Fig. 5

Longitudinal ACs that progress to Smoldering ATL and descendants of ATL patients harbor FHIT methylation. a FHIT CpG island methylation occurs in both overt smoldering ATL patients (n = 13) and ACs that progressed to smoldering ATL (n = 10). FHIT methylation was determined by BGS and unmethylated and methylated alleles are noted by white and black boxes, respectively. Due to the limited number of smoldering ATL patient samples, some patients are duplicated from previous figures (Figs. 1b and 2d). For progressors, FHIT methylation was determined at the time the patient was an AC, not when the patient developed ATL. b Graphical representation of the overall percentage of methylated (M) CpG islands (n = 31) in the FHIT gene in smoldering (ATL-S) samples (n = 13) and ACs that developed smoldering ATL (n = 10). Patients are graphed from zero CpG islands methylated (0%) to complete CpG islands methylated (100%). The values plotted represent an average value from sequencing of several BGSs. p-values were calculated by one-way ANOVA statistical test between the two groups. The f-ratio value is 2.61176. The p-value is 0.12174. c PVL does not correlate with the level of FHIT CpG methylation. PVLs were calculated as a % (as determined in a previous study [9]). PVL % was plotted against the % CpGs methylated. Pearson’s correlation coefficient and resulting p-value are indicated. d The primary descendants of two HTLV-I positive, ATL patients harbor methylation of the FHIT gene. The methylation status of the FHIT gene was determined for the immediate family members of two ATL patients’ samples. Patient samples were analyzed by BGS. Squares and circles denote male and female patients, respectively. White, grey, and black shapes represent non-HTLV-I infected, HTLV-I positive asymptomatic, and HTLV-I positive ATL, patients, respectively. For patient one (ATL A), the father, was deceased, and further analysis of the FHIT gene could not be performed. The BGS for patient B4 is identical to patient “AC carrier” in Fig. 4b