Progression was defined as 25% increase in the size of any measurable lesion; the appearance of a new lesion; or the conversion of negative cerebrospinal fluid (CSF) cytology to positive. Defined as the time interval from date on treatment until the date of first progression, medulloblastoma-related death or date of last contact for patients who have not experienced an event. All eligible medulloblastoma patients who received any methotrexate are included in this analysis.

All eligible medulloblastoma patients started methotrexate and were included (n=81). PFS estimates are reported by risk group.

Defined as the time interval from date on treatment until the date of first progression, medulloblastoma-related death or date of last contact for patients who have not experienced an event. Eligible medulloblastoma patients who received any methotrexate and had molecularly confirmed medulloblastoma are included in this analysis. Five patients were excluded as 3 had no archival tissue available and 2 were found to not be medulloblastoma by methylation profile.

Eligible patients with molecularly confirmed medulloblastoma (n=76) were included. PFS estimates are reported by methylation subgroup and risk group. There were no low-risk group 3 or group 4 patients.

Defined as the time interval from date on treatment until the date of first progression, second malignancy or death due to any cause; or date of last contact for patients who have not experienced an event. All eligible medulloblastoma patients who received any methotrexate are included in this analysis.

Eligible medulloblastoma patients (n=81) were included. EFS estimates are reported by risk group.

Amplifications and deletions (gains and losses) for chromosomes of interest are shown in the table of measured values.

Eligible medulloblastoma patients (n=81) were included in these analyses. 23 of 23 low risk patients had data available for this objective, as did 27/32 and 24/26 intermediate and high risk patients.

Gene alterations, which include single nucleotide variants (SNPs), amplifications, deletions, translocations, indels, and germline alterations are shown for specific genes of interest in the results table.

Eligible medulloblastoma patients (n=81) were included in these analyses. Not all patients had data available for each gene.

Alterations included single nucleotide variants (SNPs), amplifications, deletions, translocations, indels, and germline alterations. Cytogenetic information shows gains and losses as specified in the table of measured values.

Eligible patients with molecularly confirmed medulloblastoma (n=76) were included in these analyses. Not all patients had data available for each gene.

Successful collections will be defined as the number of patients who have frozen/fixed tumor samples available.

All eligible patients enrolled (n=290) were included in this analysis. The numbers of patients with pre-study samples were considered for these results.

EFS was measured from the date of initial treatment to the earliest date of disease progression, second malignancy or death for patients who fail; and to the date of last contact for patients who remain at risk for failure. 1-year EFS estimates are reported by risk group. EFS was compared to St. Jude historical cohorts by risk group using hazard ratios with 95% confidence intervals.

Eligible medulloblastoma patients who received any methotrexate were included in this analysis. Hazard ratios with 95% confidence intervals are reported and compare SJYC07 patients to historical controls in each risk group. As there were too few low-risk historical controls, no hazard ratio is included for the low-risk group.

OS was measured from the date of initial treatment to date of death or to date of last contact for survivors. 1-year OS estimates were reported by risk group. OS was compared to St. Jude historical cohorts by risk group using hazard ratios with 95% confidence intervals.

Eligible medulloblastoma patients who received any methotrexate were included in this analysis. Hazard ratios with 95% confidence intervals are reported and compare SJYC07 patients to historical controls in each risk group. As there were too few low-risk historical controls, no hazard ratio is included for the low-risk group.

For patients treated in the intermediate and high risk strata with residual or metastatic disease we will estimate the stratum-specific objective response rate (complete response (CR) or partial response [ PR]). All patients who receive at least 1 -dose of methotrexate are evaluable for response. Objective responses must be sustained for at least eight weeks.

Eligible intermediate and high risk group patients who received at least 1 dose of methotrexate were included in this analysis. One of the high risk patients did not start therapy and was excluded.

For the subset of patients with metastatic disease (high-risk group patients), during induction, the proportion percentage of courses during which subsequent chemotherapy administration was delayed for more than 7 days due to toxicity will be calculated. Patients were to receive 4 courses of induction and then consolidation chemotherapy.

Eligible high-risk group patients who started therapy were included in this analysis (n=76). 1 patient enrolled on the high-risk arm did not start therapy due to early disease progression and was excluded. Courses 2-4 of induction and the 1st consolidation course were used in this analysis. 76 patients (with 263 courses) were included.

For the subset of patients with metastatic disease (high-risk group patients), during consolidation, we will calculate the number and proportion of courses during which subsequent chemotherapy administration was delayed for more than 7 days due to toxicity. Patients were to received 2 courses of consolidation chemotherapy and then maintenance therapy.

Eligible high-risk group patients who started therapy were included. Course 2 of consolidation and the 1st course of maintenance were used in this analysis and assessed for delays >7 days due to toxicity. Of the 76 high-risk patients that started induction therapy, 50 started consolidation (with 47 courses included in this analysis).

For patients enrolled on the high-risk arm with measurable residual disease after induction treated with consolidation therapy, we will estimate the objective response (complete response (CR)/partial response (PR)) rate after consolidation therapy with a 95% confidence interval. Objective responses must be sustained for at least eight weeks. All patients who receive at least 1 dose of cyclophosphamide or topotecan during consolidation are evaluable for response.

Of the 50 high-risk patients that started consolidation chemotherapy, 38 had measurable residual disease after induction and were included in this result.

These data are based on patient diaries. For children <3 years of age, we will calculate the percentage of total scheduled doses each patient received per course for each of the oral maintenance courses and report the overall average number percentage of doses received per course across patients. If patients received all planned doses, their percentage would be 100%. If the average percentage was less than 75%, then feasibility would be in question.

Eligible patients less than 3 years of age (n=273) constituted the study population for this analysis; 167 of these patients started the first course of maintenance and were included in this analysis (50 low-risk, 87 intermediate-risk, and 30 high-risk patients).

Measures will be analyzed for intermediate risk participants who receive proton beam therapy (PBT) and who consent. This objective aims to assess the feasibility of using post-proton beam therapy (PBT) positron emission tomography (PET) as an in-vivo dosimetric and distal edge verification system in this patient population. To quantify the decay in signal, 134 scans from 53 patients were analyzed by recording the mean activation value (MAV), the average recorded PET signal from activation, within the target volume. With each patient being given the same dose, the percent standard deviation in the MAV can serve as a quantitative representation of signal loss due to radioactive decay.

Intermediate risk patients treated at St. Jude were eligible to receive proton beam therapy through referral to the University of Florida Proton Therapy Institute. Patients electing to receive PBT and post-treatment PET scans after the delivery of one treatment beam were included in the analysis.

Concentrations of various neurotransmitters in cerebrospinal fluid were measured at 5 timepoints. The median concentration of each neurotransmitter at each time point was calculated and provided with a full range.

Eligible patients who had cerebrospinal fluid neurotransmitter studies performed. Seventeen patients had studies performed.

Types of genetic polymorphisms of neurotransmitters were examined. We studied 3 genetic polymorphisms; these were types of genetic polymorphisms involved in dopamine metabolism. They were as follows: rs6323, rs4680, and rs6280.

Three genetic polymorphisms involved in dopamine metabolism (rs6323, rs4680, and rs6280) were studied in 17 patients with CNS neurotransmitter studies.

Frequencies of genetic polymorphisms were reported.

Eligible patients who had neurotransmitter studies performed. Seventeen patients had studies performed.

Endocrine screening and growth hormone (GH) testing were done in consenting intermediate risk patients at the end of induction therapy, the end of all therapy, and at 6, 12, 24, 36, 48, and 60 months off therapy. Endocrinopathy was defined as the presence of central hypothyroidism (free T4 concentration below normal with low or normal TSH concentration), growth hormone deficiency (peak growth hormone concentration below 5 ng/mL on dynamic testing), or ACTH deficiency (cortisol concentration below 14 ug/dL after low dose cosyntropin stimulation). Numbers of participants with endocrinopathy at each time point are reported. Please note the small numbers of participants with available data.

Endocrine screening and growth hormone (GH) testing were done in consenting intermediate risk patients.

Growth hormone secretion was measured in consenting intermediate risk patients at the end of induction therapy, the end of all therapy, and at 6, 12, 24, 36, 48, and 60 months off therapy. Mean growth hormone secretion values are reported by assessment time point. Please note the small numbers of participants with available data.

Growth hormone secretion was measured in consenting intermediate risk patients. No Intermediate Risk patients had data available at 12, 36, 48, and 60 months off therapy.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 1. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate clearance are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 1 and had samples collected for PK analysis

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 2. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate clearance are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 2 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 3. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate clearance are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 3 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 4. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate clearance are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 4 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 1. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate volume of central compartment are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 1 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 2. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate volume of central compartment are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 2 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 3. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate volume of central compartment are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 3 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 1. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate AUC0-66h (area under concentration curve from time 0 to 66 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 1 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 2. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate AUC0-66h (area under concentration curve from time 0 to 66 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 2 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 4. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate volume of central compartment are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 4 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 3. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate AUC0-66h (area under concentration curve from time 0 to 66 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 3 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 4. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate AUC0-66h (area under concentration curve from time 0 to 66 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 4 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 1. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate concentration at 42 hours post-dose are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 1 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 2. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate concentration at 42 hours post-dose are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 2 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 3. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate concentration at 42 hours post-dose are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 3 and had samples collected for PK analysis.

Methotrexate plasma concentration-time data are collected after the start of methotrexate infusion in induction cycle 4. Population parameters and inter-subject variability are estimated. Individual estimates of methotrexate concentration at 42 hours post-dose are obtained using post hoc analysis.

Eligible patients who received methotrexate during induction cycle 4 and had samples collected for PK analysis.

Cyclophosphamide plasma concentration-time data are collected on day 9 in one cycle of induction chemotherapy. Individual estimates of cyclophosphamide clearance are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during a cycle of induction therapy and had samples collected for PK analysis..

Cyclophosphamide plasma concentration-time data are collected in consolidation cycle 1. Individual estimates of cyclophosphamide clearance are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during consolidation cycle 1 and had samples collected for PK analysis.

Cyclophosphamide plasma concentration-time data are collected in consolidation cycle 2. Individual estimates of cyclophosphamide clearance are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during consolidation cycle 2 and had samples collected for PK analysis.

Cyclophosphamide plasma concentration-time data are collected on day 1 of maintenance cycle A1. Individual estimates of cyclophosphamide apparent oral clearance are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during maintenance cycle A1 and had samples collected for PK analysis.

Cyclophosphamide plasma concentration-time data are collected on day 9 in one cycle of induction chemotherapy. Individual estimates of cyclophosphamide AUC0-24h (area under concentration curve from time 0 to 24 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during a cycle of induction therapy and had samples collected for PK analysis.

Cyclophosphamide plasma concentration-time data are collected in consolidation cycle 1. Individual estimates of cyclophosphamide AUC0-24h (area under concentration curve from time 0 to 24 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during consolidation cycle 1 and had samples collected for PK analysis.

4-OH cyclophosphamide plasma concentration-time data are collected in consolidation cycle 1. Individual estimates of 4-OH cyclophosphamide AUC0-24h (area under concentration curve from time 0 to 24 hours post- dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during consolidation cycle 1 and had samples collected for PK analysis.

Cyclophosphamide plasma concentration-time data are collected in consolidation cycle 2. Individual estimates of cyclophosphamide AUC0-24h (area under concentration curve from time 0 to 24 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during consolidation cycle 2 and had samples collected for PK analysis.

Cyclophosphamide plasma concentration-time data are collected on day 1 of maintenance cycle A1. Individual estimates of cyclophosphamide AUC0-24h are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during maintenance cycle A1 and had samples collected for PK analysis.

4-OH cyclophosphamide plasma concentration-time data are collected on day 9 in one cycle of induction chemotherapy. Individual estimates of 4-OH cyclophosphamide AUC0-24h (area under concentration curve from time 0 to 24 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during a cycle of induction therapy and had samples collected for PK analysis.

4-OH cyclophosphamide plasma concentration-time data are collected in consolidation cycle 2. Individual estimates of 4-OH cyclophosphamide AUC0-24h (area under concentration curve from time 0 to 24 hours post- dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during consolidation cycle 2 and had samples collected for PK analysis.

4-OH cyclophosphamide plasma concentration-time data are collected on day 1 of maintenance cycle A1. Individual estimates of 4-OH cyclophosphamide AUC0-24h (area under concentration curve from time 0 to 24 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during maintenance cycle A1 and had samples collected for PK analysis.

Carboxyethylphosphoramide mustard (CEPM) plasma concentration-time data are collected on day 9 in one induction cycle. Individual estimates of CEPM AUC0-24h (area under concentration curve from time 0 to 24 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during a cycle of induction therapy and had samples collected for PK analysis.

Carboxyethylphosphoramide mustard (CEPM) plasma concentration-time data are collected in consolidation cycle 1. Individual estimates of CEPM AUC0-24h (area under concentration curve from time 0 to 24 hours post- dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during consolidation cycle 1 and had samples collected for PK analysis.

Carboxyethylphosphoramide mustard (CEPM) plasma concentration-time data are collected in consolidation cycle 2. Individual estimates of CEPM AUC0-24h (area under concentration curve from time 0 to 24 hours post- dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during consolidation cycle 2 and had samples collected for PK analysis.

Carboxyethylphosphoramide mustard (CEPM) plasma concentration-time data are collected on day 1 of maintenance cycle A1. Individual estimates of CEPM AUC0-24h (area under concentration curve from time 0 to 24 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received cyclophosphamide during maintenance cycle A1 and had samples collected for PK analysis.

Number of participants who successfully achieve target systemic exposure of intravenous topotecan after an empiric dosage during consolidation phase of therapy are reported.

Eligible patients who received topotecan with empirical dosage during consolidation therapy were included in this analysis. Per protocol, low-risk and intermediate-risk patients did not receive topotecan during consolidation unless they experienced disease progression during induction. One such intermediate-risk patient was included.

Number of participants who successfully achieve target systemic exposure of intravenous topotecan after a pharmacokinetic-guided dosage adjustment during consolidation phase of therapy are reported.

Eligible patients who received topotecan with PK-guided dosage adjustment during consolidation therapy were included in this analysis. Per protocol, low-risk and intermediate-risk patients did not receive topotecan during consolidation unless they experienced disease progression during induction. One such intermediate-risk patient was included.

Topotecan plasma concentration-time data are collected on day 1 of consolidation cycle 1 after a single IV dose. Individual estimates of topotecan clearance are obtained using post hoc analysis.

Eligible patients who received intravenous topotecan during consolidation cycle 1 and had PK samples collected were included in this analysis. Per protocol, low- and intermediate-risk patients did not receive topotecan during consolidation unless they experienced disease progression during induction. One such intermediate-risk patient was included.

Topotecan plasma concentration-time data are collected on day 1 of maintenance cycle A1 after a single oral dose. Individual estimates of topotecan apparent oral clearance are obtained using post hoc analysis.

Eligible patients who received oral topotecan during maintenance therapy cycle A1 and had samples collected for PK analysis.

Topotecan plasma concentration-time data are collected on day 1 of consolidation cycle 1 after a single IV dose. Individual estimates of topotecan AUC0-24h (area under concentration curve from time 0 to 24 hours post- dose) are obtained using post hoc analysis.

Eligible patients who received intravenous topotecan during consolidation cycle 1 and had PK samples collected were included in this analysis. Per protocol, low- and intermediate-risk patients did not receive topotecan during consolidation unless they experienced disease progression during induction. One such intermediate-risk patient was included.

Topotecan plasma concentration-time data are collected on day 1 of maintenance cycle A1 after a single oral dose. Individual estimates of topotecan AUC0-24h (area under concentration curve from time 0 to 24 hours post- dose) are obtained using post hoc analysis.

Eligible patients who received oral topotecan during maintenance therapy cycle A1 and had samples collected for PK analysis.

Erlotinib plasma concentration-time data are collected on day 1 of maintenance cycle B2. Individual estimates of erlotinib apparent oral clearance are obtained using post hoc analysis.

Eligible patients who received oral erlotinib during maintenance therapy cycle B2 and had samples collected for PK analysis.

Erlotinib plasma concentration-time data are collected on day 1 of maintenance cycle B2. Individual estimates of erlotinib apparent volume of central compartment are obtained using post hoc analysis.

Eligible patients who received oral erlotinib during maintenance therapy cycle B2 and had samples collected for PK analysis.

Erlotinib plasma concentration-time data are collected on day 1 of maintenance cycle B2. Individual estimates of erlotinib AUC0-24h (area under concentration curve from 0 to 24 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received oral erlotinib during maintenance therapy cycle B2 and had samples collected for PK analysis.

Erlotinib metabolite OSI-420 plasma concentration-time data are collected on day 1 of maintenance cycle B2. Individual estimates of OSI-420 AUC0-24h (area under concentration curve from 0 to 24 hours post-dose) are obtained using post hoc analysis.

Eligible patients who received oral erlotinib during maintenance therapy cycle B2 and had samples collected for PK analysis.

Local failure was defined as the interval from end of RT to date of local failure (or combined local + distant failure). Competing events were distant failure or second malignancy. Patients without an event were censored at date of last contact. The 1-year cumulative incidence was estimated and reported with a 95% confidence interval.

Eligible intermediate-risk patients who received focal radiation were included in this analysis. Of the 156 intermediate risk patients, 121 started radiation.

Distant failure was defined as the interval from end of RT to date of distant failure (or combined local + distant failure). Competing events were local failure or second malignancy. Patients without an event were censored at date of last contact. The 1-year cumulative incidence was estimated and reported with a 95% confidence interval.

Eligible intermediate-risk patients who received focal radiation were included in this analysis. Of the 156 intermediate risk patients, 121 started radiation.

Global cognitive functioning was measured based on Cognitive Composite Scores from the Bayley III instrument for subjects <3 years of age and on estimated IQ scores from the Stanford Binet V instrument for subjects ≥3 years of age. Higher scores indicate better performance. The normative mean is 100 with a standard deviation of 15.

Eligible patients with scores at any of the data collection timepoints were included. Sample sizes differ across timepoints as not all subjects had scores for all timepoints.

Scores measuring attention were obtained from the Attention Problems T-score on the BASC-2 instrument which is a parent report. Higher scores indicate more attention problems. The normative mean is 50 with a standard deviation of 10.

Eligible patients with scores at any of the data collection timepoints were included. Sample sizes differ across timepoints as not all subjects had scores for all timepoints.

Scores measuring processing speed were obtained based on the visual matching standard score from the Woodcock Johnson III instrument. Higher scores indicate better performance. The normative mean is 100 with a standard deviation of 15.

Eligible patients with scores at any of the data collection timepoints were included. Sample sizes differ across timepoints as not all subjects had scores for all timepoints.

Scores measuring executive functioning were obtained from Global Executive Composite (GEC) T-scores, which were obtained from the Behavior Rating Inventory of Executive Function (BRIEF) instrument which is a parent report. Higher scores indicate more problems. The normative mean is 50 with a standard deviation of 10.

Eligible patients with scores at any of the data collection timepoints were included. Sample sizes differ across timepoints as not all subjects had scores for all timepoints.

Scores measuring working memory were obtained from Working Memory T-scores, which were obtained from the Behavior Rating Inventory of Executive Function (BRIEF) instrument which is a parent report. Higher scores indicate more problems. The normative mean is 50 with a standard deviation of 10.

Eligible patients with scores at any of the data collection timepoints were included. Sample sizes differ across timepoints as not all subjects had scores for all timepoints.

Scores measuring verbal fluency were obtained from Retrieval Fluency standard scores on the Woodcock Johnson III instrument. Higher scores indicate better performance. The normative mean is 100 with a standard deviation of 15.

Eligible patients with scores at any of the data collection timepoints were included. Sample sizes differ across timepoints as not all subjects had scores for all timepoints.

Scores measuring visual-spatial reasoning were obtained from VMI T-scores on the Beery VMI instrument. Higher scores indicate better performance. The normative mean is 50 with standard deviation of 10.

Eligible patients with scores at any of the data collection timepoints were included. Sample sizes differ across timepoints as not all subjects had scores for all timepoints.

Scores measuring visual-spatial reasoning were obtained from Visual Perception T-scores on the Beery Visual Motor Integration (VMI) instrument. Higher scores indicate better performance. The normative mean is 50 with a standard deviation of 10.

Eligible patients with scores at any of the data collection timepoints were included. Sample sizes differ across timepoints as not all subjects had scores for all timepoints.

Quantitative MRI measures Fractional Anisotropy (FA) change per month in right frontal-lobe over time in each risk group will be assessed using a random effects model incorporating various covariates. Covariates to be considered include age at diagnosis, time since diagnosis and risk-arm. Differences in quantitative MRI measures of neurostructure volume and integrity between patient groups will be evaluated as a metric of structural neurotoxicity of therapy.

Fractional anisotropy (FA) is a scalar unitless measure that quantifies the degree of anisotropy of a diffusion process, particularly in the context of diffusion tensor imaging (DTI) used in MRI scans. FA values range from 0 to 1

Eligible infratentorial medulloblastoma, ependymoma, and pineoblastoma patients(n=75) were included.

Quantitative MRI measures Fractional Anisotropy (FA) change per month in left frontal lobe over time in each risk group will be assessed using a random effects model incorporating various covariates. Covariates to be considered include age at diagnosis, time since diagnosis and risk-arm. Differences in quantitative MRI measures of neurostructure volume and integrity between patient groups will be evaluated as a metric of structural neurotoxicity of therapy.

Fractional anisotropy (FA) is a scalar unitless measure that quantifies the degree of anisotropy of a diffusion process, particularly in the context of diffusion tensor imaging (DTI) used in MRI scans. FA values range from 0 to 1

Eligible infratentorial medulloblastoma, ependymoma, and pineoblastoma patients(n=75) were included.

Quantitative MRI measures Fractional Anisotropy (FA) change per month in right parietal lobe over time in each risk group will be assessed using a random effects model incorporating various covariates. Covariates to be considered include age at diagnosis, time since diagnosis and risk-arm. Differences in quantitative MRI measures of neurostructure volume and integrity between patient groups will be evaluated as a metric of structural neurotoxicity of therapy.

Fractional anisotropy (FA) is a scalar unitless measure that quantifies the degree of anisotropy of a diffusion process, particularly in the context of diffusion tensor imaging (DTI) used in MRI scans. FA values range from 0 to 1

Eligible infratentorial medulloblastoma, ependymoma, and pineoblastoma patients(n=75) were included.

Quantitative MRI measures Fractional Anisotropy (FA) change per month in left parietal lobe over time in each risk group will be assessed using a random effects model incorporating various covariates. Covariates to be considered include age at diagnosis, time since diagnosis and risk-arm. Differences in quantitative MRI measures of neurostructure volume and integrity between patient groups will be evaluated as a metric of structural neurotoxicity of therapy.

Fractional anisotropy (FA) is a scalar unitless measure that quantifies the degree of anisotropy of a diffusion process, particularly in the context of diffusion tensor imaging (DTI) used in MRI scans. FA values range from 0 to 1

Eligible infratentorial medulloblastoma, ependymoma, and pineoblastoma patients(n=75) were included

Quantitative MRI measures Fractional Anisotropy (FA) change per month in right occipital lobe over time in each risk group will be assessed using a random effects model incorporating various covariates. Covariates to be considered include age at diagnosis, time since diagnosis and risk-arm. Differences in quantitative MRI measures of neurostructure volume and integrity between patient groups will be evaluated as a metric of structural neurotoxicity of therapy.

Fractional anisotropy (FA) is a scalar unitless measure that quantifies the degree of anisotropy of a diffusion process, particularly in the context of diffusion tensor imaging (DTI) used in MRI scans. FA values range from 0 to 1

Eligible infratentorial medulloblastoma, ependymoma, and pineoblastoma patients(n=75) were included.

Quantitative MRI measures Fractional Anisotropy (FA) change per month in left occipital lobe over time in each risk group will be assessed using a random effects model incorporating various covariates. Covariates to be considered include age at diagnosis, time since diagnosis and risk-arm. Differences in quantitative MRI measures of neurostructure volume and integrity between patient groups will be evaluated as a metric of structural neurotoxicity of therapy.

Fractional anisotropy (FA) is a scalar unitless measure that quantifies the degree of anisotropy of a diffusion process, particularly in the context of diffusion tensor imaging (DTI) used in MRI scans. FA values range from 0 to 1

Eligible infratentorial medulloblastoma, ependymoma, and pineoblastoma patients(n=75) were included.

Quantitative MRI measures Fractional Anisotropy (FA) change per month in right temporal lobe over time in each risk group will be assessed using a random effects model incorporating various covariates. Covariates to be considered include age at diagnosis, time since diagnosis and risk-arm. Differences in quantitative MRI measures of neurostructure volume and integrity between patient groups will be evaluated as a metric of structural neurotoxicity of therapy.

Fractional anisotropy (FA) is a scalar unitless measure that quantifies the degree of anisotropy of a diffusion process, particularly in the context of diffusion tensor imaging (DTI) used in MRI scans. FA values range from 0 to 1

Eligible infratentorial medulloblastoma, ependymoma, and pineoblastoma patients(n=75) were included.

Quantitative MRI measures Fractional Anisotropy (FA) change per month in left temporal lobe over time in each risk group will be assessed using a random effects model incorporating various covariates. Covariates to be considered include age at diagnosis, time since diagnosis and risk-arm. Differences in quantitative MRI measures of neurostructure volume and integrity between patient groups will be evaluated as a metric of structural neurotoxicity of therapy.

Fractional anisotropy (FA) is a scalar unitless measure that quantifies the degree of anisotropy of a diffusion process, particularly in the context of diffusion tensor imaging (DTI) used in MRI scans. FA values range from 0 to 1

Eligible infratentorial medulloblastoma, ependymoma, and pineoblastoma patients(n=75) were included.

Quantitative MRI measures Fractional Anisotropy (FA) change per month in frontal lobe over time in each risk group will be assessed using a random effects model incorporating various covariates. Covariates to be considered include age at diagnosis, time since diagnosis and risk-arm. Differences in quantitative MRI measures of neurostructure volume and integrity between patient groups will be evaluated as a metric of structural neurotoxicity of therapy.

Fractional anisotropy (FA) is a scalar unitless measure that quantifies the degree of anisotropy of a diffusion process, particularly in the context of diffusion tensor imaging (DTI) used in MRI scans. FA values range from 0 to 1

Eligible infratentorial medulloblastoma, ependymoma, and pineoblastoma patients(n=75) were included.

Quantitative MRI measures Fractional Anisotropy (FA) change per month in right frontal-parietal region over time in each risk group will be assessed using a random effects model incorporating various covariates. Covariates to be considered include age at diagnosis, time since diagnosis and risk-arm. Differences in quantitative MRI measures of neurostructure volume and integrity between patient groups will be evaluated as a metric of structural neurotoxicity of therapy.

Fractional anisotropy (FA) is a scalar unitless measure that quantifies the degree of anisotropy of a diffusion process, particularly in the context of diffusion tensor imaging (DTI) used in MRI scans. FA values range from 0 to 1

Eligible infratentorial medulloblastoma, ependymoma, and pineoblastoma patients(n=75) were included.