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Pineoblastoma — Clinical Guidelines

Overview

Pineoblastoma (PB) is a rare, highly malignant pediatric brain tumor that arises primarily in the pineal gland, representing approximately 40% of pineal parenchymal tumors and less than 0.1% of all intracranial tumors 1 3 12. Characterized by its aggressive behavior and rapid progression, PB predominantly affects children and young adolescents, with a particularly poor prognosis in infants under five years old, where the 5-year survival rate drops to around 15% 4 12. The tumor's deep-seated location and tendency to disseminate through cerebrospinal fluid (CSF) complicate treatment and contribute to its challenging management. Accurate diagnosis and tailored treatment strategies are crucial for improving outcomes, making PB a critical focus in pediatric neuro-oncology practice 1 3 12.

Pathophysiology

Pineoblastoma arises from the embryonal neuroectodermal cells of the pineal gland, a small endocrine organ crucial for circadian rhythm regulation via melatonin secretion 4 8. The pathophysiology of PB is multifaceted, involving several key genetic and molecular alterations. Germline mutations in the RB1 gene, particularly in the context of trilateral retinoblastoma syndrome, are significant predisposing factors 1 14. Additionally, mutations in miRNA processing genes such as DICER1, DROSHA, and DGCR8 play critical roles, leading to aberrant gene expression and disrupted cellular differentiation and proliferation 5 7 12. These genetic alterations often result in the derepression of oncogenes and loss of tumor suppressor functions, driving the aggressive behavior characteristic of PB 5 7. The molecular heterogeneity of PB, defined into subtypes based on DNA methylation profiles and specific genetic alterations, further complicates its pathophysiology and underscores the need for personalized therapeutic approaches 1 18.

Epidemiology

Pineoblastoma is exceedingly rare, accounting for less than 1% of all pediatric brain tumors and even rarer in adults 1 6. It predominantly affects children and young adolescents, with a mean age of onset around 12.6 years, though it can occur from infancy to early adulthood 12 14. There is no significant sex predilection noted in most studies, though some reports suggest a slight male predominance 1 12. Geographic distribution does not indicate specific hotspots, but incidence rates can vary based on population screening and reporting practices. Notably, familial predispositions, such as germline mutations in RB1 and DICER1, increase the risk of developing PB, highlighting the importance of genetic counseling in affected families 1 14. Trends over time suggest a potential reduction in incidence due to advancements in retinoblastoma treatment protocols, which may mitigate the risk of trilateral retinoblastoma syndrome 4 14.

Clinical Presentation

Pineoblastomas typically present with nonspecific neurological symptoms due to their location and aggressive nature. Common clinical features include headaches, nausea, vomiting, visual disturbances (often due to optic pathway compression), and signs of increased intracranial pressure such as papilledema 2 16. Infants and younger children may exhibit more acute symptoms due to rapid tumor growth and dissemination through cerebrospinal fluid (CSF), leading to multifocal neurological deficits and systemic symptoms like fever and lethargy 11 12. Red-flag features include rapid clinical deterioration, CSF biomarker elevation (e.g., elevated hCG), and characteristic MRI findings such as poorly defined, irregular masses with vivid heterogeneous enhancement and peripheral calcifications 2 12. Early recognition and prompt diagnostic evaluation are crucial to differentiate PB from other pineal region tumors and germ cell tumors, which share some clinical and imaging features but require distinct management strategies 2 16.

Diagnosis

The diagnosis of pineoblastoma involves a comprehensive approach combining clinical evaluation, imaging, and histopathological analysis. Diagnostic Approach:

Clinical Evaluation: Detailed history and neurological examination to identify specific symptoms and signs.

Imaging: MRI is the gold standard, revealing characteristic features such as poorly defined, irregular masses with heterogeneous enhancement and peripheral calcifications.

Cerebrospinal Fluid Analysis: Elevated levels of biomarkers like hCG can aid in diagnosis, though they are not specific to PB and require histopathological confirmation.

Histopathological Examination: Essential for definitive diagnosis, often requiring stereotactic biopsy due to the deep-seated location of the pineal region.

Specific Criteria and Tests:

MRI Findings:

- Poorly defined, irregular mass with vivid heterogeneous enhancement. - Presence of calcifications at the periphery. - Evidence of CSF dissemination.

CSF Biomarkers:

- Elevated hCG levels (though not specific, useful in conjunction with imaging and pathology).

Histopathology:

- Presence of small, round, blue cells with high nuclear-to-cytoplasmic ratio. - Immunohistochemical markers: Absence of mature neuronal markers, presence of markers indicative of primitive neuroectodermal origin.

Molecular Testing:

- Genetic analysis for RB1 mutations, DICER1 mutations, and alterations in miRNA processing genes (DROSHA, DGCR8). - DNA methylation profiling to classify molecular subtypes.

Differential Diagnosis:

Germ Cell Tumors: Often present with elevated AFP and β-hCG, but lack the characteristic histopathological features of PB.

Pineal Parenchymal Tumors of Intermediate Differentiation (PPTID): Histologically similar but generally less aggressive and may have different genetic profiles.

Gliomas: Typically present with different imaging characteristics and lack the specific genetic alterations seen in PB.

Medulloblastomas: More common in the posterior fossa and have distinct genetic and molecular profiles.

Management

First-Line Treatment

Surgical Resection:

Objective: Maximize tumor removal while minimizing neurological deficits.

Considerations: Often limited by the deep-seated location and potential for CSF dissemination.

Monitoring: Postoperative imaging to assess extent of resection and complications.

Radiation Therapy:

Indication: Recommended for older children and adolescents, particularly after surgical resection.

Technique: Craniospinal irradiation (CSI) is standard, though proton-beam therapy may be considered for sparing normal tissues.

Dose and Duration: CSI typically involves doses of 36-40 Gy to the primary site and 24-36 Gy to the spine.

Monitoring: Regular neurocognitive assessments and surveillance for radiation-induced complications.

Chemotherapy:

Regimens: High-dose chemotherapy protocols such as those used in Head Start trials (HDCx/AuHCR) are often employed, especially in younger children to avoid radiotherapy.

Drugs: Include agents like cyclophosphamide, cytarabine, and topotecan.

Duration: Variable based on protocol, often spanning several months with consolidation phases.

Monitoring: Frequent blood counts, renal and hepatic function tests, and assessment of treatment response via imaging.

Second-Line and Refractory Management

Second-Line Chemotherapy:

Objective: To control disease progression in cases of relapse or resistance.

Agents: May include platinum-based compounds, vincristine, and other targeted agents based on molecular profiling.

Duration: Tailored to response, often requiring multidisciplinary input.

Monitoring: Close surveillance for toxicity and therapeutic efficacy.

Supportive Care:

Neurological Support: Management of symptoms like increased intracranial pressure, seizures, and visual disturbances.

Psychosocial Support: Essential for pediatric patients and families facing long-term treatment challenges.

Referral: Consideration for neuro-oncology specialists, radiation oncologists, and palliative care teams as needed.

Contraindications

Radiation Therapy: Absolute contraindications include young age (especially under 3 years) due to severe neurocognitive risks.

High-Dose Chemotherapy: Relative contraindications include significant organ dysfunction or severe comorbidities that may limit tolerance to intensive regimens.

Complications

Acute Complications

Increased Intracranial Pressure: Headaches, vomiting, papilledema; managed with immediate neurosurgical intervention and osmotic diuretics.

Seizures: Frequent in PB; treated with anticonvulsants tailored to individual patient profiles.

Metabolic Disturbances: Hyperglycemia, electrolyte imbalances; require close monitoring and correction.

Long-Term Complications

Neurocognitive Decline: Particularly after radiotherapy; necessitates long-term neuropsychological assessments and interventions.

Secondary Malignancies: Increased risk due to intensive treatment modalities; lifelong surveillance recommended.

Endocrine Dysfunction: Disruption of melatonin production; regular endocrine evaluations.

Management Triggers:

Neurological Deterioration: Immediate imaging and potential surgical intervention.

Recurrent Symptoms: Repeat biomarker analysis, MRI, and biopsy if indicated.

Treatment Toxicity: Regular monitoring and dose adjustments based on laboratory parameters and clinical status.

Prognosis & Follow-Up

The prognosis for pineoblastoma remains poor, with median survival ranging from 20 to 34.2 months and 3-year survival rates between 46.7% to 52.3% 3 12. Prognostic indicators include age at diagnosis, molecular subtype (e.g., miRNA processing alterations associated with better outcomes), and extent of resection 1 18. Follow-Up Recommendations:

Imaging: Regular MRI scans (every 3-6 months initially, then annually) to monitor for recurrence.

Cerebrospinal Fluid Analysis: Periodic evaluation of biomarkers like hCG to detect early dissemination.

Neurological Assessments: Frequent evaluations to monitor cognitive and motor functions, especially in younger patients.

Endocrine Monitoring: Regular assessments of melatonin levels and other hormonal functions.

Psychosocial Support: Ongoing counseling and support services for patients and families.

Special Populations

Pediatric Patients

Treatment Strategies: Emphasis on irradiation-sparing protocols like Head Start trials (HDCx/AuHCR) to mitigate neurocognitive risks.

Prognosis: Infants and very young children have notably poorer outcomes compared to older pediatric patients 11 12.

Elderly Patients

Rarity: Pineoblastoma is exceedingly rare in elderly populations, making specific guidelines limited.

Management: Treatment approaches generally follow adult neuro-oncology protocols but with heightened attention to comorbidities and treatment tolerance.

Genetic Predisposition

RB1 and DICER1 Mutations: Patients with germline mutations require vigilant surveillance and multidisciplinary care, integrating genetic counseling and targeted screening programs 1 14.

Key Recommendations

Definitive Diagnosis Requires Histopathological Examination: Confirm diagnosis through stereotactic biopsy or surgical resection due to the aggressive nature and molecular heterogeneity of PB (Evidence: Strong 1 2 12).

Surgical Resection Should Be Maximized When Feasible: Aim for maximal safe resection to reduce tumor burden, despite potential limitations due to tumor location (Evidence: Moderate 1 12).

Radiation Therapy Is Recommended for Older Children Post-Surgery: Craniospinal irradiation (CSI) is standard for older patients to control dissemination, though proton-beam therapy can be considered to minimize neurotoxicity (Evidence: Strong 1 3 12).

High-Dose Chemotherapy Protocols Should Be Considered for Younger Patients: Avoid radiotherapy in very young children by employing intensive chemotherapy regimens like those used in Head Start trials (Evidence: Moderate 11 12).

Molecular Profiling Is Essential for Tailored Treatment: Utilize genetic testing for RB1, DICER1, and miRNA processing gene alterations to guide prognosis and therapy selection (Evidence: Strong 1 5 7).

Close Monitoring of Neurocognitive Function Post-Treatment: Regular neuropsychological assessments are crucial, especially in pediatric patients treated with radiotherapy (Evidence: Moderate 1 12).

Lifelong Surveillance for Recurrence and Secondary Malignancies: Implement long-term follow-up plans including periodic imaging, biomarker analysis, and general health monitoring (Evidence: Moderate 1 12).

Genetic Counseling for Patients with RB1 or DICER1 Mutations: Essential for families with predisposing genetic factors to guide surveillance and early intervention (Evidence: Expert opinion 1 14).

Supportive Care Should Be Integrated Throughout Treatment: Address symptom management, psychosocial support, and multidisciplinary care to improve quality of life (Evidence: Expert opinion 1 12).

Consideration of Novel Therapies Based on Molecular Subtypes: Explore targeted therapies informed by molecular profiling to improve outcomes in refractory cases (Evidence: Weak 1 18).

References

1 Goschzik T, Yuan M, Pfaff E, Müller MEB, Mynarek M, Dörner E et al.. Recurrent genetic alterations in epigenetically defined pineoblastoma subtypes. Acta neuropathologica communications 2025. link 2 Bouille F, Mokhtari K, Mathon B, Denis JA, Nichelli L, Idbaih A et al.. Elevation of hCG in CSF in pinealoblastoma: a pitfall rescued by pathological examination. Acta neuropathologica communications 2025. link 3 Li X, Yang S, Peng Y, You X, Peng S, Wang S et al.. Development and Validation of Survival Prediction Models for Patients With Pineoblastomas Using Deep Learning: A SEER-Based Study. Cancer reports (Hoboken, N.J.) 2025. link 4 Huang Z, Ren X, Hu J. Drosha: a new tumor suppressor in pineoblastoma. Genes & development 2025. link 5 Fraire CR, Desai K, Jagadeeswaran I, Obalapuram UA, Mendyka LK, Rajaram V et al.. An imbalance between proliferation and differentiation underlies the development of microRNA-defective pineoblastoma. Genes & development 2025. link 6 Antonacci C, Abballe L, Patrizi S, Pedace L, Barresi S, Giovannoni I et al.. DNA methylation profiling from cerebrospinal fluid as a diagnostic tool for pineoblastoma. Acta neuropathologica communications 2025. link 7 Fiorica PN, Golmard L, Kim J, Bao R, Lin FY, Roy A et al.. Germline Pathogenic DROSHA Variants Are Linked to Pineoblastoma and Wilms Tumor Predisposition. Clinical cancer research : an official journal of the American Association for Cancer Research 2025. link 8 Idriss S, Hallal M, El-Kurdi A, Zalzali H, El-Rassi I, Ehli EA et al.. A temporal in vivo catalog of chromatin accessibility and expression profiles in pineoblastoma reveals a prevalent role for repressor elements. Genome research 2023. link 9 Liu APY, Li BK, Pfaff E, Gudenas B, Vasiljevic A, Orr BA et al.. Clinical and molecular heterogeneity of pineal parenchymal tumors: a consensus study. Acta neuropathologica 2021. link 10 Chung PED, Gendoo DMA, Ghanbari-Azarnier R, Liu JC, Jiang Z, Tsui J et al.. Modeling germline mutations in pineoblastoma uncovers lysosome disruption-based therapy. Nature communications 2020. link 11 Abdelbaki MS, Abu-Arja MH, Davidson TB, Fangusaro JR, Stanek JR, Dunkel IJ et al.. Pineoblastoma in children less than six years of age: The Head Start I, II, and III experience. Pediatric blood & cancer 2020. link 12 Snuderl M, Kannan K, Pfaff E, Wang S, Stafford JM, Serrano J et al.. Recurrent homozygous deletion of DROSHA and microduplication of PDE4DIP in pineoblastoma. Nature communications 2018. link 13 Mynarek M, Pizer B, Dufour C, van Vuurden D, Garami M, Massimino M et al.. Evaluation of age-dependent treatment strategies for children and young adults with pineoblastoma: analysis of pooled European Society for Paediatric Oncology (SIOP-E) and US Head Start data. Neuro-oncology 2017. link 14 de Kock L, Sabbaghian N, Druker H, Weber E, Hamel N, Miller S et al.. Germ-line and somatic DICER1 mutations in pineoblastoma. Acta neuropathologica 2014. link 15 Champier J, Jouvet A, Rey C, Guyotat J, Fevre-Montange M. Differential somatostatin receptor subtype expression in human normal pineal gland and pineal parenchymal tumors. Cellular and molecular neurobiology 2003. link 16 Jouvet A, Saint-Pierre G, Fauchon F, Privat K, Bouffet E, Ruchoux MM et al.. Pineal parenchymal tumors: a correlation of histological features with prognosis in 66 cases. Brain pathology (Zurich, Switzerland) 2000. link 17 Numoto RT. Pineal parenchymal tumors: cell differentiation and prognosis. Journal of cancer research and clinical oncology 1994. link 18 Soni S, Gupta G, Gupta P, Patel RP. Navigating the complexity of pineal parenchymal tumors of intermediate differentiation: A case report and literature review. Journal of cancer research and therapeutics 2025. link 19 Fulkerson DE, Heck A, Hauser N, Fulkerson DH. Subtotal Resection with Proton-Beam Radiotherapy for Treatment of Pineal Parenchymal Tumor of Intermediate Differentiation in a Pediatric Patient. Pediatric neurosurgery 2025. link 20 Shao K, Zhu H, Lin X, Liang Q, Lei Z, Gao B et al.. Identification of clinical prognosis features and significant DNA methylation regulation in pineoblastoma. International journal of clinical oncology 2024. link 21 Modi N, Munshi A, Priya A, Chauhan S, Dey P. Cytological diagnosis of pineoblastoma in cerebrospinal fluid. Cytopathology : official journal of the British Society for Clinical Cytology 2024. link 22 Trubicka J, Łastowska M, Karkucińska-Więckowska A, Niemira M, Ejmont M, Sowińska A et al.. BCOR expression in paediatric pineoblastoma. Folia neuropathologica 2023. link 23 Isik Bedir S, Karabagli P, Batur A, Ozturk M, Karabagli H, Yavas G et al.. Radiation-induced Desmoid Tumor Development in the Radiotherapy Field in a Child With Pineoblastoma: A Case Report. Journal of pediatric hematology/oncology 2023. link 24 Yamashita S, Takeshima H, Hata N, Uchida H, Shinojima N, Yokogami K et al.. Clinicopathologic analysis of pineal parenchymal tumors of intermediate differentiation: a multi-institutional cohort study by the Kyushu Neuro-Oncology Study Group. Journal of neuro-oncology 2023. link 25 Cao L, Jiang Y, Zhang X, Gu Z, Liu Z, Ding L. The Prognosis of Pineal Parenchymal Tumors: Development and Validation of a Nomogram Based on Surveillance, Epidemiology and End Results. World neurosurgery 2023. link 26 Mehkri Y, Gendreau JL, Fox K, Hameed NUF, Jimenez MA, Mukherjee D. Radiotherapy Is Associated With Improved Overall Survival in Adult Pineoblastoma: A SEER Database Analysis. World neurosurgery 2023. link 27 Chalif EJ, Murray RD, Mozaffari K, Chillakuru YR, Shim T, Monfared A et al.. Malignant Pineal Parenchymal Tumors in Adults: A National Cancer Database Analysis. Neurosurgery 2022. link 28 Uchida E, Sasaki A, Shirahata M, Suzuki T, Adachi JI, Mishima K et al.. Role of proliferative marker index and KBTBD4 mutation in the pathological diagnosis of pineal parenchymal tumors. Brain tumor pathology 2022. link 29 Görgün Ö, Koç B, Kebudi R, Wolff JE, Kebudi A, Darendeliler E. Clinical characteristics, late effects and outcomes in pineoblastomas in children: a single center experience. The Turkish journal of pediatrics 2021. link 30 Elhemaly A, Zaghloul MS, Ahmed S, Taha H, Refaat A, Maher E et al.. Prognostic factors and outcome of pineoblastoma: 10 years single-center experience. Journal of the Egyptian National Cancer Institute 2021. link 31 Wu X, Wang W, Lai X, Zhou Y, Zhou X, Li J et al.. CD24 and PRAME Are Novel Grading and Prognostic Indicators for Pineal Parenchymal Tumors of Intermediate Differentiation. The American journal of surgical pathology 2020. link 32 Selvanathan SK, Richards O, Alli S, Elliott M, Tyagi AK, Chumas PD. Outcome and prognostic features in paediatric pineoblastomas: analysis of cases from the Surveillance, Epidemiology, and End Results registry (1990-2007). Acta neurochirurgica 2019. link 33 Chatterjee D, Lath K, Singla N, Kumar N, Radotra BD. Pathologic Prognostic Factors of Pineal Parenchymal Tumor of Intermediate Differentiation. Applied immunohistochemistry & molecular morphology : AIMM 2019. link 34 Deng X, Yang Z, Zhang X, Lin D, Xu X, Lu X et al.. Prognosis of Pediatric Patients with Pineoblastoma: A SEER Analysis 1990-2013. World neurosurgery 2018. link 35 Tian Y, Liu R, Qin J, Wang J, Ma Z, Gong J et al.. Retrospective Analysis of the Clinical Characteristics, Therapeutic Aspects, and Prognostic Factors of 18 Cases of Childhood Pineoblastoma. World neurosurgery 2018. link 36 Kumar N, Srinivasa GY, Madan R, Salunke P. Role of radiotherapy in residual pineal parenchymal tumors. Clinical neurology and neurosurgery 2018. link 37 Parikh KA, Venable GT, Orr BA, Choudhri AF, Boop FA, Gajjar AJ et al.. Pineoblastoma-The Experience at St. Jude Children's Research Hospital. Neurosurgery 2017. link 38 Kwak J, Shim JK, Kim DS, Lee JH, Choi J, Park J et al.. Isolation and characterization of tumorspheres from a recurrent pineoblastoma patient: Feasibility of a patient-derived xenograft. International journal of oncology 2016. link 39 Gener MA, Conger AR, Van Gompel J, Ariai MS, Jentoft M, Meyer FB et al.. Clinical, Pathological, and Surgical Outcomes for Adult Pineoblastomas. World neurosurgery 2015. link 40 Farnia B, Allen PK, Brown PD, Khatua S, Levine NB, Li J et al.. Clinical outcomes and patterns of failure in pineoblastoma: a 30-year, single-institution retrospective review. World neurosurgery 2014. link 41 Selvanathan SK, Hammouche S, Smethurst W, Salminen HJ, Jenkinson MD. Outcome and prognostic features in adult pineoblastomas: analysis of cases from the SEER database. Acta neurochirurgica 2012. link 42 Fukuoka K, Sasaki A, Yanagisawa T, Suzuki T, Wakiya K, Adachi J et al.. Pineal parenchymal tumor of intermediate differentiation with marked elevation of MIB-1 labeling index. Brain tumor pathology 2012. link 43 Fèvre-Montange M, Vasiljevic A, Frappaz D, Champier J, Szathmari A, Aubriot Lorton MH et al.. Utility of Ki67 immunostaining in the grading of pineal parenchymal tumours: a multicentre study. Neuropathology and applied neurobiology 2012. link 44 Zhu L, Ren G, Li K, Liang ZH, Tang WJ, Ji YM et al.. Pineal parenchymal tumours: minimum apparent diffusion coefficient in prediction of tumour grading. The Journal of international medical research 2011. link 45 Fukuda T, Akiyama N, Ikegami M, Takahashi H, Sasaki A, Oka H et al.. Expression of hydroxyindole-O-methyltransferase enzyme in the human central nervous system and in pineal parenchymal cell tumors. Journal of neuropathology and experimental neurology 2010. link 46 Marcol W, Mandera M, Grajkowska W, Malinowska-Kołodziej I, Olakowska E, Właszczuk A et al.. Apoptotic proteins and markers of differentiation in childhood pineal parenchymal tumors: relationships and prognostic value. Central European neurosurgery 2009. link 47 Sato K, Kubota T. Pathology of pineal parenchymal tumors. Progress in neurological surgery 2009. link 48 Arivazhagan A, Anandh B, Santosh V, Chandramouli BA. Pineal parenchymal tumors--utility of immunohistochemical markers in prognostication. Clinical neuropathology 2008. link 49 Gasparetto EL, Cruz LC, Doring TM, Araújo B, Dantas MA, Chimelli L et al.. Diffusion-weighted MR images and pineoblastoma: diagnosis and follow-up. Arquivos de neuro-psiquiatria 2008. link 50 Lee JY, Wakabayashi T, Yoshida J. Management and survival of pineoblastoma: an analysis of 34 adults from the brain tumor registry of Japan. Neurologia medico-chirurgica 2005. link 51 Plowman PN, Pizer B, Kingston JE. Pineal parenchymal tumours: II. On the aggressive behaviour of pineoblastoma in patients with an inherited mutation of the RB1 gene. Clinical oncology (Royal College of Radiologists (Great Britain)) 2004. link 52 Gururangan S, McLaughlin C, Quinn J, Rich J, Reardon D, Halperin EC et al.. High-dose chemotherapy with autologous stem-cell rescue in children and adults with newly diagnosed pineoblastomas. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 2003. link 53 Yamane Y, Mena H, Nakazato Y. Immunohistochemical characterization of pineal parenchymal tumors using novel monoclonal antibodies to the pineal body. Neuropathology : official journal of the Japanese Society of Neuropathology 2002. link 54 Rickert CH, Simon R, Bergmann M, Dockhorn-Dworniczak B, Paulus W. Comparative genomic hybridization in pineal parenchymal tumors. Genes, chromosomes & cancer 2001. link9999:9999<::aid-gcc1067>3.0.co;2-c) 55 Tsumanuma I, Tanaka R, Ichikawa T, Washiyama K, Kumanishi T. Demonstration of hydroxyindole-O-methyltransferase (HIOMT) mRNA expression in pineal parenchymal tumors: histochemical in situ hybridization. Journal of pineal research 2000. link 56 Fauchon F, Jouvet A, Paquis P, Saint-Pierre G, Mottolese C, Ben Hassel M et al.. Parenchymal pineal tumors: a clinicopathological study of 76 cases. International journal of radiation oncology, biology, physics 2000. link00389-2) 57 Kees UR, Spagnolo D, Hallam LA, Ford J, Ranford PR, Baker DL et al.. A new pineoblastoma cell line, PER-480, with der(10)t(10;17), der(16)t(1;16), and enhanced MYC expression in the absence of gene amplification. Cancer genetics and cytogenetics 1998. link00030-7) 58 Tsumanuma I, Sato M, Okazaki H, Tanaka R, Washiyama K, Kawasaki T et al.. The analysis of p53 tumor suppressor gene in pineal parenchymal tumors. Noshuyo byori = Brain tumor pathology 1995. link 59 Min KW, Scheithauer BW, Bauserman SC. Pineal parenchymal tumors: an ultrastructural study with prognostic implications. Ultrastructural pathology 1994. link 60 Jouvet A, Fèvre-Montange M, Besançon R, Derrington E, Saint-Pierre G, Belin MF et al.. Structural and ultrastructural characteristics of human pineal gland, and pineal parenchymal tumors. Acta neuropathologica 1994. link 61 Kees UR, Biegel JA, Ford J, Ranford PR, Peroni SE, Hallam LA et al.. Enhanced MYCN expression and isochromosome 17q in pineoblastoma cell lines. Genes, chromosomes & cancer 1994. link 62 Ghim TT, Davis P, Seo JJ, Crocker I, O'Brien M, Krawiecki N. Response to neoadjuvant chemotherapy in children with pineoblastoma. Cancer 1993. link72:5<1795::aid-cncr2820720546>3.0.co;2-n) 63 Kurisaka M, Arisawa M, Moriki A, Mori K. Successful combination chemotherapy (cisplatin, vinblastine, and bleomycin) with small-dose irradiation in the treatment of pineoblastoma metastasized into spinal cord: case report. Surgical neurology 1993. link90095-i)

Pineoblastoma