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      Call for Papers: Supportive Care - Essential for Modern Oncology

      Submit here before December 31, 2024

      About Oncology Research and Treatment: 2.0 Impact Factor I 3.2 CiteScore I 0.521 Scimago Journal & Country Rank (SJR)

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      A Husband and a Wife with Simultaneous Presentation of Glioblastoma Multiforme: A Case Report

      case-report

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          Abstract

          Glioblastoma multiforme (GBM) is the most lethal subtype of glioma, classified as a WHO grade 4 infiltrative glioma. The etiology of GBM remains unknown and risk factors can be identified only in a small minority. We report the synchronous occurrence of GBM in an otherwise unrelated married couple, i.e. a husband and his wife, who developed GBM within an interval of 1 month. No specific causative environmental factors were identified for both patients, and the genetic screens were negative for hereditary syndromes. Family history was negative for tumors, and no other incidence of cancer in either siblings, parents or other children was reported. An analysis of the couple's exposure to nonionizing electromagnetic fields and ionizing radiations revealed values within the normal ranges usually found in homes. Overall, conjugal tumors are rarely reported. However, the case reported herein raises important questions about possible etiologic factors.

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          Brain tumors.

          L M DeAngelis (2001)
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            Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas.

            Hiroko Ohgaki, Paul Kleihues (2005)
            Published data on prognostic and predictive factors in patients with gliomas are largely based on clinical trials and hospital-based studies. This review summarizes data on incidence rates, survival, and genetic alterations from population-based studies of astrocytic and oligodendrogliomas that were carried out in the Canton of Zurich, Switzerland (approximately 1.16 million inhabitants). A total of 987 cases were diagnosed between 1980 and 1994 and patients were followed up at least until 1999. While survival rates for pilocytic astrocytomas were excellent (96% at 10 years), the prognosis of diffusely infiltrating gliomas was poorer, with median survival times (MST) of 5.6 years for low-grade astrocytoma WHO grade II, 1.6 years for anaplastic astrocytoma grade III, and 0.4 years for glioblastoma. For oligodendrogliomas the MSTwas 11.6 years for grade II and 3.5 years for grade III. TP53 mutations were most frequent in gemistocytic astrocytomas (88%), followed by fibrillary astrocytomas (53%) and oligoastrocytomas (44%), but infrequent (13%) in oligodendrogliomas. LOH 1p/19q typically occurred in tumors without TP53 mutations and were most frequent in oligodendrogliomas (69%), followed by oligoastrocytomas (45%), but were rare in fibrillary astrocytomas (7%) and absent in gemistocytic astrocytomas. Glioblastomas were most frequent (3.55 cases per 100,000 persons per year) adjusted to the European Standard Population, amounting to 69% of total incident cases. Observed survival rates were 42.4% at 6 months, 17.7% at one year, and 3.3% at 2 years. For all age groups, survival was inversely correlated with age, ranging from an MST of 8.8 months ( 80 years). In glioblastomas, LOH 10q was the most frequent genetic alteration (69%), followed by EGFR amplification (34%), TP53 mutations (31%), p16INK4a deletion (31%), and PTEN mutations (24%). LOH 10q occurred in association with any of the other genetic alterations, and was the only alteration associated with shorter survival of glioblastoma patients. Primary (de novo) glioblastomas prevailed (95%), while secondary glioblastomas that progressed from low-grade or anaplastic gliomas were rare (5%). Secondary glioblastomas were characterized by frequent LOH 10q (63%) and TP53 mutations (65%). Of the TP53 mutations in secondary glioblastomas, 57% were in hot-spot codons 248 and 273, while in primary glioblastomas, mutations were more evenly distributed. G:C-->A:T mutations at CpG sites were more frequent in secondary than primary glioblastomas, suggesting that the acquisition of TP53 mutations in these glioblastoma subtypes may occur through different mechanisms.
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              Carcinogenicity of radiofrequency electromagnetic fields.

              Robert Baan, Yann Grosse, Béatrice Lauby-Secretan … (2011)
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                Author and article information

                Journal
                Journal ID (publisher-id): CRO
                Journal ID (pmc): CRO
                Journal ID (doi): 10.1159/issn.1662-6575
                Title: Case Reports in Oncology
                Publisher: S. Karger AG
                ISSN (Electronic): 1662-6575
                Publication date Subscription-year: 2013
                Publication date Collection: September – December 2013
                Publication date (Electronic): 30 October 2013
                Volume: 6
                Issue: 3
                Pages: 538-543
                Affiliations
                aMedical Oncology Unit, bUnit NINT Neuroimaging and Neurointervention, Department of Neurological and Sensorineural Sciences, cDepartment of Human Pathology and Oncology Section of Pathological Anatomy, and dSection of Radiological Sciences, Department of Human Pathology and Oncology, Azienda Opedaliera Universitaria Senese, Policlinico ‘Santa Maria alle Scotte', Siena, Italy
                Author notes
                *Giandomenico Roviello, MD, Medical Oncology Unit, University of Siena, Policlinico ‘Santa Maria alle Scotte', Viale Bracci 11, IT-53100 Siena (Italy), E-Mail giandomenicoroviello@hotmail.it
                Article
                Publisher ID: 356098 Pmcid ID: PMC3843927 Other ID: Case Rep Oncol 2013;6:538-543
                DOI: 10.1159/000356098
                PMC ID: PMC3843927
                PubMed ID: 24348390
                SO-VID: ece82878-d126-43b5-a240-19e93b5522ba
                Copyright © © 2013 S. Karger AG, Basel
                License:

                Open Access License: This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) ( http://www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Figures: 2, Pages: 6
                Categories
                Subject: Published: October 2013

                ScienceOpen disciplines: Oncology & Radiotherapy,Pathology,Surgery,Obstetrics & Gynecology,Pharmacology & Pharmaceutical medicine,Hematology
                Keywords: Glioblastoma multiforme,Familial risk,Synchronous occurrence
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy, Pathology, Surgery, Obstetrics & Gynecology, Pharmacology & Pharmaceutical medicine, Hematology
                Keywords: Glioblastoma multiforme, Familial risk, Synchronous occurrence

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