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 |
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).
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).
TOX3 methylation in primary lung tumors was marginally more prevalent in never smokers compared to current or former smokers (pā=ā0.05).
TOX3 methylation in primary lung tumors was more prevalent in squamous cell carcinoma compared to adenocarcinoma (pā=ā0.05).