On the genetic involvement of apoptosis-related genes in Crohn's disease as revealed by an extended association screen using 245 markers: no evidence for new predisposing factors

Table 2 P values for microsatellite markers located intragenically or in the immediate vicinity of represented genes after the initial step and individual genotyping.

	p values
gene (as represented by the respective marker)	after analysis with pooled DNA	after summation of alleles beneath 5%	after analyses of each single allele (most significant allele)	after individual genotyping ¹ (p ^c value)	after correction by Q-value of pooled data
FLIP	0.2871	0.1936	0.0100	0.0044 (p^c > 0.05; c = 9)	n.s.
BCL2A1	0.0948	0.0948	0.0275	n.s.	n.s.
BAG1	0.2541	0.2541	0.0163	n.s.	n.s.
BPI	0.0011	0.0011	0.0031	n.s.	n.s.
erbB3	0.0760	0.0932	0.0100	n.s.	n.s.
TP73	0.5928	0.3535	0.0302	n.s.	n.s.
TLR9	0.3004	0.3004	0.0300	n.s.	n.s.
TNFRSF17	0.0012	0.0014	0.0014	0.0012 (p^c < 0.01; c = 6)	n.s.
CARD15	0.0083	0.0247	0.0054	0.0050 (p^c < 0.04; c = 7)	n.s.

P values were generated using three different procedures as described in the methods' section. Briefly, data were analysed by means of contingency tables, initially comparing allele distributions represented by the AIF (after analyses with pooled DNA), then after summation of alleles < 5% in order to focus on the major alleles and, finally, after comparison of each single allele between the control and patient cohorts. For analysing the results of the individual genotyping χ² testing was utilised.
¹Genotyping was performed with the same individuals used in the pooling procedure, and, when remaining significant, further individuals were added to the analyses (FLIP: CD = 134, controls = 150; TNFRSF17: CD = 147, controls = 135; CARD15: CD = 144, controls = 165).

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