Pediatric Brain Tumors Pre, Intra & Post Op Evaluation and Management
Total Page:16
File Type:pdf, Size:1020Kb

Load more
Recommended publications
-
Endothelial-Tumor Cell Interaction in Brain and CNS Malignancies
International Journal of Molecular Sciences Review Endothelial-Tumor Cell Interaction in Brain and CNS Malignancies Maria Peleli 1,2,3,*, Aristidis Moustakas 1 and Andreas Papapetropoulos 2,3 1 Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, Uppsala University, Box 582, SE-751 23 Uppsala, Sweden; [email protected] 2 Clinical, Experimental Surgery and Translational Research Center, Biomedical Research Foundation of the Academy of Athens, 115 27 Athens, Greece; [email protected] 3 Laboratory of Pharmacology, Faculty of Pharmacy, National and Kapodistrian University of Athens, 157 71 Athens, Greece * Correspondence: [email protected]; Tel.: +46-768-795-270 Received: 28 August 2020; Accepted: 3 October 2020; Published: 6 October 2020 Abstract: Glioblastoma and other brain or CNS malignancies (like neuroblastoma and medulloblastoma) are difficult to treat and are characterized by excessive vascularization that favors further tumor growth. Since the mean overall survival of these types of diseases is low, the finding of new therapeutic approaches is imperative. In this review, we discuss the importance of the interaction between the endothelium and the tumor cells in brain and CNS malignancies. The different mechanisms of formation of new vessels that supply the tumor with nutrients are discussed. We also describe how the tumor cells (TC) alter the endothelial cell (EC) physiology in a way that favors tumorigenesis. In particular, mechanisms of EC–TC interaction are described such as (a) communication using secreted growth factors (i.e., VEGF, TGF-β), (b) intercellular communication through gap junctions (i.e., Cx43), and (c) indirect interaction via intermediate cell types (pericytes, astrocytes, neurons, and immune cells). -
Central Nervous System Tumors General ~1% of Tumors in Adults, but ~25% of Malignancies in Children (Only 2Nd to Leukemia)
Last updated: 3/4/2021 Prepared by Kurt Schaberg Central Nervous System Tumors General ~1% of tumors in adults, but ~25% of malignancies in children (only 2nd to leukemia). Significant increase in incidence in primary brain tumors in elderly. Metastases to the brain far outnumber primary CNS tumors→ multiple cerebral tumors. One can develop a very good DDX by just location, age, and imaging. Differential Diagnosis by clinical information: Location Pediatric/Young Adult Older Adult Cerebral/ Ganglioglioma, DNET, PXA, Glioblastoma Multiforme (GBM) Supratentorial Ependymoma, AT/RT Infiltrating Astrocytoma (grades II-III), CNS Embryonal Neoplasms Oligodendroglioma, Metastases, Lymphoma, Infection Cerebellar/ PA, Medulloblastoma, Ependymoma, Metastases, Hemangioblastoma, Infratentorial/ Choroid plexus papilloma, AT/RT Choroid plexus papilloma, Subependymoma Fourth ventricle Brainstem PA, DMG Astrocytoma, Glioblastoma, DMG, Metastases Spinal cord Ependymoma, PA, DMG, MPE, Drop Ependymoma, Astrocytoma, DMG, MPE (filum), (intramedullary) metastases Paraganglioma (filum), Spinal cord Meningioma, Schwannoma, Schwannoma, Meningioma, (extramedullary) Metastases, Melanocytoma/melanoma Melanocytoma/melanoma, MPNST Spinal cord Bone tumor, Meningioma, Abscess, Herniated disk, Lymphoma, Abscess, (extradural) Vascular malformation, Metastases, Extra-axial/Dural/ Leukemia/lymphoma, Ewing Sarcoma, Meningioma, SFT, Metastases, Lymphoma, Leptomeningeal Rhabdomyosarcoma, Disseminated medulloblastoma, DLGNT, Sellar/infundibular Pituitary adenoma, Pituitary adenoma, -
Gliomatosis Cerebri with Neurofibromatosis: an Autopsy-Proven Case
Child's Nerv Syst (1999) 15:219-221 © Springer-Verlag 1999 BRILF Önal Gliomatosis cerebri with neurofibromatosis: Çiçek an autopsy-proven case Gliomatosis cerebri Received: 15 July 1998 Abstract is a stereotactic ante-mortem diagnosis glial neoplastic process that is dif- and the other after autopsy. in this fusely distributed through neural paper. the autopsy-proven case Ç. Önal (BI) 1 • Ç. structures, whose anatomical config- of this rare disease with coexistent Department of Neurosurgery, uration remains Among the neurofibromatosis - the sixth lstanbul School of Medicine, more than 19,000 cases hospitalized case reported in the literature - Universitv of Istanbul, Çapa. Turkey in Istanbul University Istanbul is presented. School of Medicine Department of address: 1 Cad. Özenç Sok .. 4/9. Neurosurgery throughout the past Key words Gliomatosis cerebri · TR-81080 Erenköy-lstanbul. Turkey 45 years, only 2 cases were diag- Neurofibromatosis · Autopsy · Fax: +90-422-34 !O 726 nosed as gliomatosis cerebri. 1 by GFAP tened gyri showing diffuse oedema and no enhancement lntroduction (Fig. 1 Antibiotic and therapy was begun when the initial diagnosis of meningitis was made. No change was noted on Gliomatosis cerebri is a rare tumour of neuroepithelial or- follow-up CT performed 5 days later. MRI studie~ showed diffuse igin with vague presentation [l. 3. 5-8). Even hypo-isointense lesions in T1 and extensive lesions in with the aid T2-weighted and proton density tPDJ images (Figs. 2. 3). The me- of the most sophisticated techniques, ante-mortem diagno- dulla spinalis was in spite of an therapy. her condi- sis is difficult [2, 8). -
Risk-Adapted Therapy for Young Children with Embryonal Brain Tumors, High-Grade Glioma, Choroid Plexus Carcinoma Or Ependymoma (Sjyc07)
SJCRH SJYC07 CTG# - NCT00602667 Initial version, dated: 7/25/2007, Resubmitted to CPSRMC 9/24/2007 and 10/6/2007 (IRB Approved: 11/09/2007) Activation Date: 11/27/2007 Amendment 1.0 dated January 23, 2008, submitted to CPSRMC: January 23, 2008, IRB Approval: March 10, 2008 Amendment 2.0 dated April 16, 2008, submitted to CPSRMC: April 16, 2008, (IRB Approval: May 13, 2008) Revision 2.1 dated April 29, 2009 (IRB Approved: April 30, 2009 ) Amendment 3.0 dated June 22, 2009, submitted to CPSRMC: June 22, 2009 (IRB Approved: July 14, 2009) Activated: August 11, 2009 Amendment 4.0 dated March 01, 2010 (IRB Approved: April 20, 2010) Activated: May 3, 2010 Amendment 5.0 dated July 19, 2010 (IRB Approved: Sept 17, 2010) Activated: September 24, 2010 Amendment 6.0 dated August 27, 2012 (IRB approved: September 24, 2012) Activated: October 18, 2012 Amendment 7.0 dated February 22, 2013 (IRB approved: March 13, 2013) Activated: April 4, 2013 Amendment 8.0 dated March 20, 2014. Resubmitted to IRB May 20, 2014 (IRB approved: May 22, 2014) Activated: May 30, 2014 Amendment 9.0 dated August 26, 2014. (IRB approved: October 14, 2014) Activated: November 4, 2014 Un-numbered revision dated March 22, 2018. (IRB approved: March 27, 2018) Un-numbered revision dated October 22, 2018 (IRB approved: 10-24-2018) RISK-ADAPTED THERAPY FOR YOUNG CHILDREN WITH EMBRYONAL BRAIN TUMORS, HIGH-GRADE GLIOMA, CHOROID PLEXUS CARCINOMA OR EPENDYMOMA (SJYC07) Principal Investigator Amar Gajjar, M.D. Division of Neuro-Oncology Department of Oncology Section Coordinators David Ellison, M.D., Ph.D. -
Malignant CNS Solid Tumor Rules
Malignant CNS and Peripheral Nerves Equivalent Terms and Definitions C470-C479, C700, C701, C709, C710-C719, C720-C725, C728, C729, C751-C753 (Excludes lymphoma and leukemia M9590 – M9992 and Kaposi sarcoma M9140) Introduction Note 1: This section includes the following primary sites: Peripheral nerves C470-C479; cerebral meninges C700; spinal meninges C701; meninges NOS C709; brain C710-C719; spinal cord C720; cauda equina C721; olfactory nerve C722; optic nerve C723; acoustic nerve C724; cranial nerve NOS C725; overlapping lesion of brain and central nervous system C728; nervous system NOS C729; pituitary gland C751; craniopharyngeal duct C752; pineal gland C753. Note 2: Non-malignant intracranial and CNS tumors have a separate set of rules. Note 3: 2007 MPH Rules and 2018 Solid Tumor Rules are used based on date of diagnosis. • Tumors diagnosed 01/01/2007 through 12/31/2017: Use 2007 MPH Rules • Tumors diagnosed 01/01/2018 and later: Use 2018 Solid Tumor Rules • The original tumor diagnosed before 1/1/2018 and a subsequent tumor diagnosed 1/1/2018 or later in the same primary site: Use the 2018 Solid Tumor Rules. Note 4: There must be a histologic, cytologic, radiographic, or clinical diagnosis of a malignant neoplasm /3. Note 5: Tumors from a number of primary sites metastasize to the brain. Do not use these rules for tumors described as metastases; report metastatic tumors using the rules for that primary site. Note 6: Pilocytic astrocytoma/juvenile pilocytic astrocytoma is reportable in North America as a malignant neoplasm 9421/3. • See the Non-malignant CNS Rules when the primary site is optic nerve and the diagnosis is either optic glioma or pilocytic astrocytoma. -
Meningioma ACKNOWLEDGEMENTS
AMERICAN BRAIN TUMOR ASSOCIATION Meningioma ACKNOWLEDGEMENTS ABOUT THE AMERICAN BRAIN TUMOR ASSOCIATION Meningioma Founded in 1973, the American Brain Tumor Association (ABTA) was the first national nonprofit advocacy organization dedicated solely to brain tumor research. For nearly 45 years, the ABTA has been providing comprehensive resources that support the complex needs of brain tumor patients and caregivers, as well as the critical funding of research in the pursuit of breakthroughs in brain tumor diagnosis, treatment and care. To learn more about the ABTA, visit www.abta.org. We gratefully acknowledge Santosh Kesari, MD, PhD, FANA, FAAN chair of department of translational neuro- oncology and neurotherapeutics, and Marlon Saria, MSN, RN, AOCNS®, FAAN clinical nurse specialist, John Wayne Cancer Institute at Providence Saint John’s Health Center, Santa Monica, CA; and Albert Lai, MD, PhD, assistant clinical professor, Adult Brain Tumors, UCLA Neuro-Oncology Program, for their review of this edition of this publication. This publication is not intended as a substitute for professional medical advice and does not provide advice on treatments or conditions for individual patients. All health and treatment decisions must be made in consultation with your physician(s), utilizing your specific medical information. Inclusion in this publication is not a recommendation of any product, treatment, physician or hospital. COPYRIGHT © 2017 ABTA REPRODUCTION WITHOUT PRIOR WRITTEN PERMISSION IS PROHIBITED AMERICAN BRAIN TUMOR ASSOCIATION Meningioma INTRODUCTION Although meningiomas are considered a type of primary brain tumor, they do not grow from brain tissue itself, but instead arise from the meninges, three thin layers of tissue covering the brain and spinal cord. -
Marginal Tumor Cysts As a Diagnostic MR Finding
Sinonasal Esthesioneuroblastoma with Intracranial Extension: Marginal Tumor Cysts as a Diagnostic MR Finding Peter M. Som, Mika Lidov, Margaret Brandwein, Peter Catalano, and Hugh F. Biller PURPOSE: To determine whether the MR finding of cysts along the intracranial margin of sinonasal esthesioneuroblastomas can be considered to suggest this tumor. METHODS: MR scans of 54 patients who had sinonasal lesions with intracranial extension were examined specifically for cysts along the intracranial margins of the lesions. RESULTS: Only 3 of the 54 patients had these cysts, and all 3 of these patients had esthesioneuroblastoma. Surgical pathologic findings of one speci men showed the cyst to be marginally located within the tumor. CONCLUSION: If cysts are seen on MR along the intracranial margin of a sinonasal mass, this finding highly suggests esthesia neuroblastoma. Index terms: Esthesioneuroblastoma; Nose, magnetic resonance AJNR Am J Neuroradio/15:1259-1262, Aug 1994 Radiologists often seem on a constant quest amelanotic melanomas, and embryonal rhab to give histologic diagnosis for disease seen on domyosarcomas ( 2). All of these neoplasms are sectional imaging studies. Rarely can this be undifferentiated, small-cell tumors, and like es accomplished. However, sometimes the pres thesioneuroblastoma can occur in the nasal ence of one or more imaging findings can allow fossa, with spread to the paranasal sinuses and the radiologist to offer a histologic diagnosis that anterior cranial fossa. Electron microscopy and has a very high degree of reliability. With this histochemical testing are required to establish a aim in mind, we examined the imaging studies definitive diagnosis (3). of 54 patients who had sinonasal masses with Initially, there was hope that radiologists extension into the anterior cranial fossa. -
COMMON BRAIN TUMORS Yarema Bezchlibnyk MD, Phd Assistant Professor of Neurosurgery Morsani School of Medicine, University of South Florida 2
1 COMMON BRAIN TUMORS Yarema Bezchlibnyk MD, PhD Assistant Professor of Neurosurgery Morsani School of Medicine, University of South Florida 2 OVERVIEW • To review the epidemiology, diagnosis, management, and prognosis of common brain tumors, including: • Metastatic tumors • Meningiomas • Glial tumors • High-grade astrocytomas/GBM • Anaplastic gliomas (AA, AO, AOA) • Low-grade gliomas (LGG) 3 EPIDEMIOLOGY OF BRAIN TUMORS • Overall incidence of brain tumors • ~21/100 000 • Metastases are the most common brain tumor seen clinically in adults • ~50% of brain tumors • Meningiomas = ~18% • Gliomas = ~12% • GBM = ~7% • Anaplastic and low-grade gliomas = ~5% • Pituitary adenomas = ~7% • Schwanommas = ~5% • Other = ~8% METASTATIC BRAIN TUMORS EPIDEMIOLOGY OF METASTATIC BRAIN TUMORS • 98,000-170,000 new cases diagnosed each year in U.S. • Peak age 50-70 • 25% of patients with systemic cancer have CNS metastasis on autopsy • 50-80% are multiple TUMOR TYPE AND INCIDENCE/RISK OF BRAIN METS LOCATION OF BRAIN METASTASES Most commonly found at the grey-white matter junction and superficial distal arterial fields The distribution reflects the blood flow to different regions 80% in cerebrum 15% cerebellum 5% brainstem Brem: Neurosurgery, Volume 57(5) Supplement.November 2005.S4-5-S4-9 CLINICAL PRESENTATION • 80% = Metachronous (>2 month after diagnosis of cancer) • 20% = Precocious (1st sign of cancer) or Synchronous (identified at or around the time of the cancer diagnosis) • Neurological symptoms may develop gradually or acutely • Headache, alteration in cognitive function • Other symptoms depending on location: • Focal weakness, ataxia, gait disturbance, cranial nerve findings, hydrocephalus, headache • 20% develop seizures • 15% present with brain bleed IMAGING 10 MANAGEMENT: OVERVIEW • Look for primary cancer • Stage the disease • Precocious • Biopsy or resection for tissue diagnosis • Synchronous or metachronous • Resection vs. -
2004 Implementation Guidelines: Collaborative Staging and Benign/Borderline Intracranial and CNS Tumors
NAACCR 2004 Implementation Guidelines: Collaborative Staging and Benign/Borderline Intracranial and CNS Tumors November 6, 2003 Revised November 14, 2003 NORTH AMERICAN ASSOCIATION OF CENTRAL CANCER REGISTRIES 2004 Implementation Guidelines Table of Contents NAACCR Collaborative Staging Implementation Work Group ............................................5 Benign Brain Tumor Implementation Work Group................................................................6 Acronyms and Abbreviations Used............................................................................................8 1 Introduction..........................................................................................................................9 1.1 Collaborative Staging.......................................................................................9 1.2 Benign and Borderline Intracranial and Central Nervous System Tumors ...10 2 Collaborative Staging System...........................................................................................11 2.1 Standard Setting Organization Collaborative Staging Reporting Requirements 11 2.1.1 CoC Reporting Requirements.........................................................................11 2.1.2 NPCR Reporting Requirements......................................................................12 2.1.3 SEER Reporting Requirements ......................................................................12 2.1.4 Canadian Council of Cancer Registries..........................................................13 2.2 -
Medulloblastoma with Patient Ips Cell-Derived Neural Stem Cells
Modeling SHH-driven medulloblastoma with patient iPS cell-derived neural stem cells Evelyn Susantoa, Ana Marin Navarroa, Leilei Zhoua, Anders Sundströmb, Niek van Breea, Marina Stantica, Mohsen Moslemc, Jignesh Tailord,e, Jonne Rietdijka, Veronica Zubillagaa, Jens-Martin Hübnerf,g, Holger Weishauptb, Johanna Wolfsbergera, Irina Alafuzoffb, Ann Nordgrenh,i, Thierry Magnaldoj, Peter Siesjök,l, John Inge Johnsenm, Marcel Koolf,g, Kristiina Tammimiesm, Anna Darabil, Fredrik J. Swartlingb, Anna Falkc,1, and Margareta Wilhelma,1 aDepartment of Microbiology, Tumor and Cell biology (MTC), Karolinska Institutet, 171 65 Stockholm, Sweden; bDepartment of Immunology, Genetics, and Pathology, Science For Life Laboratory, Uppsala University, 751 85 Uppsala, Sweden; cDepartment of Neuroscience, Karolinska Institutet, 171 65 Stockholm, Sweden; dDevelopmental and Stem Cell Biology Program, The Hospital for Sick Children, Toronto, ON M5G 0A4, Canada; eDivision of Neurosurgery, University of Toronto, Toronto, ON M5S 1A8, Canada; fHopp Children’s Cancer Center (KiTZ), 69120 Heidelberg, Germany; gDivision of Pediatric Neurooncology, German Cancer Research Center (DKFZ), and German Cancer Research Consortium (DKTK), 69120 Heidelberg, Germany; hDepartment of Molecular Medicine and Surgery, Center for Molecular Medicine, Karolinska Institutet, 171 76 Stockholm, Sweden; iDepartment of Clinical Genetics, Karolinska University Hospital, 171 76 Stockholm, Sweden; jInstitute for Research on Cancer and Aging, CNRS UMR 7284, INSERM U1081, University of Nice Sophia Antipolis, Nice, France; kDivision of Neurosurgery, Department of Clinical Sciences, Skane University Hospital, 221 85 Lund, Sweden; lGlioma Immunotherapy Group, Division of Neurosurgery, Department of Clinical Sciences, Lund University, 221 85 Lund, Sweden; and mDepartment of Women’s and Children’s Health, Karolinska Institutet, 171 76 Stockholm, Sweden Edited by Matthew P. -
Headmirror's ENT in a Nutshell Esthesioneuroblastoma Experts: Garret Choby, M.D. and Jamie Van Gompel, M.D. Presentation (0:28
Headmirror’s ENT in a Nutshell Esthesioneuroblastoma Experts: Garret Choby, M.D. and Jamie Van Gompel, M.D. Presentation (0:28) - Symptomatology o Nasal obstruction o Hyposmia or anosmia o Epistaxis o Headache, vision changes o Rare presentation cervical metastasis (5% patients) - Physical Examination o High nasal vault tumor (olfactory cleft) o Fleshy mass, moderately vascular o Thorough cranial nerve and neck examination - Epidemiology o Bimodal age distribution o SEER database middle to late age (40-60s) - Differential Diagnosis o Squamous cell carcinoma o Sinonasal undifferentiated carcinoma o Sinonasal neuroendocrine carcinoma o Lymphoma (imaging can look very similar) o Rhabdomyosarcoma o Ewing Sarcoma o Sinonasal mucosal melanoma Pathophysiology (2:20) - Theorized to arise from bipolar cell from nasal epithelium (upper 1.5 cm of the nasal vault) - Small blue round cell tumor or neuroendocrine tumor - Homer-Wright rosettes (1/3 of patients) - Flexner wintersteiner rosettes Workup (6:00) - Imaging o CT scan . Boney erosion at the skull base o MRI . Uniformly enhancing mass in the upper nasal vault with possible extension into the paranasal sinuses and intracranially . Dumbbell appearance is not reliable sign clincally o PET-CT scan . Especially for Kadish C-D lesions . Metastatic work up usually not performed for small lesions or Hyams grade 1-2 - Biopsy o Most important next step after imaging, especially in clinic - Grading System o Kadish Staging System . A: confined into the nasal cavity . B: extension into the paranasal sinuses . C: tumor beyond nasal cavity and paranasal sinus which can include cribiform plate, erosion of skull base, intracranial cavity or orbital invasion . D: cervical nodes or distant metastasis o Hyams Grading System . -
Parapharyngeal Space Tumors
IJHNS 10.5005/jp-journals-10001-1059 REVIEW ARTICLE Parapharyngeal Space Tumors Parapharyngeal Space Tumors Pratima S Khandawala Senior Registrar, Department of ENT, Holy Family Hospital, Bandra, Mumbai, Maharashtra, India Correspondence: Pratima S Khandawala, Senior Registrar, Department of ENT, Holy Family Hospital, Bandra, Mumbai Maharashtra, India, e-mail: [email protected] ABSTRACT Parapharyngeal space is a potential space in the neck extending from skull base to the greater cornu of hyoid bone. It is divided in prestyloid and poststyloid compartment by the fascia joining styloid process to tensor veli palatini. Tumors of parapharyngeal space are uncommon, comprising of less than 1% of all head and neck neoplasms. CT Scanning and MRI investigations is complimentary and both studies should be performed for evaluation of lesions in this area. Complete surgical excision is the mainstay of treatment. Keywords: Parapharyngeal space, Prestyloid, Poststyloid, CT scan, MRI. ANATOMY It is continuous with the retropharyngeal space and also communicates with other cervical and cranial fascial spaces The parapharyngeal space (or lateral pharyngeal space) is a as well as the mediastinum. potential space in the neck shaped like an inverted pyramid. Divisions and Contents (Fig. 2) Boundaries (Fig. 1) The parapharyngeal space is divided into prestyloid and • Inferior greater cornu of the hyoid bone forming the apex poststyloid compartments by the fascia joining the styloid • Superior—base of skull (sphenoid and temporal bones), process to the tensor veli palatini. this area includes the jugular and hypoglossal foramen These lymphatics receive afferent drainage from the oral and the foramen lacerum cavity, oropharynx, paranasal sinuses and thyroid.