, the identification of molecular differences between brain and extracranial metastases would support the need for the development of organ-specific therapeutic approaches. Hotspot mutations, copy number variations (CNV), global mRNA expression patterns, and protein expression and activation, quantitatively analyzed by molecular inversion probe arrays, microarrays and reverse phase protein array (RPPA) were evaluated in pairs of melanoma brain metastases and extracranial metastases from patients who had undergone surgical resection for both types of tumors. Seventy-two samples from 52 brain (except for patient 01, who had a spinal cord metastasis) and extracranial metastases of melanoma were analyzed. Available biological replicates (different parts of the same tumor) were included.

2014-05-08 | E-GEOD-50493 | biostudies-arrayexpress

Somatic copy number variation profiling in matched brain and extracranial metastases of melanoma

Project description:An improved understanding of the molecular pathogenesis of brain metastases, one of the most common and devastating complications of advanced melanoma, may identify and prioritize rational therapeutic approaches for this disease. In particular, the identification of molecular differences between brain and extracranial metastases would support the need for the development of organ-specific therapeutic approaches. Hotspot mutations, copy number variations (CNV), global mRNA expression patterns, and protein expression and activation, quantitatively analyzed by mass-array genotyping, molecular inversion probe arrays, microarrays and reverse phase protein array (RPPA) were evaluated in pairs of melanoma brain metastases and extracranial metastases from patients who had undergone surgical resection for both types of tumors. Somatic copy number variation (CNV) in 47 melanoma brain metastases (BM, except for patient 01, who had a spinal cord metastasis) and extracranial metastases (EM) were analyzed by molecular inversion probe (MIP) array (Affymetrix OncoScan FFPE Express 2.0). DNA were extracted from regions with >70% viable tumor cells from formalin-fixed and paraffin-embedded (FFPE) tissues. Of the 47 tumor samples, 22 were matched BM and EM from the same patients. In addition, 24 DNA samples from normal tissues were included as diploid controls.

2014-05-08 | E-GEOD-50495 | biostudies-arrayexpress

Gene expression profiling of oncogenic NRAS driven mouse melanomas that have developed resistance to NRAS withdrawal

Project description:Targeted therapies have the potential to revolutionize cancer care by providing personalized treatment strategies that are less toxic and more effective but it is clear that for most solid tumors suppression of a single target is not sufficient to prevent development of resistance. A powerful method to identify mechanisms of resistance and targets for combination therapy is to use an in vivo genetic approach. We have developed a novel retroviral gene delivery mouse model of melanoma that permits control of gene expression post-delivery using the tetracycline (tet)-regulated system. In this study we used this melanoma model to select for resistant tumors following genetic inhibition of mutant NRAS. Analysis of tumors that became resistant to NRAS suppression revealed that the most common mechanism of resistance was overexpression of the Met receptor tyrosine kinase (RTK). Importantly, inhibition of Met overcomes NRAS resistance in this context. Analysis of NRAS mutant human melanoma cells revealed that inhibition of MEK is also associated with adaptive RTK signaling. Furthermore, co-inhibition of RTK signaling and MEK overcomes acquired MEK inhibitor resistance in NRAS mutant melanoma. These data suggest that combined inhibition of RTK and MEK signaling is a rational therapeutic strategy in mutant NRAS driven melanoma. Reversible NRAS Q61R expression in the melanocytes of DCT-TVA;Ink4a/Arf lox/lox mice (FVB/n) was achieved by transducing the animals with Tet-off and TRE-NRASQ61R-IRES-Cre avian leukosis viruses. After tumor initiation, the expression of NRAS Q61R was turned off by administrating doxycycline. Despite initial regression, tumors in 40% of mice developed resistance to NRAS Q61R withdraw. Seven resistant tumors and one control tumor where NRAS Q61R expression was not interrupted were subjected to genome-wide gene expression profiling.

2014-10-31 | E-GEOD-51906 | biostudies-arrayexpress

DNA copy number gain at 1q23.3 is associated with poor survival in metastatic bladder cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-07-07 | E-GEOD-39282 | biostudies-arrayexpress

Genomic analysis of low-grade serous ovarian carcinomas

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-10-01 | E-GEOD-57280 | biostudies-arrayexpress

Genomic analysis of low-grade serous ovarian carcinomas [ILOEF]

Project description:Low-grade serous ovarian carcinomas are typically Ras-pathway mutated, TP53 wild-type, have limited chromosomal aberration, and are frequently associated with borderline tumors. By contrast, high-grade serous ovarian carcinoma lack Ras-pathway mutations, are invariably TP53 mutated, show widespread genomic change, and are commonly BRCA-pathway disrupted.We sought to identify differences in genomic copy number changes between co-existing borderline and invasive components of serous carcinoma. Paired co-existing borderline and invasive tumor components were sampled and profiled from formalin-fixed paraffin embedded tumors from 6 patients

2014-10-01 | E-GEOD-57276 | biostudies-arrayexpress

SNP array profiling of leiomyosarcoma

Project description:SNP arrays were use to identify recurrent affected genomic regions in leiomyosarcoma.

2018-07-02 | E-MTAB-5773 | biostudies-arrayexpress

Identification of copy number alterations associated with the progression of DCIS to Invasive Ductal Carcinoma

Project description:Ductal carcinoma in situ (DCIS) is a non-obligate precursor to invasive ductal carcinoma (IDC). Annotation of the genetic differences between the two lesions may assist in the identification of genes that promote the invasive phenotype. Matched IDC and DCIS showed highly similar copy number profiles (average of 83% of the genome shared) indicating a common clonal orgin although there is evidence that the DCIS continues to evolve in parallel with the co-existing IDC. Four chromosomal regions of loss (3q, 6q, 8p and 11q) and four regions of gain (5q, 16p, 19q and 20) were recurrently affected in IDC but not in DCIS. CCND1 and MYC showed increased amplitude of gain in IDC. One region of loss (17p11.2) was specific to DCIS. 21 cases of synchronous DCIS and IDC were microdissected from FFPE tissue and analysed by molecular inversion probe (MIP) copy number arrays. The arrays were early release OncoScan arrays and the data in this submission are CN values for the ~300,000 probes common to two batches performed. Raw data is retained by Affymetrix.

2012-09-04 | E-GEOD-31892 | biostudies-arrayexpress

Liver tumor/normal pairs

Project description:A major challenge to the study of tumor DNA copy number (CN) in clinical specimens is the lack of appropriate fresh frozen samples and thus a dependence on Formalin-Fixed Paraffin Embedded (FFPE) banked samples, which typically have more extensive clinical follow up information. However, on most high density CN platforms, DNA from FFPE tissues generally underperforms or suffers high failure rates compared to fresh frozen samples because of DNA degradation and cross-linking. Molecular Inversion Probe (MIP) technology has been applied successfully to obtain high quality CN and genotype data from DNA isolated from cell lines and frozen tumor samples. Since the MIP probes require only a small (~40 bp) target binding site, we reasoned they may be well suited to assess FFPE samples. In this study, we successfully applied MIP technology with a panel of 50,000 markers to CN determination in FFPE samples. Using an input of 37 ng genomic DNA, we demonstrated high quality CN data with MIP technology from 93 FFPE samples from seven diverse collections. We found that the performance of FFPE DNA for CN determination was comparable to that of DNA obtained from matched frozen tumor, with only a modest loss in performance of DNA. Tumor FFPE were analyzed using matched normal FFPE as the reference. Tumor and normal pairs: 01-02, 12-13, 16-17, 08-09, 20-21, 24-25, 28-29, and 35-36. Tumor 32 has no matched normal sample.

2009-01-22 | E-GEOD-14353 | biostudies-arrayexpress

DNA copy number gain at 1q23.3 is associated with poor survival in metastatic bladder cancer [Agilent]

Project description:Metastatic urothelial carcinoma (UC) of the bladder is associated with multiple somatic copy number alterations (SCNAs). We evaluated SCNAs to identify predictors of poor survival in patients with metastatic UC treated with platinum chemotherapy. We obtained overall survival (OS) and DNA copy number data from UC patients in a Spanish discovery cohort and three validation cohorts. GISTIC was used to identify altered regions, and associations between copy number gains/losses and OS were determined by a Cox proportional hazard model adjusting for performance status and visceral disease The output files of the GISTIC 2.0 software are linked as supplementary files on Series record along with readme.txt file describing the contents of each file/column.

2013-07-07 | E-GEOD-39281 | biostudies-arrayexpress

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