Pediatric Cancer

SS 14 - Pediatrics 2

101 - Increased Risk of Pseudoprogression Among Pediatric Low-Grade Glioma Patients Treated With Proton Versus Photon Radiation Therapy

Monday, October 22
11:05 AM - 11:15 AM
Location: Room 008

Increased Risk of Pseudoprogression Among Pediatric Low-Grade Glioma Patients Treated With Proton Versus Photon Radiation Therapy
E. B. Ludmir1, A. Mahajan2,3, A. C. Paulino3,4, J. Y. Jones4,5, L. Ketonen3, J. L. Ater3, J. M. Su4, D. R. Grosshans6, A. M. Adesina4, R. C. Dauser4, J. S. Weinberg3, and M. Chintagumpala4; 1The University of Texas MD Anderson Cancer Center, Division of Radiation Oncology, Houston, TX, 2Department of Radiation Oncology, Mayo Clinic, Rochester, MN, 3The University of Texas MD Anderson Cancer Center, Houston, TX, 4Texas Children's Cancer Center, Baylor College of Medicine, Houston, TX, 5Nationwide Children's Hospital, Columbus, OH, 6University of Texas MD Anderson Cancer Center, Houston, TX

Purpose/Objective(s): Pseudoprogression (PsP) is a recognized post-radiation therapy (RT) phenomenon for high-grade glioma, but is poorly characterized for low-grade glioma (LGG). We sought to evaluate magnetic resonance imaging (MRI) changes for pediatric patients treated with photon-based intensity-modulated RT (IMRT) or proton beam therapy (PBT) for LGG.

Materials/Methods: Eighty-three pediatric LGG patients managed at two institutions between 1998 and 2017 were identified, and serial MRI scans of these patients were evaluated. PsP was scored when a new or progressive contrast-enhancing lesion occurred within the RT field within the first year after RT, and subsequently decreased or stabilized in size for at least a year without therapy.

Results: Thirty-two patients (39%) were treated with IMRT, and 51 (61%) were treated with PBT. Median age at time of RT was 10.0 years (range 1.0 – 17.2). The most common diagnoses were pilocytic astrocytoma (50/83, 60%) and grade 2 astrocytoma (22/83, 27%). Median RT dose for the cohort was 50.4Gy(RBE) (range 45 – 59.4Gy[RBE]). No differences in age at RT, RT dose, treatment volume, or histology were identified between the IMRT and PBT groups. Post-RT radiographic tumor enlargement consistent with PsP was identified in 31 patients (37%), including 8/32 IMRT patients (25%) and 23/51 PBT patients (45%). PBT patients were significantly more likely to have PsP (HR 2.15, 95% confidence interval [CI] 1.06 – 4.38, p=0.048). RT dose ≥54Gy(RBE) similarly predicted higher rates of PsP (HR 3.93, 95% CI 1.29 – 12.00, p=0.016). No other analyzed variables predicted subsequent development of PsP (including age at RT, treatment volume, histology, and pre- or post-RT chemotherapy). On multivariable analysis, both treatment with PBT (HR 2.92, p=0.014) and RT dose ≥54Gy(RBE) (HR 3.69, p=0.003) remained significant predictors of PsP. For patients with PsP, radiographic enlargement peaked at a median of 4 months post-RT (range 1 – 8 months), with a median bidirectional diameter tumor increase of 22% (range 5 – 259%). Median time to stabilization was 12 months, with a median of 15 and 9.5 months to stabilization for the IMRT and PBT cohorts, respectively (p=0.001). Confirmed local progression occurred in 10 patients: 7/32 IMRT patients (22%) and 3/51 PBT patients (6%); 5-year local control rates were 78% and 90% for the IMRT and PBT patients, respectively, with a trend toward improved local control for patients treated with PBT (HR 0.34, 95% CI 0.10 – 1.18, p=0.099). Local progression occurred at a median of 39.8 months following RT (range 15.0 – 61.1 months).

Conclusion: These data highlight substantial rates of PsP among patients treated with PBT, and further follow-up may elucidate whether these higher rates of PsP are associated with improved local disease control. PsP should be considered when assessing response to RT in LGG, particularly within the first year after RT.

Author Disclosure: E.B. Ludmir: None. A. Mahajan: Secretary; PTCOG-NA. Membership; PROS. A.C. Paulino: Royalties for text book; Elsevier Inc. Committee Member; ABR. J.Y. Jones: Employee; PCCA. L. Ketonen: None. J.L. Ater: None. J.M. Su: None. D.R. Grosshans: None. A.M. Adesina: None. J.S. Weinberg: None. M. Chintagumpala: None.

Ethan Ludmir, MD

MD Anderson Cancer Center

Disclosure:
Employment
The University of Texas MD Anderson Cancer Center: Resident physician: Employee

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