Table 4.
PFS multivariate modeling of clinical, histologic, and molecular factors in pediatric low-grade gliomas
| Variable | HR | 95% CI | P | Variable | HR | 95% CI | P |
|---|---|---|---|---|---|---|---|
| Age <5 y | 1.58 | 0.72–3.44 | .25 | Age <5 y | 1.45 | 0.67–3.28 | .32 |
| Midline location | 3.87 | 1.84–8.11 | .0003 | Midline location | 4.60 | 2.18–9.69 | .0001 |
| Grade I vs II | 1.65 | 0.45–6.00 | .45 | Grade I vs II | 1.54 | 0.45–5.26 | .49 |
| P53 high | 1.53 | 0.66–3.54 | .32 | P53 high | 1.40 | 0.56–3.49 | .47 |
| P16 deleted | 2.88 | 1.03–8.08 | .04 | P16 deleted | 2.50 | 0.91–6.82 | .07 |
| MIB1 >10% | 2.29 | 0.98–5.33 | .05 | MIB1 >10% | 1.87 | 0.77–4.55 | .17 |
| BRAF rearranged | 0.64 | 0.29–1.42 | .27 | BRAF V600E | 2.39 | 0.93–6.15 | .07 |
| Age <5 y | 1.25 | 0.57–2.75 | .57 | Age <5 y | 1.57 | 0.70–3.53 | .27 |
| Midline location | 3.98 | 1.78–8.92 | .0008 | Midline location | 4.54 | 2.08–9.91 | .0001 |
| Grade I vs II | 1.56 | 0.42–5.82 | .51 | Grade I vs II | 1.96 | 0.53–7.21 | .31 |
| P53 high | 1.48 | 0.59–3.73 | .40 | P53 high | 1.60 | 0.63–4.07 | .32 |
| P16 deleted | 2.37 | 0.82–6.80 | .11 | P16 deleted | 3.25 | 1.09–9.65 | .03 |
| MIB1 >10% | 2.01 | 0.81–4.98 | .13 | MIB1 >10% | 2.19 | 0.89–5.42 | .09 |
| Any BRAF abnormality | 0.78 | 0.32–1.91 | .59 | BRAF rearranged | 0.54 | 0.23–1.25 | .15 |
| BRAF V600E | 2.48 | 0.94–6.56 | .07 | ||||
Abbreviations: HR, hazard ratio; CI, confidence interval.
Several models of progression-free survival (PFS) showed that the most consistent powerful marker of shorter PFS was a tumor located in the midline vs either cerebellum or cerebrum. The strongest molecular marker for reduced PFS was homozygous p16 deletion, while high MIB1 similarly trended toward shorter PFS. Interestingly, BRAF rearrangement trended weakly toward longer PFS, yet BRAF V600E strongly trended toward shorter PFS. No variable showed independent prognostic significance for OS in any model. N = 104 (upper left), 96 (upper right), 97 (lower left), and 90 (lower right).