2019 Neoplasms of the BRAIN/CNS CDC & Florida DOH Attribution
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Neurofibromatosis Type 2 (NF2)
International Journal of Molecular Sciences Review Neurofibromatosis Type 2 (NF2) and the Implications for Vestibular Schwannoma and Meningioma Pathogenesis Suha Bachir 1,† , Sanjit Shah 2,† , Scott Shapiro 3,†, Abigail Koehler 4, Abdelkader Mahammedi 5 , Ravi N. Samy 3, Mario Zuccarello 2, Elizabeth Schorry 1 and Soma Sengupta 4,* 1 Department of Genetics, Cincinnati Children’s Hospital, Cincinnati, OH 45229, USA; [email protected] (S.B.); [email protected] (E.S.) 2 Department of Neurosurgery, University of Cincinnati, Cincinnati, OH 45267, USA; [email protected] (S.S.); [email protected] (M.Z.) 3 Department of Otolaryngology, University of Cincinnati, Cincinnati, OH 45267, USA; [email protected] (S.S.); [email protected] (R.N.S.) 4 Department of Neurology, University of Cincinnati, Cincinnati, OH 45267, USA; [email protected] 5 Department of Radiology, University of Cincinnati, Cincinnati, OH 45267, USA; [email protected] * Correspondence: [email protected] † These authors contributed equally. Abstract: Patients diagnosed with neurofibromatosis type 2 (NF2) are extremely likely to develop meningiomas, in addition to vestibular schwannomas. Meningiomas are a common primary brain tumor; many NF2 patients suffer from multiple meningiomas. In NF2, patients have mutations in the NF2 gene, specifically with loss of function in a tumor-suppressor protein that has a number of synonymous names, including: Merlin, Neurofibromin 2, and schwannomin. Merlin is a 70 kDa protein that has 10 different isoforms. The Hippo Tumor Suppressor pathway is regulated upstream by Merlin. This pathway is critical in regulating cell proliferation and apoptosis, characteristics that are important for tumor progression. -
Charts Chart 1: Benign and Borderline Intracranial and CNS Tumors Chart
Charts Chart 1: Benign and Borderline Intracranial and CNS Tumors Chart Glial Tumor Neuronal and Neuronal‐ Ependymomas glial Neoplasms Subependymoma Subependymal Giant (9383/1) Cell Astrocytoma(9384/1) Myyppxopapillar y Desmoplastic Infantile Ependymoma Astrocytoma (9412/1) (9394/1) Chart 1: Benign and Borderline Intracranial and CNS Tumors Chart Glial Tumor Neuronal and Neuronal‐ Ependymomas glial Neoplasms Subependymoma Subependymal Giant (9383/1) Cell Astrocytoma(9384/1) Myyppxopapillar y Desmoplastic Infantile Ependymoma Astrocytoma (9412/1) (9394/1) Use this chart to code histology. The tree is arranged Chart Instructions: Neuroepithelial in descending order. Each branch is a histology group, starting at the top (9503) with the least specific terms and descending into more specific terms. Ependymal Embryonal Pineal Choro id plexus Neuronal and mixed Neuroblastic Glial Oligodendroglial tumors tumors tumors tumors neuronal-glial tumors tumors tumors tumors Pineoblastoma Ependymoma, Choroid plexus Olfactory neuroblastoma Oligodendroglioma NOS (9391) (9362) carcinoma Ganglioglioma, anaplastic (9522) NOS (9450) Oligodendroglioma (9390) (9505 Olfactory neurocytoma Ganglioglioma, malignant (()9521) anaplastic (()9451) Anasplastic ependymoma (9505) Olfactory neuroepithlioma Oligodendroblastoma (9392) (9523) (9460) Papillary ependymoma (9393) Glioma, NOS (9380) Supratentorial primitive Atypical EdEpendymo bltblastoma MdllMedulloep ithliithelioma Medulloblastoma neuroectodermal tumor tetratoid/rhabdoid (9392) (9501) (9470) (PNET) (9473) tumor -
Paraganglioma (PGL) Tumors in Patients with Succinate Dehydrogenase-Related PCC–PGL Syndromes: a Clinicopathological and Molecular Analysis
T G Papathomas and others Non-PCC/PGL tumors in the SDH 170:1 1–12 Clinical Study deficiency Non-pheochromocytoma (PCC)/paraganglioma (PGL) tumors in patients with succinate dehydrogenase-related PCC–PGL syndromes: a clinicopathological and molecular analysis Thomas G Papathomas1, Jose Gaal1, Eleonora P M Corssmit2, Lindsey Oudijk1, Esther Korpershoek1, Ketil Heimdal3, Jean-Pierre Bayley4, Hans Morreau5, Marieke van Dooren6, Konstantinos Papaspyrou7, Thomas Schreiner8, Torsten Hansen9, Per Arne Andresen10, David F Restuccia1, Ingrid van Kessel6, Geert J L H van Leenders1, Johan M Kros1, Leendert H J Looijenga1, Leo J Hofland11, Wolf Mann7, Francien H van Nederveen12, Ozgur Mete13,14, Sylvia L Asa13,14, Ronald R de Krijger1,15 and Winand N M Dinjens1 1Department of Pathology, Josephine Nefkens Institute, Erasmus MC, University Medical Center, PO Box 2040, 3000 CA Rotterdam, The Netherlands, 2Department of Endocrinology, Leiden University Medical Center, Leiden,The Netherlands, 3Section for Clinical Genetics, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, 4Department of Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands, 5Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands, 6Department of Clinical Genetics, Erasmus MC, University Medical Center, Rotterdam, The Netherlands, 7Department of Otorhinolaryngology, Head and Neck Surgery, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany, 8Section for Specialized Endocrinology, -
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, -
Ganglioneuroma of the Sacrum
https://doi.org/10.14245/kjs.2017.14.3.106 KJS Print ISSN 1738-2262 On-line ISSN 2093-6729 CASE REPORT Korean J Spine 14(3):106-108, 2017 www.e-kjs.org Ganglioneuroma of the Sacrum Donguk Lee1, Presacral ganglioneuromas are extremely rare benign tumors and fewer than 20 cases have been reported in the literature. Ganglioneuromas are difficult to be differentiated preoperatively Woo Jin Choe1, from tumors such as schwannomas, meningiomas, and neurofibromas with imaging modalities. 2 So Dug Lim The retroperitoneal approach for resection of presacral ganglioneuroma was performed for gross total resection of the tumor. Recurrence and malignant transformation of these tumors is rare. 1 Departments of Neurosurgery and Adjuvant chemotherapy or radiation therapy is not indicated because of their benign nature. 2Pathology, Konkuk University Medical Center, Konkuk University We report a case of a 47-year-old woman with a presacral ganglioneuroma. School of Medicine, Seoul, Korea Key Words: Ganglioneuroma, Presacral, Anterior retroperitoneal approach Corresponding Author: Woo Jin Choe Department of Neurosurgery, Konkuk University Medical Center, displacing the left sacral nerve roots, without 120-1 Neungdong-ro, Gwangjin-gu, INTRODUCTION Seoul 05030, Korea any evidence of bony invasion (Fig. 2). We performed surgery via anterior retrope- Tel: +82-2-2030-7625 Ganglioneuroma is an uncommon benign tu- ritoneal approach and meticulous adhesiolysis Fax: +82-2-2030-7359 mor of neural crest origin which is mainly loca- was necessary because of massive abdominal E-mail: [email protected] lized in the posterior mediastinum, retroperito- adhesion due to the previous gynecologic sur- 1,6) Received: August 16, 2017 neum, and adrenal gland . -
Updates in Assessment of the Breast After Neoadjuvant Treatment
Updates in Assessment of The Breast After Neoadjuvant Treatment Laila Khazai 3/3/18 AJCC, 8th Edition AJCC • Pathologic Prognostic Stage is not applicable for patients who receive neoadjuvant therapy. • Pathologic staging includes all data used for clinical staging, plus data from surgical resection. • Information recorded should include: – Clinical Prognostic Stage. – The category information for either clinical (ycT and ycN) response to therapy if surgery is not performed, or pathologic (ypT and ypN) if surgery is performed. – Degree of response (complete, partial, none). AJCC • Post -treatment size should be estimated based on the best combination of imaging, gross, and microscopic histological findings. • The ypT is determined by measuring the largest single focus of residual invasive tumor, with a modifier (m) indicating multiple foci of residual tumor. • This measurement does not include areas of fibrosis within the tumor bed. • When the only residual cancer intravascular or intralymphatic (LVI), the yPT0 category is assigned, but it is not classified as complete pathologic response. A formal system (i.e. RCB, Miller-Payne, Chevalier, …) may be offered in the report. Otherwise, description of the distance over which tumor foci extend, the number of tumor foci present, or the number of tumor slides/blocks in which tumor appears might be offered. AJCC • The ypN categories are the same as those used for pN. • Only the largest contiguous focus of residual tumor is used for classification (treatment associated fibrosis is not included). • Inclusion of additional information such as distance over which tumor foci extend and the number of tumor foci present, may assist the clinician in estimating the extent of residual disease. -
Downloaded 09/30/21 01:49 PM UTC NF2 Patients There Were Often Multiple Meningiomas
Neurosurg Focus 4 (3):Article 1, 1998 Neurofibromatosis type 2 and central neurofibromatosis Leonard I. Malis, M.D. The Mount Sinai School of Medicine, New York City, New York Neurofibromatosis type 2 (NF2) is a rare disease, affecting only approximately 1000 patients in the entire United States. The diagnosis requires the presence of bilateral acoustic neuromas, but many other tumors of the nervous system are also present. It is a very different disease from von Recklinghausen's neurofibromatosis, NF1. The remarkable genetic research in recent years has defined the origin of NF2 to be the lack of a specific suppressor protein, known as Merlin. While we await a method to replace this protein, the neurosurgical care of these patients is a formidable problem. The author reviews his personal series of 41 patients with NF2 treated during the past 30 years and presents 10 cases in detail to demonstrate their considerable range of differences and the treatment problems they have posed. Key Words * neurofibromatosis type 2 * bilateral acoustic neurofibromatosis * central neurofibromatosis * bilateral acoustic neuromas * bilateral vestibular schwannomas * Merlin * schwannomin This review is based on my personal series of 41 surgically treated patients with neurofibromatosis type 2 (NF2). The patients were cared for in the microsurgical era between 1970 and 1995 and received minimum follow-up care of 3 years (median 12 years). All of these people were referred because of bilateral acoustic neuromas. This was a quite young group, with the average age only 20 years, much younger than my patients with solitary acoustic neuromas. The youngest patient was 8 years old and the oldest 40 years old when first referred. -
Ambient Mass Spectrometry for the Intraoperative Molecular Diagnosis of Human Brain Tumors
Ambient mass spectrometry for the intraoperative molecular diagnosis of human brain tumors Livia S. Eberlina, Isaiah Nortonb, Daniel Orringerb, Ian F. Dunnb, Xiaohui Liub, Jennifer L. Ideb, Alan K. Jarmuscha, Keith L. Ligonc, Ferenc A. Joleszd, Alexandra J. Golbyb,d, Sandro Santagatac, Nathalie Y. R. Agarb,d,1, and R. Graham Cooksa,1 aDepartment of Chemistry and Center for Analytical Instrumentation Development, Purdue University, West Lafayette, IN 47907; and Departments of bNeurosurgery, cPathology, and dRadiology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115 Edited by Jack Halpern, The University of Chicago, Chicago, IL, and approved December 5, 2012 (received for review September 11, 2012) The main goal of brain tumor surgery is to maximize tumor resection at Brigham and Women’s Hospital (BWH), created an opportu- while preserving brain function. However, existing imaging and nity for collecting information about the extent of tumor resection surgical techniques do not offer the molecular information needed during surgery (5, 6). Although brain tumor resection typically to delineate tumor boundaries. We have developed a system to requires multiple hours, intraoperative MRI can be completed rapidly analyze and classify brain tumors based on lipid information and information evaluated within an hour. However, MRI has acquired by desorption electrospray ionization mass spectrometry limited ability to distinguish residual tumor from surrounding (DESI-MS). In this study, a classifier was built to discriminate gliomas normal brain (9). In consequence, there is a need for more de- and meningiomas based on 36 glioma and 19 meningioma samples. tailed molecular information to be acquired on a timescale closer The classifier was tested and results were validated for intraoper- to real time than can be supplied by MRI. -
The Updated AJCC/TNM Staging System (8Th Edition) for Oral Tongue Cancer
166 Editorial The updated AJCC/TNM staging system (8th edition) for oral tongue cancer Kyubo Kim, Dong Jin Lee Department of Otorhinolaryngology-Head and Neck Surgery, Hallym University College of Medicine, Seoul, South Korea Correspondence to: Dong Jin Lee, MD, PhD. 1 Singil-ro, Yeongdeungpo-gu, Seoul 150-950, South Korea. Email: [email protected]. Comment on: Almangush A, Mäkitie AA, Mäkinen LK, et al. Small oral tongue cancers (≤ 4 cm in diameter) with clinically negative neck: from the 7th to the 8th edition of the American Joint Committee on Cancer. Virchows Arch 2018;473:481-7. Submitted Dec 22, 2018. Accepted for publication Dec 28, 2018. doi: 10.21037/tcr.2019.01.02 View this article at: http://dx.doi.org/10.21037/tcr.2019.01.02 An increasing amount of literature shows solid evidence that updated classification system and the applicability of DOI as the depth of invasion (DOI) of oral cavity squamous cell a predictor of clinical behavior for early-stage OTSCC. carcinoma is an independent predictor for occult metastasis, The AJCC 8th edition employs a cut-off value of 5 mm recurrence, and survival (1-3). Furthermore, the DOI of the DOI for upstaging from stage T1 to T2 and 10 mm for primary tumor has been a major criterion when deciding to upstaging to T3. This may be questionable as it has been perform elective neck dissection on oral cavity squamous shown that an invasion depth of more than 4 mm increases cell carcinoma patients since as early as the mid-1990s (4). the risk of locoregional metastasis and is associated with a A cut-off value of 4 mm has conventionally been used poor prognosis (9-11), but with the new staging system, a when determining the need for elective neck dissection, large number of invasive tumors in which the DOI is less based on a study by Kligerman et al. -
Diagnostic Value of Preoperative Inflammatory Markers in Patients with Glioma: a Multicenter Cohort Study
CLINICAL ARTICLE J Neurosurg 129:583–592, 2018 Diagnostic value of preoperative inflammatory markers in patients with glioma: a multicenter cohort study *Shi-hao Zheng, MD,1 Jin-lan Huang, PhD,2,4 Ming Chen, MD,3 Bing-long Wang, BS,2 Qi-shui Ou, PhD,2 and Sheng-yue Huang, BS1 1Department of Neurosurgery, Fujian Provincial Hospital; 2Department of Clinical Laboratory, First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian; 3Department of Neurosurgery, Xin Hua Hospital, Affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai; and 4Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, People’s Republic of China OBJECTIVE Glioma is the most common form of brain tumor and has high lethality. The authors of this study aimed to elucidate the efficiency of preoperative inflammatory markers, including neutrophil/lymphocyte ratio (NLR), derived NLR (dNLR), platelet/lymphocyte ratio (PLR), lymphocyte/monocyte ratio (LMR), and prognostic nutritional index (PNI), and their paired combinations as tools for the preoperative diagnosis of glioma, with particular interest in its most aggressive form, glioblastoma (GBM). METHODS The medical records of patients newly diagnosed with glioma, acoustic neuroma, meningioma, or nonle- sional epilepsy at 3 hospitals between January 2011 and February 2016 were collected and retrospectively analyzed. The values of NLR, dNLR, PLR, LMR, and PNI were compared among patients suffering from glioma, acoustic neuroma, meningioma, and nonlesional epilepsy and healthy controls by using nonparametric tests. Correlations between NLR, dNLR, PLR, LMR, PNI, and tumor grade were analyzed. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic significance of NLR, dNLR, PLR, LMR, PNI, and their paired combinations for glioma, particularly GBM. -
Central Neurocytoma SNP Array Analyses, Subtel FISH, and Review
Pathology - Research and Practice 215 (2019) 152397 Contents lists available at ScienceDirect Pathology - Research and Practice journal homepage: www.elsevier.com/locate/prp Case report Central neurocytoma: SNP array analyses, subtel FISH, and review of the T literature Caroline Sandera,1, Marco Wallenborna,b,1, Vivian Pascal Brandtb, Peter Ahnertc, Vera Reuscheld, ⁎ Christan Eisenlöffele, Wolfgang Kruppa, Jürgen Meixensbergera, Heidrun Hollandb, a Dept. of Neurosurgery, University of Leipzig, Liebigstraße 26, 04103 Leipzig, Germany b Saxonian Incubator for Clinical Translation, University of Leipzig, Philipp-Rosenthal Str. 55, 04103 Leipzig, Germany c Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig, Haertelstraße 16-18, 04107 Leipzig, Germany d Dept. of Neuroradiology, University of Leipzig, Liebigstraße 22a, 04103 Leipzig, Germany e Dept. of Neuropathology, University of Leipzig, Liebigstraße 26, 04103 Leipzig, Germany ARTICLE INFO ABSTRACT Keywords: The central neurocytoma (CN) is a rare brain tumor with a frequency of 0.1-0.5% of all brain tumors. According Central neurocytoma to the World Health Organization classification, it is a benign grade II tumor with good prognosis. However, Cytogenetics some CN occur as histologically “atypical” variant, combined with increasing proliferation and poor clinical SNP array outcome. Detailed genetic knowledge could be helpful to characterize a potential atypical behavior in CN. Only FISH few publications on genetics of CN exist in the literature. Therefore, we performed cytogenetic analysis of an intraventricular neurocytoma WHO grade II in a 39-year-old male patient by use of genome-wide high-density single nucleotide polymorphism array (SNP array) and subtelomere FISH. Applying these techniques, we could detect known chromosomal aberrations and identified six not previously described chromosomal aberrations, gains of 1p36.33-p36.31, 2q37.1-q37.3, 6q27, 12p13.33-p13.31, 20q13.31-q13.33, and loss of 19p13.3-p12. -
Oncology 101 Dictionary
ONCOLOGY 101 DICTIONARY ACUTE: Symptoms or signs that begin and worsen quickly; not chronic. Example: James experienced acute vomiting after receiving his cancer treatments. ADENOCARCINOMA: Cancer that begins in glandular (secretory) cells. Glandular cells are found in tissue that lines certain internal organs and makes and releases substances in the body, such as mucus, digestive juices, or other fluids. Most cancers of the breast, pancreas, lung, prostate, and colon are adenocarcinomas. Example: The vast majority of rectal cancers are adenocarcinomas. ADENOMA: A tumor that is not cancer. It starts in gland-like cells of the epithelial tissue (thin layer of tissue that covers organs, glands, and other structures within the body). Example: Liver adenomas are rare but can be a cause of abdominal pain. ADJUVANT: Additional cancer treatment given after the primary treatment to lower the risk that the cancer will come back. Adjuvant therapy may include chemotherapy, radiation therapy, hormone therapy, targeted therapy, or biological therapy. Example: The decision to use adjuvant therapy often depends on cancer staging at diagnosis and risk factors of recurrence. BENIGN: Not cancerous. Benign tumors may grow larger but do not spread to other parts of the body. Also called nonmalignant. Example: Mary was relieved when her doctor said the mole on her skin was benign and did not require any further intervention. BIOMARKER TESTING: A group of tests that may be ordered to look for genetic alterations for which there are specific therapies available. The test results may identify certain cancer cells that can be treated with targeted therapies. May also be referred to as genetic testing, molecular testing, molecular profiling, or mutation testing.