Netteke Schouten-van Meeteren

Princess Máxima Center

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Helena J. H. van der Pal

Princess Máxima Center

Jan Köster

Amsterdam University Medical Centers

Wim J. E. Tissing

Princess Máxima Center

Cécile M. Ronckers

Johannes Gutenberg University Mainz

Jop C. Teepen

Princess Máxima Center

Leontien C.M. Kremer

Emma Kinderziekenhuis

Eelco W. Hoving

Princess Máxima Center

Lisanne C. Verbruggen

Princess Máxima Center

Nicole J. Ullrich

Boston Children's Hospital

Meike W. Vernooij

Erasmus University Rotterdam

Cooperative Institutions

Princess Máxima Center

Amsterdam University Medical Centers

University of Amsterdam

Emma Kinderziekenhuis

Academic Medical Center

University Medical Center Utrecht

Amsterdam UMC Location VUmc

Vrije Universiteit Amsterdam

Cancer Center Amsterdam

Utrecht University

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MEK/MELK inhibition and blood–brain barrier deficiencies in atypical teratoid/rhabdoid tumors

Neuro-Oncology (2019)

Michaël H. Meel Míriam Guillén Navarro Mark C. de Gooijer Dennis S. Metselaar Piotr Waranecki

Atypical teratoid/rhabdoid tumors (AT/RT) are rare, but highly aggressive. These entities are of embryonal origin occurring in the central nervous system (CNS) of young children. Molecularly these tumors are driven by a single hallmark mutation, resulting in inactivation of SMARCB1 or SMARCA4. Additionally, activation of the MAPK signaling axis and preclinical antitumor efficacy of its inhibition have been described in AT/RT.We established and validated a patient-derived neurosphere culture and xenograft model of sonic hedgehog (SHH) subtype AT/RT, at diagnosis and relapse from the same patient. We set out to study the vascular phenotype of these tumors to evaluate the integrity of the blood-brain barrier (BBB) in AT/RT. We also used the model to study combined mitogen-activated protein kinase kinase (MEK) and maternal embryonic leucine zipper kinase (MELK) inhibition as a therapeutic strategy for AT/RT.We found MELK to be highly overexpressed in both patient samples of AT/RT and our primary cultures and xenografts. We identified a potent antitumor efficacy of the MELK inhibitor OTSSP167, as well as strong synergy with the MEK inhibitor trametinib, against primary AT/RT neurospheres. Additionally, vascular phenotyping of AT/RT patient material and xenografts revealed significant BBB aberrancies in these tumors. Finally, we show in vivo efficacy of the non-BBB penetrable drugs OTSSP167 and trametinib in AT/RT xenografts, demonstrating the therapeutic implications of the observed BBB deficiencies and validating MEK/MELK inhibition as a potential treatment.Altogether, we developed a combination treatment strategy for AT/RT based on MEK/MELK inhibition and identify therapeutically exploitable BBB deficiencies in these tumors.

Trametinib

Neurosphere

10.1093/neuonc/noz151

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Citations (36)

LTBK-02. Safety of growth hormone replacement therapy in childhood craniopharyngioma

Neuro-Oncology (2022)

Jiska van Schaïk Eline Kormelink Netteke Schouten-van Meeteren Evelien de Vos‐Kerkhof Boudewijn Bakker

Abstract Introduction: Treatment for childhood-onset craniopharyngioma (cCP) has shifted from complete to limited resection aiming to avoid additional hypothalamic morbidity. Up to 90% of cCP patients develop growth hormone deficiency (GHD). GH replacement therapy (GHRT) is of high importance for linear growth and metabolic state. Hardly any studies evaluated the optimal time to start GHRT in relation to tumor progression or recurrence. Our aim was to assess the effect of GHRT in cCP on tumor progression/recurrence. Methods: Patients with cCP diagnosed between 2001 and 2022, with at least one year of follow-up were included. Tumor progression/recurrence was defined as tumor progression/recurrence requiring intervention. Kaplan Meier and multivariable cox regression analyses were estimated for tumor progression/recurrence. Comparison was made between cCP patients with GHRT and without GHRT. Of the cCP patients receiving GHRT, those given GHRT ≤ 1 year of cCP diagnosis were compared to those given GHRT >1 year after cCP diagnosis. Results: Of 59 cCP patients, 52 were diagnosed with GHD and 51 (86.4%) received GHRT. Sixteen cCP patients (31.4%) developed tumor progression/recurrence during GHRT compared to four cCP patients (50.0%) without GHRT. Mean progression free survival (PFS) did not differ between cCP patients with or without GHRT (GHRT: 5.55 years 95% CI 3.74 - 7.36 vs. no GHRT: 3.69 years 95% CI 1.44 - 5.93). Of cCP patients who started GHRT ≤1 year after cCP diagnosis, 36.4% developed tumor progression/recurrence compared to 27.6% of cCP patients who received GHRT > 1 year after diagnosis (PFS: 8.45 years CI 95% 5.54 – 11.36 vs. 7.99 years CI 95% 6.03 – 9.94). Limited surgery was associated to tumor progression/recurrence (HR 6.99 CI 95% 2.10 – 23.25). Conclusion: GHRT does not seem to influence tumor progression/recurrence in cCP. These results support early initiation of GHRT in cCP patients to optimize linear growth and metabolic outcome.

Craniopharyngioma

Tumor progression

10.1093/neuonc/noac079.714

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Hersentumoren bij jonge kinderen.

Netteke Schouten-van Meeteren W.P. Vandertop Corrie Gidding

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Clinical characteristics of subsequent histologically confirmed meningiomas in long-term childhood cancer survivors: A Dutch LATER study

European Journal of Cancer (2021)

Lisanne C. Verbruggen Judith L. Kok Jop C. Teepen Geert O. Janssens Charlotte M. de Boer

Medical record

Record Linkage

Childhood Cancer

Malignant meningioma

10.1016/j.ejca.2021.03.021

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Integrated Genomics Identifies Five Medulloblastoma Subtypes with Distinct Genetic Profiles, Pathway Signatures and Clinicopathological Features

PLoS ONE (2008)

Marcel Kool Jan Köster Jens Bunt Nancy E. Hasselt Arjan Lakeman

Background Medulloblastoma is the most common malignant brain tumor in children. Despite recent improvements in cure rates, prediction of disease outcome remains a major challenge and survivors suffer from serious therapy-related side-effects. Recent data showed that patients with WNT-activated tumors have a favorable prognosis, suggesting that these patients could be treated less intensively, thereby reducing the side-effects. This illustrates the potential benefits of a robust classification of medulloblastoma patients and a detailed knowledge of associated biological mechanisms. Methods and Findings To get a better insight into the molecular biology of medulloblastoma we established mRNA expression profiles of 62 medulloblastomas and analyzed 52 of them also by comparative genomic hybridization (CGH) arrays. Five molecular subtypes were identified, characterized by WNT signaling (A; 9 cases), SHH signaling (B; 15 cases), expression of neuronal differentiation genes (C and D; 16 and 11 cases, respectively) or photoreceptor genes (D and E; both 11 cases). Mutations in β-catenin were identified in all 9 type A tumors, but not in any other tumor. PTCH1 mutations were exclusively identified in type B tumors. CGH analysis identified several fully or partly subtype-specific chromosomal aberrations. Monosomy of chromosome 6 occurred only in type A tumors, loss of 9q mostly occurred in type B tumors, whereas chromosome 17 aberrations, most common in medulloblastoma, were strongly associated with type C or D tumors. Loss of the inactivated X-chromosome was highly specific for female cases of type C, D and E tumors. Gene expression levels faithfully reflected the chromosomal copy number changes. Clinicopathological features significantly different between the 5 subtypes included metastatic disease and age at diagnosis and histology. Metastatic disease at diagnosis was significantly associated with subtypes C and D and most strongly with subtype E. Patients below 3 yrs of age had type B, D, or E tumors. Type B included most desmoplastic cases. We validated and confirmed the molecular subtypes and their associated clinicopathological features with expression data from a second independent series of 46 medulloblastomas. Conclusions The new medulloblastoma classification presented in this study will greatly enhance the understanding of this heterogeneous disease. It will enable a better selection and evaluation of patients in clinical trials, and it will support the development of new molecular targeted therapies. Ultimately, our results may lead to more individualized therapies with improved cure rates and a better quality of life.

Comparative genomic hybridization

Monosomy

PTCH1

Chromosome instability

10.1371/journal.pone.0003088

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Citations (703)

Heterogeneity of ASL perfusion MRI in low-grade paediatric glioma as imaging biomarker to assess treatment effect

Proceedings on CD-ROM - International Society for Magnetic Resonance in Medicine. Scientific Meeting and Exhibition/Proceedings of the International Society for Magnetic Resonance in Medicine, Scientific Meeting and Exhibition (2023)

Lejla Alić Sanneke Willekens Henk J. M. M. Mutsaerts Jan Petr Netteke Schouten-van Meeteren

ASL-MRI is reported as an option to assess potentially heterogeneous physiological processes important for tumour treatment. Therefore, we explored the heterogeneity in normalised CBF as an imaging biomarker for assessment of treatment effect in pLGG. There is a noticeable effect of chemotherapy observed as a change in texture of healthy appearing brain tissue. A high difference in texture between treated and non-treated patients for non-enhancing tumour part is observed, suggesting that texture, based on co-occurrence matrices, is suitable as an imaging biomarker for assessment of treatment effect in pLGG.

Imaging biomarker

10.58530/2022/2792

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RARE-03 CENTRAL NERVOUS SYSTEM TUMORS IN CHILDREN WITH NEUROFIBROMATOSIS TYPE 1, A COHORT FROM A NATIONAL PEDIATRIC ONCOLOGY CENTER

Neuro-Oncology (2021)

Kim Vandenput Lisethe Meijer Netteke Schouten-van Meeteren

Abstract Approximately 15% of the children with Neurofibromatosis type 1 (NF1) develop a central nervous system (CNS) tumor, predominantly optic pathway glioma. However, other brain tumor types are also frequent, resulting in a heterogenous population regarding tumor type, symptoms and treatment. Even though many tumors are indolent, clinical deterioration or radiological progression requires surveillance and treatment. Pediatric oncology care in the Netherlands has been centralized into the Princess Máxima Center since June 2018, providing care for the majority of Dutch NF1 CNS tumor patients. This retrospective cohort study describes the course of disease in NF1 patients with a CNS tumor diagnosed between 2005–2020, based on data from patient files. The population consisted of 95 patients (48 males), median age at diagnosis 4.3 (range 0.8–17.2) and 12.6 (range 2.9–19.9) years at follow up, 27% familiar NF1, mostly nonsense or frameshift mutations. Neurological and/or visual symptoms were present in 64 (67.4%) patients. 63.6% of the tumors was in the optic pathway, 9.1% in the cerebellum. Biopsy in 19/95 revealed 1 ependymoma and 18 low grade glioma, with rarely additional molecular changes besides NF1. Kaplan Meier median PFS was 24 months (range 3–174.5, n=65) in symptomatic presenting patients, 34 months (range 5–165, n=20) in asymptomatic patients with abnormal ophthalmological and/or neurological exam and 67.3 months (range 7–130, n=10) in asymptomatic patients without abnormalities at exam. Treatment was indicated in 53 (55.8%), predominantly chemotherapy (n=49), with substantial toxicity. Carboplatin allergy was seen in 29/44 (65.9%) patients, peripheral neuropathy in 21/46 (45.7%) patients receiving vincristine, and 5/10 patients receiving irinotecan and bevacizumab ended treatment early due to toxicity. In conclusion: analysis of our extensive cohort of NF1 patients with a CNS tumor indicates the relevance of regular screening of NF1 patients without complaints and critical surveillance and systematical documentation of treatment toxicity.

Ependymoma

Brain tumor

10.1093/neuonc/noab090.164

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Surveillance for subsequent neoplasms of the CNS for childhood, adolescent, and young adult cancer survivors: a systematic review and recommendations from the International Late Effects of Childhood Cancer Guideline Harmonization Group

The Lancet Oncology (2021)

Daniel C. Bowers Lisanne C. Verbruggen Leontien C.M. Kremer Melissa M. Hudson Roderick Skinner

Guideline

Harmonization

10.1016/s1470-2045(20)30688-4

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