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. 2012 Apr 4;7(4):e34850. doi: 10.1371/journal.pone.0034850

Table 1. Prevalence for promoter CpG island hypermethylation of TOX subfamily of genes.

Sample Type Methylated (%)
TOX TOX2 TOX3 TOX4
Normal tissue
NHBEC 0/20 (0) 0/20 (0) 0/20 (0) 0/20 (0)
HBEC 0/5 (0) 0/5 (0) 0/5 (0) 0/5 (0)
PBMC 0/10 (0) 0/10 (0) 0/10 (0) 0/10 (0)
DNLT 0/8 (0) 0/8 (0) 0/8 (0) 0/8 (0)
Breast cancer
Cell lines 3/4 (75) 3/4 (75) 2/4 (50) 0/4 (0)
Primary tumors 34/80 (43)A 18/80 (23) 24/80 (30)A ND
Lung cancer
Cell lines 4/20 (20) 4/20 (20) 5/20 (25) 0/20 (0)
Primary tumors 9/190 (5) 54/190 (28) 110/190 (58) ND
Adenocarcinoma 7/171 (4) 51/171 (30) 95/171 (56) ND
Current smokers 1/37 (3) 16/37 (43)B 18/37 (49) ND
Former smokers 4/59 (7) 17/59 (29) 29/59 (49) ND
Never smokers 2/75 (3) 18/75 (24) 48/75 (64)C ND
Squamous cell carcinoma 2/19 (11) 3/19 (16) 15/19 (79)D ND
A

Methylation of TOX was significantly more prevalent in breast than lung tumor (p<0.001). In contrast, TOX3 methylation was more common in lung than breast tumor (p<0.001).

B

Among NSCLC patients, the prevalence for TOX2 methylation in current smokers was significantly higher than never smokers (p<0.05) as well as current non-smokers (former and never smokers combined) (p<0.05).

C

TOX3 methylation in primary lung tumors was marginally more prevalent in never smokers compared to current or former smokers (pā€Š=ā€Š0.05).

D

TOX3 methylation in primary lung tumors was more prevalent in squamous cell carcinoma compared to adenocarcinoma (pā€Š=ā€Š0.05).