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Books on the topic 'Glioma brain tumor'

Author: Grafiati
Published: 4 June 2025
Last updated: 23 June 2025

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1

J, Apuzzo Michael L., and AANS Publications Committee., eds. Benign cerebral glioma. American Association of Neurological Surgeons, 1995.

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2

G, Broggi, and Gerosa M. A, eds. Cerebral gliomas: Proceedings of the International Workshop on Brain Tumors, held in Santa Margherita Ligure, Italy, 20-22 June 1988. Excerpta Medica, 1989.

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3

Michaud, Dominique, David Savitz, and Lorelei Mucci. Brain Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0024.

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cBrain tumors constitute an array of histologic types, the most common being meningioma and glioma. Unlike other cancers, both benign and malignant brain tumors are concerning for survival because of their anatomic location. Two-thirds of brain tumors are benign. The most well established risk factor is high dose ionizing radiation, based on studies of atomic bomb survivors as well as children treated for tinea capitis. In contrast, nonionizing radiation including from cellular telephones, is not a risk factor. Tobacco use does not appear to be associated with glioma or meningioma. There is fairly consistent evidence of an inverse association between allergies and asthma with risk of glioma, potentially through levels of IgE. Finally, occupational epidemiology studies suggest potential positive associations with specific exposures. The identification of modifiable risk factors for brain tumors has been challenging, due in part to the diversity of tumor subtypes.
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4

Biological aspects of brain tumors: Proceedings of the 8th Nikko Brain Tumor Conference, Karatsu (Saga) 1990. Springer-Verlag, 1991.

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5

Woolf, Eric C., and Adrienne C. Scheck. Ketogenic Diet as Adjunctive Therapy for Malignant Brain Cancer. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0013.

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Malignant brain tumors are devastating, and increased survival requires new therapeutic modalities. Metabolic dysregulation results in an increased need for glucose in tumor cells, suggesting that reduced tumor growth could be achieved with decreased glucose availability either through pharmacological means or use of a high-fat, low-carbohydrate ketogenic diet (KD). KD provides increased blood ketones to support energy needs of normal tissues and has been shown to reduce tumor growth, angiogenesis, inflammation, peritumoral edema, migration, and invasion. Furthermore, this diet can enhance the activity of radiation and chemotherapy in a mouse model of glioma, thus increasing survival. In vitro studies indicate that increasing ketones in the absence of glucose reduction can also inhibit cell growth and potentiate the effects of radiation. Thus, emerging data provide strong support for the use of KD in the treatment of malignant gliomas and thus far has led to a limited number of clinical trials.
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6

Sanai, Nader. Low-Grade Gliomas. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0027.

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Low grade gliomas encompass multiple histologic diagnoses of primary brain tumors, most commonly grade 2 oligodendroglioma and grade 2 astrocytoma. This chapter presents a case of a patient with a left temporal low grade glioma who presented with seizures, which are a common presenting symptom for this tumor type. Management of patients with a newly diagnosed low grade glioma typically begins with maximal safe surgical resection for surgically accessible tumors. Surgical planning may involve functional imaging such as with fMRI. Genetic and molecular markers help distinguish subtypes of low grade gliomas, and this subtyping has implications for the type and timing of adjuvant therapy.
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7

Kaley, Thomas J. Oligodendrogliomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0128.

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Gliomas represent the most common symptomatic primary brain tumors, of which oligodendrogliomas are the least common subtype of glioma.1 The traditional thinking is that although the rarest, they also offer patients the best prognosis and they are deemed to be the most sensitive to treatment. However, although they may have a longer average survival than most other gliomas, nearly all patients with an oligodendroglioma will ultimately succumb to their illness due to either progressive and recurrent tumor or malignant transformation into a higher grade tumor. Optimal treatment of oligodendroglial tumors, especially those harboring a 1P/19Q codeletion, remains controversial.
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8

A new diffusely infiltrating glioma mouse model reveals neuronal alterations in the brain tumor microenvironment. [publisher not identified], 2018.

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9

Eseonu, Chikezie I., Jordina Rincon-Torroella, and Alfredo Quiñones-Hinojosa. Unusual Gliomas. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0002.

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Patients with intra-axial brain tumors often present with neurologic symptoms based on the anatomic location of their tumor. Workup for a brain tumor includes cranial imaging such as magnetic resonance imaging and computed tomography, as well as systemic imaging to assess for primary tumor if metastasis is suspected. Maximal safe resection optimizes outcomes including overall survival. Surgical decisions are based on variables such as medical comorbidities and anatomic location of the tumor. Gliomas in eloquent areas may require intraoperative cortical and subcortical mapping of motor and/or language areas to optimize safety and help maximize resection. Adjuvant chemotherapy and radiation lead to a median survival of 14.6 months for patients with glioblastoma. Rapidly recurring glioblastoma after surgery has a poor prognosis.
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10

Huntoon, Kristin, and J. Bradley Elder. High-Grade Gliomas. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0001.

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Glioblastoma is the most common primary malignant brain tumor. This chapter discusses the clinical presentation and initial workup for a patient with a suspected glioblastoma, as well as the optimal treatment strategy and prognosis. Diagnosis is typically made using magnetic resonance imaging. Optimal treatment involves maximal safe surgical resection followed by adjuvant chemotherapy and radiation therapy. Surgical adjuncts including intraoperative imaging modalities and brain mapping techniques help improve neurologic morbidity associated with surgery. Despite maximal treatment, virtually all patients with glioblastoma will experience recurrence of their tumor and may be considered for clinical trials or second-line therapy. This chapter highlights important pearls associated with management of patients with glioblastoma and written for those who are interested in neuro-oncology, neurosurgery, and the field of brain tumors.
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11

Cerebral gliomas: Proceedings of the International Workshop on Brain Tumors, held in Santa Margherita Ligure, Italy, 20-22 June 1988 (International congress series). Sole distributors for the USA and Canada, Elsevier Science Pub. Co, 1989.

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12

Barnett, Gene H. High-Grade Gliomas: Diagnosis and Treatment (Current Clinical Oncology). Humana Press, 2006.

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13

Barnett, Gene H. High-grade Gliomas: Diagnosis and Treatment. Humana P.,U.S., 2006.

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14

Apuzzo, Michael L., and Micheal L. J. Apuzzo. Benign Cerebral Glioma, Volume II. American Association of Neurological Surgeons, 1995.

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15

Taillandier, Luc, Laurent Capelle, and Hugues Duffau. New Therapeutic Strategies in Low-grade Gliomas. Nova Science Publishers, 2006.

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16

Tonn, J. C., M. Westphal, and Z. Ram. Local Therapies for Glioma: Present Status and Future Developments. Springer Wien, 2012.

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17

(Editor), M. Westphal, J. C. Tonn (Editor), and Z. Ram (Editor), eds. Local Therapies for Glioma: Present Status and Future Developments (Acta Neurochirurgica Supplementum). Springer, 2004.

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18

Modern Management Of High Grade Glioma. W.B. Saunders Company, 2012.

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19

Pandey, Sanjeet, Dr Sheshang Degadwala, and Dr Vineet Kumar Singh. BRAIN TUMOR CLASSIFICATION INTO HIGH AND LOW GRADE GLIOMAS. Scholars' Press, 2021.

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20

Hayat, M. A. Tumors of the Central Nervous System, Volume 1 : Gliomas: Glioblastoma. Springer, 2013.

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21

Hayat, M. A. Tumors of the Central Nervous System, Volume 2 : Gliomas: Glioblastoma. Springer, 2013.

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22

Norden, Andrew D., David A. Reardon, and Patrick C. Y. Wen. Primary Central Nervous System Tumors: Pathogenesis and Therapy. Humana Press, 2011.

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23

Hayat, M. A. Pediatric Cancer, Volume 2: Teratoid/Rhabdoid, Brain Tumors, and Glioma. Springer London, Limited, 2012.

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24

Hayat, M. A. Pediatric Cancer, Volume 2: Teratoid/Rhabdoid, Brain Tumors, and Glioma. Springer, 2016.

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25

James M., M.D. Markert (Editor), Vincent T. Devita (Editor), Samuel Hellman (Editor), and Steven A. Rosenberg (Editor), eds. Glioblastoma Multiforme. Jones & Bartlett Publishers, 2004.

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26

Norden, Andrew D., David A. Reardon, and Patrick C. Y. Wen. Primary Central Nervous System Tumors: Pathogenesis and Therapy. Humana Press, 2013.

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27

Therapeutic Ribonucleic Acids In Brain Tumors. Springer, 2009.

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28

Barciszewski, Jan, Volker A. Erdmann, and Guido Reifenberger. Therapeutic Ribonucleic Acids in Brain Tumors. Springer Berlin / Heidelberg, 2014.

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29

Amirian, E. Susan, Quinn T. Ostrom, Yanhong Liu, Jill Barnholtz-Sloan, and Melissa L. Bondy. Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0056.

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Although brain and other nervous system tumors are relatively rare, constituting up to 4% of incident primary cancer diagnoses, they are often associated with high morbidity and mortality. Several etiologic factors have been examined in relation to nervous system tumors, with the majority of studies focusing on central nervous system tumors. Despite decades of research, the only established risk factors for brain tumors are family history and moderate to high levels of ionizing radiation exposure. Differences in study designs, case ascertainment, control selection, and accuracy of exposure assessment are challenges associated with studying risk factors for nervous system tumors, and may partly explain why the majority of risk for these tumors remains unexplained. There is now substantial evidence that gliomas are inversely associated with allergies and atopy and positively associated with taller height.
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30

Lee, Eudocia Q. Convulsion in a Pregnant Woman. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0033.

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The management and treatment of brain tumors is the same regardless of patient gender, except when considering fertility and pregnancy. Fortunately, brain tumors are rare during pregnancy. Because the lives of the mother and the fetus may be at risk, the care of pregnant women with brain tumors has ethical implications and requires a multidisciplinary approach involving obstetrics, maternal-fetal medicine, neurosurgery, anesthesiology, neurology, medical oncology, and radiation oncology. Chemotherapy and radiation are generally considered incompatible with normal fetal development. Only a few chemotherapeutic drugs have been tested in pregnancy, and therefore most are considered contraindicated during pregnancy. Radiation can have long-term implications for the fetus, including increased risks of cancer and mental retardation. This chapter will review the management of low-grade gliomas in pregnancy.
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31

Davis, Devra, Margaret E. Sears, Anthony B. Miller, and Riina Bray. Microwave/Radiofrequency Radiation and Human Health. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190490911.003.0010.

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Radiation from wireless transmitting devices can cause or worsen acute and chronic health conditions. Outdated exposure limits for cell phones and other wireless devices emitting microwave radiation, a form of radiofrequency radiation, are based solely on avoiding an increase in temperature and do not accommodate increasing evidence of nonthermal effects on reproductive, neurologic, developmental and cardiac health, and cancer. In 2016, the U.S. National Toxicology Program reported significantly greater risks of brain (i.e. gliomas) and heart tumors in the largest rodent study ever conducted. Case-control studies found that regular and heavy cell phone users incurred increased risks of these tumors. Increasing trends of aggressive gliomas among young people have been reported. Chapter 10 provides an overview of microwave chemistry and in vitro, in vivo, epidemiologic, and clinical study findings. Guidance from international authorities addresses history taking, clinical management of relevant exposures, and promotion of safer technologic approaches and policies.
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32

Gruber-Page, Marcia, and Thomas Gruber. Navigating Glioblastoma and High-Grade Glioma: A Patient and Family Guide to Primary Brain Tumors. Advantage Media Group, 2022.

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33

Kleihues, Paul, Elisabeth Rushing, and Hiroko Ohgaki. The 2016 revision of the WHO classification of tumours of the central nervous system. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0001.

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The revised fourth edition of the WHO classification of Tumours of the Central Nervous System, published in 2016, comprises several newly recognized tumour entities, and a significant restructuring of the classification, mainly based on genetic profiling. Glioblastomas are now classified into two major types. Isocitrate dehydrogenase (IDH)-wildtype glioblastoma (primary glioblastoma IDH-wildtype) develops rapidly de novo without a recognizable precursor lesion. IDH-mutant glioblastoma (secondary glioblastoma IDH-mutant) develops more slowly through malignant progression from diffuse or anaplastic astrocytoma. Medulloblastomas are now defined by combining histological patterns (classic, desmoplastic/nodular, extensive nodularity, anaplastic) and genetic hallmarks (WNT-activated; SHH-activated, TP53-mutant; SHH-activated, TP53-wildtype; non-WNT/non-SHH). Other newly recognized tumour entities include diffuse midline glioma, H3 K27M-mutant; ependymoma, RELA fusion-positive; and embryonal tumour with multilayered rosettes. The new classification is a significant step forward and will facilitate the development of novel targeted therapies of brain tumours.
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34

Hodgkiss, Andrew. Psychiatric consequences of particular cancers. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0004.

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Certain tumour types can cause psychopathology through direct biological mechanisms such as metastatic spread to the brain, release of onconeuronal antibodies, ectopic hormone secretion, or release of pro-inflammatory cytokines. Lung cancers, adenocarcinoma of the pancreas, brain tumours, and ovarian tumours are considered in detail. Confusional states due to brain metastases, syndrome of inappropriate ADH secretion, hypercalcaemia of malignancy, and anti-Hu encephalitis are found in lung cancers. Severe depression, due to interleukin-6 release and its actions on the HPA axis and tryptophan metabolism, is common in adenocarcinoma of the pancreas. Anti-NMDA-receptor limbic encephalitis, clinically indistinguishable from acute schizophrenia, can complicate teratomas. Gliomas, pituitary tumours, and thyroid, adrenal, and testicular tumours can also disrupt mental health through various biological mechanisms described here.
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35

(Editor), Jörg-Christian Tonn, Manfred Westphal (Editor), James T. Rutka (Editor), and Stuart A. Grossman (Editor), eds. Neuro-Oncology of CNS Tumors. Springer, 2005.

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36

Glioblastoma: Molecular mechanisms of pathogenesis and current therapeutic strategies. Springer, 2010.

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37

Ray, Swapan K. Glioblastoma : : Molecular Mechanisms of Pathogenesis and Current Therapeutic Strategies. Springer, 2011.

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38

Ray, Swapan K. Glioblastoma : : Molecular Mechanisms of Pathogenesis and Current Therapeutic Strategies. Springer, 2009.

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39

Ray, Swapan K. Glioblastoma : : Molecular Mechanisms of Pathogenesis and Current Therapeutic Strategies. Springer, 2014.

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40

(Editor), Wei Zhang, and Gregory N. Fuller (Editor), eds. Genomic and Molecular Neuro-Oncology. Jones & Bartlett Publishers, 2003.

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41

Mason, Peggy. Cells of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0002.

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The nervous system is made up of neurons and glia that derive from neuroectoderm. Since neurons are terminally differentiated and do not divide, primary intracranial tumors do not arise from mature neurons. Tumors outside the nervous system may metastasize inside the brain or may release a substance that negatively affects brain function, termed paraneoplastic disease. Neurons receive information through synaptic inputs onto dendrites and soma and send information to other cells via a synaptic terminal. Most neurons send information to faraway locations and for this, an axon that connects the soma to synaptic terminals is required. Glial cells wrap axons in myelin, which speeds up information transfer. Axonal transport is necessary to maintain neuronal function and health across the long distances separating synaptic terminals and somata. A common mechanism of neurodegeneration arises from impairments in axonal transport that lead to protein aggregation and neuronal death.
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