TABLE 2.
Site(s) | Sample type (total no.) | No. of samples showing:
|
% of amplifiable samples with methylation | |
---|---|---|---|---|
Methylation | No methylation | |||
Brazil | Asymptomatic (14) | 8 | 6 | 57.1 |
CIN I (3) | 0 | 3 | 0 | |
Invasive cancer (16) | 2 | 14 | 12.5 | |
New Mexico | Asymptomatic (11) | 5 | 6 | 45.4 |
CIN I (10) | 3 | 7 | 30 | |
CIN III (10) | 2 | 8 | 20 | |
Invasive cancer (17) | 0 | 17 | 0 | |
Bothb | Asymptomatic (25) | 13 | 12 | 52 |
CIN I and III (23) | 5 | 18 | 21.7 | |
Invasive cancer (33) | 2 | 31 | 6.1 |
CpG methylation was determined by cleavage of the DNA preparations with the restriction enzyme McrBC and subsequent PCR amplification of a genomic segment of HPV-16 corresponding to the promoter and E6 gene as shown in Fig. 3.
Data from both cohorts were combined, results with CIN I and CIN III were united into one group of precursor lesions, and DNA preparations that could not be amplified were omitted.