In our dataset, a threshold concentration of 370 pg/mL revealed the optimal combination of specificity (80%) and sensitivity (56%) in predicting SVR patients. We then determined our optimal IP-10 level to correctly predict both SVR as well as nonresponse. A threshold value of 550 pg/mL yielded the

highest rate of true positives or negatives (69%), and correlated well with the 600 pg/mL cutoff (68% true positives or negatives predicted in our dataset). Finally, logistic regression analysis Selleckchem Selumetinib of pretreatment IP-10 concentrations enabled fitting the probability of SVR for specific IP-10 levels measured in individual patients, and demonstrated a highly significant effect of IP-10 (P< 0.0001; Supporting Fig. 1, gray curve). When comparing pretreatment IP-10 serum levels of CA and AA patients, no significant differences were observed in separate analyses of responders (P = 0.75) and nonresponders (P = 0.97) (Table 1).

The significant (P = 0.015) difference in baseline serum IP-10 level between CA and AA patients that was observed in the overall buy Ferrostatin-1 study cohort can most likely be explained by the unbalanced composition of the cohort (IFN treatment response rate in the CA subgroup was 75% versus 40% in the AA subgroup). The highly significant difference in IP-10 serum level between responders and nonresponders to IFN therapy was found both in CA and AA patients (Table 1). Logistic regression analyses of baseline IP-10 levels were used to generate treatment response curves for CA and AA patients (Supporting Fig. 1). The response curves for AA and CA patients revealed a significant effect of both IP-10 (P< 0.0001) and race (P< 0.0001), but no significant interaction between IP-10 and race (P = 0.08). Of the 210 patients genotyped, 30% were CC, 49% were CT, and 21% were TT. A significant association between IL28B

see more genotype and treatment response was observed: corresponding SVR rates were 87% for CC, 50% for CT, and 39% for TT (P< 0.0001) (Table 2). For CA patients, 49% were CC with an SVR of 91%, 41% were CT with an SVR of 67%, and 10% were TT with an SVR of 45% (P< 0.001). For AA patients, only 9% were CC with an SVR of 67%, 58% were CT with an SVR of 35%, and 33% were TT with an SVR of 36% (P = 0.20). Mean serum IP-10 levels were similar for all patients regardless of IL28B genotype both in CA patients (P = 0.27) and AA patients (P = 0.58) (Fig. 2). This lack of correlation between serum IP-10 and IL28B genotype indicates that the associations with SVR observed for both of these markers are independent. Using the 600 pg/mL cutoff for pretreatment IP-10 levels, the SVR rate for our cohort of patients with both serum IP-10 and IL28B genotype data available (n = 210) was 69% for those with a low IP-10 level (<600 pg/mL) and 35% for those with a high IP-10 level (>600 pg/mL) (P< 0.0001).