GEPAS, an experiment-oriented pipeline for the analysis of microarray gene expression data

Vaquerizas, Juan M.; Conde, Lucía; Yankilevich, Patricio; Cabezón, Amaya; Mínguez, Pablo; Dı́az-Uriarte, Ramón; Al‐Shahrour, Fátima; Herrero, Javier; Dopazo, Joaquı́n

doi:10.1093/nar/gki500

Cited by 84 publications

(82 citation statements)

References 26 publications

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“…Briefly, in the array data analysis, aCGH normalization was carried using the DNMAD application (Vaquerizas et al, 2004). The normalized profiles were processed using the Binary Segmentation algorithm implemented in the Insilico CGH software (Vaquerizas et al, 2005). This algorithm defines genomic segments, which have an estimative copy number value in log 2 ratio (that is, the median log 2 ratio of the contained clones).…”

Section: Tumor Samples and Patientsmentioning

confidence: 99%

Distinct genomic aberration patterns are found in familial breast cancer associated with different immunohistochemical subtypes

et al. 2007

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Five breast cancer subtypes have been described in sporadic breast cancer (SBC) using expression arrays: basal-like, ERBB2, normal breast-like, luminal A and B. These molecular subtypes show different genomic aberration patterns (GAPs). Recently, our group described these breast cancer subtypes in 50 non-BRCA1/2 familial tumors using immunohistochemistry assays. We extended this study to the other classes of familial breast cancer (FBC), including 62 tumors (18 BRCA1, 16 BRCA2 and 28 non-BRCA1/2), with the same panel of 25 immunohistochemical (IHC) markers and histological grade obtaining a similar classification. We combined these data with results generated by a 1 Mb BAC array-based CGH study to evaluate the genomic aberrations of each group. We found that BRCA1-related tumors are preferentially basal-like, whereas non-BRCA1/2 familial tumors are mainly luminal A subtype. We described distinct GAPs related to each IHC subtype. Basal tumors had a greater number of gains/losses, while luminal B tumors had more high-level DNA amplifications. Our data are similar to those obtained in SBC studies, highlighting the existence of distinct genetic pathways of tumor evolution, common to both SBC and FBC.

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Section: Tumor Samples and Patientsmentioning

confidence: 99%

Distinct genomic aberration patterns are found in familial breast cancer associated with different immunohistochemical subtypes

et al. 2007

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“…Categorized copy number values (0, 1 or À1 indicating no change, gain or loss, respectively) were obtained using Insilico array CGH software. 23 We defined a genomic aberration (GA) as a group of at least two consecutive probes showing the same non-zero categorized copy number value. Single-probe aberrations did not score as genomic aberrations.…”

Section: Arraycgh and Management Of Genetic Polymorphismsmentioning

confidence: 99%

“…23 Associations between genomic instability and other clinical parameters were assessed using Fisher's exact test for qualitative variables and the KruskalWallis test for quantitative factors. Kaplan-Meyer curves were drawn and the log-rank test and multivariate Cox regression applied using SPSS v13.0 (Lead Technologies, Inc., Charlotte, NC, USA) to test for differences in overall survival between groups.…”

Section: Bioinformatics and Statistical Analysismentioning

confidence: 99%

DNA profiling analysis of 100 consecutive de novo acute myeloid leukemia cases reveals patterns of genomic instability that affect all cytogenetic risk groups

et al. 2007

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We have carried out a high-resolution whole genome DNA profiling analysis on 100 bone marrow samples from a consecutive series of de novo acute myeloid leukemia (AML) cases. After discarding copy number changes that are known to be genetic polymorphisms, we found that genomic aberrations (GA) in the form of gains or losses of genetic material were present in 74% of the samples, with a median of 2 GA per case (range 0-35). In addition to the cytogenetically detected aberration, GA were present in cases from all cytogenetic prognostic groups: 79% in the favorable group, 60% in the intermediate group (including 59% of cases with normal karyotype) and 83% in the adverse group. Five aberrant deleted regions were recurrently associated with cases with a highly aberrant genome (e.g., a 1.5 Mb deletion at 17q11.2 and a 750 kb deletion at 5q31.1). Different degrees of genomic instability showed a statistically significant impact on survival curves, even within the normal karyotype cases. This association was independent of other clinical and genetic parameters. Our study provides, for the first time, a detailed picture of the nature and frequency of DNA copy number aberrations in de novo AML.

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“…GSE3193 was made up from dual channel cDNA arrays and the others from single channel Affymetrix U133A platforms. To analyze the cDNA datasets, the missing values (!30%) were initially filtered out and imputed by the knearest neighbor method using a GEPAS web server [36]. The average values of gene expression were calculated from replicate probes.…”

Section: Transcriptomics Reveals Upregulations Of Coronin 1a and P34-mentioning

confidence: 99%

Proteomic analysis of breast cancer tissue reveals upregulation of actin‐remodeling proteins and its relevance to cancer invasiveness

Kim

Bae

Lee

et al. 2009

Proteomics Clinical Apps

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There is an emerging interest in protein expression profiling with the aim of identifying novel diagnostic markers and therapeutic targets in breast cancer. We analyzed breast cancer tissues by 2-D DIGE using a narrow range IPG strip (pH 5.5-6.7) after the immunodepletion of serum albumin and Ig. Sixty-three protein spots were detected with more than 61.8-fold differences (p ,0.05 for three technical replicates) from a set of tissue samples in which three tumor and three nontumor samples were randomly selected from six breast cancer subjects and pooled separately. Of these, 53 proteins were successfully identified by MS. Among the proteins whose levels were increased, we identified three novel WD-repeat-motifbearing proteins that have been known to be involved in actin remodeling: Arp2/3 complex subunit 2 (p34-Arc), coronin-1A and WD-repeat protein 1 (Wdr1). Significantly increased amounts of p34-Arc and coronin-1A in breast cancer were also shown by Western blot analysis of matched tumor and nontumor tissue samples (N = 11, p ,0.05), and were consistent with the mRNA levels retrieved from publicly available microarray databases. The siRNA knockdown of p34-Arc attenuated the invasion of SK-BR3 breast cancer cells into Matrigel. In contrast, the overexpression of coronin-1A increased this invasive activity. Taken together, the cellular levels of p34-Arc and coronin-1A were linked to cancer development and migration. The data obtained from the present study provides new insight into the management of breast cancer.

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GEPAS, an experiment-oriented pipeline for the analysis of microarray gene expression data

Cited by 84 publications

References 26 publications

Distinct genomic aberration patterns are found in familial breast cancer associated with different immunohistochemical subtypes

Distinct genomic aberration patterns are found in familial breast cancer associated with different immunohistochemical subtypes

DNA profiling analysis of 100 consecutive de novo acute myeloid leukemia cases reveals patterns of genomic instability that affect all cytogenetic risk groups

Proteomic analysis of breast cancer tissue reveals upregulation of actin‐remodeling proteins and its relevance to cancer invasiveness

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