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. 2018 Jun 30;8(6):e020427. doi: 10.1136/bmjopen-2017-020427

Table 2.

Models aiming to predict progression to OADC

Author/year Study type Patient no (P:NP) Model used Result
Clément et al 200635 Retrospective cohort 28*
(12:16)
APC+TIMP3+TERT Hypermethylation in P versus NP (P 81% vs NP 26% P<0.0001)
Jin et al 200941 Retrospective cohort 195*
(50:145)
Biomarker panel (p16, HPP1, RUNX3, CDH13, TAC1, NELL1, AKAP12, SST) AUROC 0.72
Biomarker panel+age
(p16, HPP1, RUNX3, CDH13, TAC1, NELL1, AKAP12, SST)
AUROC 0.85
Sato et al 200840 Retrospective cohort 62
(28:34)
Methylation index (p16, HPP1, RUNX3) Hypermethylation in P versus NP
AUROC 0.75 (no CI stated)
Methylation index (p16, HPP1, RUNX3), segment length, pathology AUROC 0.79
(95% CI 0.6968 to 0.8853)
Sensitivity 91.4
Specificity 51.8
Schulmann et al 200539 Retrospective cohort 53
(8:45)
Age, segment length, HPP1, TIMP3, APC, p16, CRBP1, RUNX3 HPP1, p16, RUNX3 independent risk factors in multivariate analyses
Model combined HR index >5 leads to an increased likelihood of progression within 2 years
Wang et al 200938 Retrospective cohort 57
(7:50)
P16+APC Hypermethylation of both APC and p16 OR 14.97 (95% CI 1.73 to ∞, P=0.012) for neoplastic progression

*Number of lesions, no patient numbers described in the study; number of progressor lesions (P), number of non-progressor lesions (NP).

AUROC, area under receiver operating characteristic; NP, non-progressing patients; OADC, oesophageal adenocarcinoma; P, progressing patients.