Table 1.

Strand asymmetry of CpG transitions in p53 genes: Gene resolution

CpG transition class
Silent CpG transitions
Germ line p53 retropseudogenes
p53 genes in human tumors*
Nonsilent CpG transitions
Germinal, including Li–Flaumeni syndrome
Singlets in human tumors
Multiplets in human tumors
Multiplets with silent hitchhikers†

p53 doublets composed of nonsilent CpG  transitions	↓ Homostrand C → T, C → T	↘↙ Heterostrand C → T, G → A	↓ Homostrand G → A, G → A
All cancers in databases (13, 20)‡	5	26	6
Colorectal and skin cancers	4	4	2
All but colorectal and skin cancers§	1	22	4

^*Although the sample size is too small for reliable statistical inference, the observed ratio (6 C → T:12 G → A) fits the expected ratio of 1:2 (Td hypothesis) much better than 1:1 (Rd hypothesis). 

^†Three multiplets from “p53 late” colorectal cancers are excluded. Similarly, although the sample size is too small, the observed data do not fit the 1:1 ratio predicted by the Rd hypothesis. 

^‡A nonparametric goodness of fit test was performed to ascertain the significance of the deviation from 1:2:1 ratio predicted by the Rd hypothesis. It was found significant at the 93.6% level (0.064 P value), an almost significant deviation from the 1:2:1 ratio. 

^§Same, with 0.005 P value (indicating highly significant deviation from the 1:2:1 ratio).