spiapcc: SPIA-PCC: Signaling pathway impact analysis incorporated the...

Description Usage Arguments Details Examples

Description

This function uses the previous SPIA method and integrate the change of of genes Pearson coefficient(PCC) from two groups. We proposed a set of three pathway analysis methods based on the change of PCC. We applied these approaches to colorectal cancer, lung cancer and Alzheimer's disease datasets and so on.

Usage

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spiapcc(de = NULL, all = NULL, gse_madat2 = gse_madat2, normal = NULL,
  tumor = NULL, organism = "hsa", data.dir = NULL, pathids = NULL,
  nB = 2000, plots = FALSE, verbose = TRUE, beta = NULL,
  combine = "fisher", flag = -1)

Arguments

de

The number of differential genes

all

All genes in human

normal

the number of normal samples

tumor

the number of tumor samples

flag

flag = 1,0,-1 , if flag = 1 from normal to tumor, flag = -1 from tumor to normal, flag = 0 stand for absolute value between tow groups

Details

We used a compendium of 22 GEO datasets obtained from the KEGGdzPathwaysGEO and the KEGGandMetacoreDzPathwaysGEO benchmark sets(Tarca et al., 2012; Tarca et al., 2013) in this study. These datasets have been specifically chosen as they study a certain human disease in a corresponding KEGG pathway (e.g. Alzheimer's disease). These pathways are regarded as the target pathways in the following. We investigate first how well the individual set- and network-based methods detect the target

The expression data sets involved 11 conditions and 17 tissues.

Examples

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#import EnrichmentBrowser, KEGGandMetacoreDzPathwaysGEO, KEGGdzPathwaysGEO and SPIA package
library(EnrichmentBrowser)
library(KEGGandMetacoreDzPathwaysGEO)
library(SPIA)
data("GSE8671")
# Get expression profile of GSE8671
exprs_all <- exprs(GSE8671)
# Add the gene symbol
all.eset <- probe.2.gene.eset(GSE8671)
head(featureNames(all.eset))
before.norm <- exprs(all.eset)
# Gene normalization
all.eset <- normalize(all.eset, norm.method="quantile")
after.norm <- exprs(all.eset)
exprs_all1 <- data.frame(after.norm)
table(pData(all.eset)$Group)
pData(all.eset)$GROUP <- ifelse(pData(all.eset)$Group == "d", 1, 0)
normal <- length(which(pData(all.eset)$GROUP == '0'))
tumor <- length(which(pData(all.eset)$GROUP == '1'))
# Get the differential expression genes in limmar package
all.eset <- de.ana(all.eset)
head(fData(all.eset), n=4)
all_de <- fData(all.eset)
tg <- all_de[all_de$ADJ.PVAL < 0.1,]
DE_colorectal = tg$FC
names(DE_colorectal)<-as.vector(rownames(tg))
ALL_colorectal = rownames(all_de)
#The result of spia method
res_spia = spia(de = DE_colorectal, all=ALL_colorectal, organism="hsa",nB=2000,plots=FALSE,beta=NULL,combine="fisher",verbose=TRUE)
gse_madat2 <- exprs_all1
# The results of SPIA_PCC_NT method
res_nt = spiapcc(de=DE_colorectal, all=ALL_colorectal, gse_madat2 = gse_madat2,normal = normal, tumor = tumor,norganism="hsa",nB=2000,plots=FALSE,
                  beta=NULL,combine="fisher",verbose=T, flag = 1)
#The results of SPIA_PCC_TN method
res_tn = spiapcc(de=DE_colorectal, all=ALL_colorectal, gse_madat2 = gse_madat2, normal = normal, tumor = tumor,organism="hsa",nB=2000,plots=FALSE,
                  beta=NULL,combine="fisher",verbose=T, flag = -1)
#The results of SPIA_PCC_ABS method
res_abs = spiapcc(de = DE_colorectal, all=ALL_colorectal , gse_madat2 = gse_madat2,normal = normal, tumor = tumor,organism="hsa",nB=2000,plots=FALSE,
                  beta=NULL,combine="fisher",verbose=T, flag = 0)

eshinesimida/spiapcc documentation built on May 17, 2019, 6:11 a.m.