Skip to main content

Table 1 Overrepresentation of different classes of genes (GWAS-associated genes or smoking response genes as defined in the smoking reversibility analysis section) in the regulatory network of four TFs

From: Smoking-associated gene expression alterations in nasal epithelium reveal immune impairment linked to lung cancer risk

GWAS genes

Response genes

  

Hard threshold

Lenient threshold

No threshold

All genes

TF

Regulon size

# Hit

FDR

# Hit

FDR

# Hit

FDR

# Hit

P-value

FDR

IRF1

318

10 (1.5)

2.9 1e−07

34 (12.5)

2.0 1e−07

83 (60)

0.07

37 (11.5)

5.19 1e−11

7.67 1e−08

CIITA

372

9 (1.5)

2.4e−08

26 (13)

0.08

83 (69)

1

45 (13.2)

1.31 1e−13

1.96 1e−10

SPIB

174

6 (0.5)

2.9e−04

14 (5.8)

0.6

43 (30.7)

1

14 (6.16)

0.0013

NS

ETV7

171

4 (0.8)

0.088

14 (5.4)

0.5

35 (28.7)

1

14 (6.08)

0.0011

NS

  1. Regulon size, the number of genes in the regulatory network for each TF; # hit, the number of genes, among each TF regulatory network that we annotate as a GWAS-linked gene (in parenthesis: expected number of GWAS genes in the regulatory network of the TF); FDR, false discovery rate of the overrepresentation of GWAS hits in the TF regulatory network (hypergeometric test; see the ‘Methods’ section). For the GWAS genes, each test is performed for 3 sets of genes defined using a hard (P < 1e−06; 44 genes); lenient (P < .05; 569 genes) or no threshold (3181 genes) on eQTL significance levels. For the ‘response genes’, only one test is performed with all the response genes