Risk and survival outcomes of radiation-induced CNS tumors

Abstract

Patients treated with cranial radiation are at risk of developing secondary CNS tumors. Understanding the incidence, treatment, and long-term outcomes of radiation-induced CNS tumors plays a role in clinical decision-making and patient education. Additionally, as meningiomas and pituitary tumors have been detected at increasing rates across all ages and may potentially be treated with radiation, it is important to know and communicate the risk of secondary tumors in children and adults. After conducting an extensive literature search, we identified publications that report incidence and long-term outcomes of radiation-induced CNS tumors. We reviewed 14 studies in children, which reported that radiation confers a 7- to 10-fold increase in subsequent CNS tumors, with a 20-year cumulative incidence ranging from 1.03 to 28.9 %. The latency period for secondary tumors ranged from 5.5 to 30 years, with gliomas developing in 5-10 years and meningiomas developing around 15 years after radiation. We also reviewed seven studies in adults, where the two strongest studies showed no increased risk while the remaining studies found a higher risk compared to the general population. The latency period for secondary CNS tumors in adults ranged from 5 to 34 years. Treatment and long-term outcomes of radiation-induced CNS tumors have been documented in four case series, which did not conclusively demonstrate that secondary CNS tumors fared worse than primary CNS tumors. Radiation-induced CNS tumors remain a rare occurrence that should not by itself impede radiation treatment. Additional investigation is needed on the risk of radiation-induced tumors in adults and the long-term outcomes of these tumors.

Molecular and translational advances in meningiomas

“…91,92 Children who have received only 1-2 Gy of radiation are at a 9.5-fold increased risk of developing a meningioma in their lifetime. 93 These tumors exhibit concerning histopathological features, such as hypercellularity, pleomorphic nuclei, and increased mitotic index, 91,94 Neuro-Oncology and in line with this, display aggressive clinical phenotype with increased tumor recurrence rates. 91,93,94 The mutational signature of RIMs is distinct from their sporadic counterparts.…”

“…93 These tumors exhibit concerning histopathological features, such as hypercellularity, pleomorphic nuclei, and increased mitotic index, 91,94 Neuro-Oncology and in line with this, display aggressive clinical phenotype with increased tumor recurrence rates. 91,93,94 The mutational signature of RIMs is distinct from their sporadic counterparts. 91,95 RIMs invariably have a more complex cytogenetic architecture, with higher rates of recurrent losses of chromosomes 1p and 22q in comparison to sporadic meningiomas.…”

Dosimetry of the brain and hypothalamus predicting acute lymphopenia and the survival of glioma patients with postoperative radiotherapy

“…This comprehensive therapy modality causes 40% of high‐grade glioma (HGG) patients to develop severe lymphopenia (grade III‐IV toxicity) within 2 months after course initiation . The state of immunosuppression is persistent and detrimentally affects patients with increased susceptibility to opportunistic infections, additional risk of secondary central nervous system (CNS) tumors, and deteriorated survival time …”

Therapeutic radiation for childhood cancer drives structural aberrations of NF2 in meningiomas

“…1990; Lee et al 2 2004). These tumors occur 10–30 years following radiotherapy for primary childhood cancer 3 – 5 , and demonstrate distinct and more aggressive clinical features than sporadic meningiomas 6 – 14 . Furthermore, RIMs display more aggressive clinicaland biologic behavior than sporadic meningiomas, including higher recurrence rates, greater cellularity, more pleomorphic nuclei and frequent mitoses, and are more often atypical and multifocal 6 – 14 .…”