Astrocytoma

Classification according to ICD-10
D33	Benign neoplasm of the brain and central nervous system
D33.0	Brain, supratentorial
D33.1	Brain, infratentorial
D33.2	Brain, unspecified
D33.3	Cranial nerves
D33.4	Spinal cord
D33.7	Other parts of the central nervous system
D33.9	Central nervous system, unspecified
D43	New formation of unsafe or unknown behavior in the brain and central nervous system
D43.0	Brain, supratentorial
D43.1	Brain, infratentorial
D43.2	Brain, unspecified
D43.3	Cranial nerves
D43.4	Spinal cord
D43.7	Other parts of the central nervous system
D43.9	Central nervous system, unspecified
C71	Malignant neoplasm of the brain
C71.0	Cerebrum, excluding lobes and ventricles
C71.1	Frontal lobes
C71.2	Temporal lobe
C71.3	Parietal lobes
C71.4	Occipital lobe
C71.5	Cerebral ventricle
C71.6	cerebellum
C71.7	Brain stem
C71.8	Brain, overlapping several areas
C71.9	Brain, unspecified
C72	Malignant neoplasm of the spinal cord, cranial nerves, and other parts of the central nervous system
C72.0	Spinal cord
C72.1	Cauda equina
C72.2	Nn. olfactorii (I. cranial nerve)
C72.3	N. opticus (2nd cranial nerve)
C72.4	Vestibulocochlear nerve (VIII. Cranial nerve)
C72.5	Other and unspecified cranial nerves
C72.8	Brain and other parts of the central nervous system, overlapping several areas
C72.9	Central nervous system, unspecified
ICD-10 online (WHO version 2019)

Astrocytomas are among the most common tumors of the brain and occur mainly in middle age. They have their origin in the astrocytes , which belong to the supporting tissue (glial cells) of the central nervous system , and are therefore classified as gliomas . The degree of malignancy is determined microscopically after a tissue sample using established criteria.

introduction

So far, a wide variety of tumor-inducing stimuli ( oncogenes ) have been proposed for astrocytomas. Of these, over 70% of the less differentiated (WHO grade II and III) have a genetic change for the cytosolic enzyme isocitrate dehydrogenase (IDH). For undifferentiated tumors (WHO grade IV) - glioblastomas - this rate of genetic change ( mutation ) is 100%. In the IDH mutation, a single amino acid at position 132 - arginine for histidine - is replaced. This IDH1-R132H mutation affects the usual conversion of isocitrate to alpha-ketoglutarate . Instead, there is a direct reduction of alpha-ketoglutarate to 2-hydroxyglutarate , the increased level of which is a risk for the development of brain tumors. In addition, exposure to petroleum-related chemicals (petrochemicals) and radiation from mobile phones were considered a risk factor, but this could not be confirmed in relevant studies. The symptoms depend on the location of the tumor in the brain or in the spinal canal . As a rule, they begin with persistent pain , sensory disturbances or even epilepsy . Neurological deficits (for example paralysis ) in the affected regions often occur later. The detection is carried out by means of contrast media in CT or magnetic resonance imaging and, in order to obtain the corresponding cells, by means of a biopsy . The aim of the treatment is to surgically remove the tumor as completely as possible . In the case of higher-grade tumors, subsequent irradiation of the tumor area may be necessary. A cure through chemotherapy alone , e.g. B. with temozolomide is currently (2009) not possible. In combination with radiation therapy, however, this can improve the probability of survival.

Classification of "common" astrocytomas

"Ordinary" astrocytomas are now classified according to different principles. This classification of tumors is complicated by the following problems:

• The tumor mass is not uniform. For a tumor the size of a walnut , the tissue may be different in different places. Since it when taking samples (brain biopsy ) only a small amount of tumor tissue extracts, and also in the investigation of a tumor resected after surgical removal, the entire fabric can not be investigated, there is sampling error , so-called "sampling errors": It may happen that you only get to see tissue of one classification level. However, the most malignant part of the tumor, which is not always contained in small tissue samples, is decisive for the further course and thus the prognosis. This falsely leads to the assumption that the degree of malignancy is too low.
• A classification is just a snapshot. Since tumors change over time, a classification may only be valid for a few months.
• The location of a tumor can be more important for the prognosis of the disease than the type of tissue. A tumor located in the brain stem can cause more damage if it is small than a much larger one in the cerebral hemisphere .

The WHO classification of brain tumors

→ Main article : WHO classification of central nervous system tumors

The term astrocytoma encompasses a heterogeneous group of gliomas . According to the current WHO criteria for brain tumors , astrocytomas are classified as follows:

Astrocytic tumor	WHO degree
Subependymal giant cell astrocytoma	I.
Pilocytic astrocytoma	I.
- Pilomyxoid astrocytoma	II
Pleomorphic xanthoastrocytoma	II
Diffuse astrocytoma	II
- Protoplasmic astrocytoma	II
- Gemistocytic astrocytoma	II
- Fibrillary astrocytoma	II
Anaplastic astrocytoma	III
Glioblastoma	IV
- Giant cell glioblastoma	IV
- gliosarcoma	IV
Gliomatosis cerebri	III

In 1979 a consensus conference in Geneva proposed a classification scheme that divides the biological behavior and thus the malignancy of ordinary astrocytomas into four degrees of severity, I to IV. This scheme was published by Zülch in 1979 and subsequently developed further. The current WHO classification of tumors of the central nervous system dates from 2007. This means that the low-malignant astrocytoma in adults is assigned the classification WHO grade II, the anaplastic astrocytoma the classification WHO grade III and the glioblastoma the classification WHO grade IV. The pilocytic Astrocytoma was assigned WHO grade I and is separated from the other astrocytomas because of its mostly benign course. The WHO classification of tumors of the central nervous system has meanwhile become the internationally valid classification. The vast majority of specialist publications refer to this classification scheme. In Germany, the neuropathological institutes and especially the brain tumor reference centers of the German Society for Neuropathology and Neuroanatomy in Bonn and Düsseldorf only classify according to WHO.

Pilocytic astrocytomas WHO grade I are benign tumors that can mostly be found in children and adolescents , but sometimes also in adults. They are sometimes associated with type 1 neurofibromatosis . WHO grade II astrocytomas are most commonly observed in 30 to 40 year olds and anaplastic WHO grade III astrocytomas in 40 to 60 year olds. WHO grade IV glioblastomas reach a maximum incidence between 50 and 60 years and a further maximum in patients over 70 years of age. However, all of the mentioned gliomas are also found in children.

The NBTSG scheme according to Burger

In 1985, Burger proposed a three-part classification scheme as part of the National Brain Tumor Group Study (NBTGS). This scheme only took into account the “ordinary” astrocytomas, ie ignored the “special” astrocytomas. The group of fibrillary astrocytic neoplasms was now divided into three groups: the astrocytomas , the anaplastic astrocytomas and the glioblastomas . In Burger's scheme, two observations are crucial: whether the tumor shows vascular enrichment and whether necrosis (tissue breakdown) occurs. An astrocytoma is defined by the fact that there are no vascular proliferation and no necrosis. For the diagnosis of glioblastoma, both phenomena must be present. The anaplastic astrocytoma occupies an intermediate position.

The Daumas-Duport classification system

In 1988 Daumas-Duport and her team presented a classification system that is designed to search for four characteristics, for each of which points are awarded. The criteria are: atypical cell nuclei, mitoses, endothelial proliferation and necrosis. The score then determines the degree of the tumor. The system is simple and the results of different investigators therefore agree well. It also has the advantage that the graduation gives an excellent prognostic value.
Since this scheme represents a significant advance in the study of astrocytomas, details are discussed here. Daumas-Duport et al. Retrospectively examined the medical histories and tissue samples of around 350 patients who were treated with a diagnosis of astrocytoma in the Mayo Clinic between 1960 and 1969 . At the follow-up examination, 287 patients were found with a common astrocytoma. At the time of the start of the study in 1984/85, only one patient from the original collective of 287 was still alive. 2 of 287 = 0.7% were classified as grade 1, these had a survival rate of 11 and 15 years. 17% (about 50) were classified as grade 2, these had a survival rate of four years. 18% (about 50) were classified as Grade 3, they had a survival rate of one and a half years, and 65% (about 180) were classified as Grade 4, these had a survival rate of about nine months. The agreement in the assessments of different examiners was up to 96%. This classification scheme is therefore considered to be simple, easily reproducible and meaningful. However, this classification scheme has not caught on internationally and is not used outside of some centers in France. The WHO classification is used in Germany.

Classification using imaging and genetics

In order to circumvent the restrictions to which the histological assessments of brain tumors are subject, efforts have been made to contribute to a meaningful grading by means of further technical processes .
In 2005, Cha and co-workers at UCSF presented a study in which it was possible to differentiate low-malignant astrocytomas (WHO grade II, NBTSG grade I) from low-malignant oligodendrogliomas on the basis of radiological criteria. They examined 25 untreated patients (11 with astrocytoma, 14 with oligodendroglioma) with a histologically confirmed diagnosis and used a special MRI (dynamic susceptibility contrast-enhanced MR imaging) method that allows blood volume measurements in the tumor tissue. The two types of tumor differed significantly, which allows radiological differentiation of the tumors.
In 2005, Barbashina and coworkers at the Sloan-Kettering Institute examined allele losses in tumor tissues. Two regions on chromosome 1 and chromosome 19 were examined. From a total population of 205 patients, 112 tumor samples could be examined for an allele loss of both chromosomes. It was shown that in about 70% (total number 39) of the examined samples of oligodendrogliomas there was a combined allele loss in the range 1p and 19q. This was not observed in any of the astrocytomas investigated. In addition, a very small “minimally deleted region” with a size of 150 kb on chromosome 1p36 could be determined. There is a brain-specific transcription factor (CAMTA1). (See also the work of Brat and Kleihues on this .)

The Kernohan scheme

This classification system is no longer in use today, but is often used for comparison purposes, for example to show improvements to newer systems. Kernohan distinguished astrocytomas on the basis of the occurrence of so-called anaplasias , diversity (pleomorphism) of the cell nuclei and the number of mitoses . The astrocytomas were thus divided into four groups with increasing malignancy. The scheme has not lost its fundamental validity until today, so that Kernohan is considered a pioneer of the astrocytoma classification.

Low-malignant astrocytomas

The low-malignant astrocytoma (Grade II WHO) (synonym: English Low Grade Astrocytoma ) is a tumor of the brain that originates from a certain type of cell in the nervous system (the astrocytes ) and thus belongs to the so-called gliomas . It mainly affects young adults, in whom the disease usually becomes noticeable with a first-time epileptic seizure . The findings of an astrocytoma are similar to those of an ischemic cerebral infarction . The therapy consists in the surgical removal of the tumor, if necessary with subsequent radiation . The 5-year survival rate for patients is 40 to 50%.

General consideration

Brain biopsy using stereotaxy

This article or the following section is not adequately provided with supporting documents ( e.g. individual evidence ). Information without sufficient evidence could be removed soon. Please help Wikipedia by researching the information and including good evidence.

Astrocytomas are brain tumors that are not initially assumed to be malignant. Like many tumors, they do not cause any symptoms at the onset of the disease. They can even get very large before symptoms appear. Often they are therefore only discovered at an advanced stage, but can then still be benign. Often the tumor is noticed on a computed tomography , which was caused because of a first-time epileptic seizure. The diagnosis “astrocytoma” can only be confirmed by a tissue removal ( biopsy ) from the corresponding brain region.

The treatment planning begins with the question whether the initially benign tumor to be treated at all. Given the tightness of space in the cranial cavity , the size and growth of the tumor are of great importance. Since there are no effective drugs against astrocytomas ( chemotherapy is not effective) and radiation only helps in certain cases, surgery is often the only option. An attempt is often made to surgically remove the astrocytoma. In turn, surgery is usually not considered necessary immediately after the initial diagnosis.

The need for surgery is related to the tendency of astrocytomas to develop into malignant forms. There is strong evidence that astrocytomas can initially develop into so-called anaplastic astrocytomas ( astrocytoma grade III WHO , tumors that are more advanced on the way to malignancy) and finally into glioblastomas ( astrocytoma grade IV WHO , very malignant brain tumor). In some of the patients it seems to be clear early on whether an astrocytoma will develop into a malignant tumor. In these cases, regardless of the treatment method , the prognosis is poor. Another part of the patients will not develop a glioblastoma; the prognosis for them is good, regardless of whether they have an operation sooner or later. How an astrocytoma will develop cannot be predicted.

Epidemiology

The average annual incidence rate (new cases) of low-grade astrocytomas is 0.9 per 100,000 population. The mean age of the patients with this tumor is 35 years. 55 to 65% of the patients are men. There is no accumulation of astrocytomas within ethnic groups. Patients with phacomatosis (hereditary tumor disease with malformations of the skin and the nervous system) have an increased risk of developing astrocytoma. In neurofibromatosis type 1 , optic giomas (tumors of the optic nerve ) are often found . Astrocytomas make up 15% of the gliomas in the brain stem , cerebral cortex, and cerebellum of these patients. Patients with tuberous sclerosis develop subependymal giant cell astrocytomas in the area of ​​the Monroi foramen in 5% of cases in adolescence .

Preferred sites for tumor localization

Midbrain astrocytoma with compression- induced hydrocephalus

Astrocytomas are mainly found in the convex area (outer areas of the cerebrum) and there in the frontal and temporal lobes . The tumors develop in the area of ​​the white matter (nerve cell fiber bundles ) of the hemispheres (cerebral hemispheres) and are usually "below" the cerebral cortex (subcortical) . Low-grade gliomas can also occur in all other sections of the brain and spinal cord.

Symptoms

By far the most common first clinical symptom in over 50% of patients is an epileptic seizure . The mechanism of the symptoms is the infiltration and destruction of neighboring neurons . " Cranial pressure " occurs through displacement pressure . The most common common sign of these mechanisms is papillary edema (bulging of the papilla, the exit point of the optic nerve in the retina, without loss of vision). Headache, lethargy and personality changes are also common signs of the onset of intracranial pressure. Focal neurological signs ( paralysis , disturbance of the cranial nerve function , headache) often precede the diagnosis by years.

Technical examination results

Astrocytoma

The technical findings of an astrocytoma are similar to those of an ischemic cerebral infarction :

The cranial computed tomography (CCT) without contrast agent exhibits occasionally blurred hypodensities , sometimes a "Marklagerödem", but also "cystic" formations. With contrast media, round, highly parietal or frontotemporal hypodensities with a local mass effect without enrichment of contrast media ("infarct areas") can be identified. Patients in whom there is an accumulation of contrast medium in the tumor have a seven times higher risk of relapse .

The spinal fluid is normal in patients with an astrocytoma usually.

Astrocytomas typically show no pathological blood vessel architecture (vascularization) on brain angiography .

In magnetic resonance imaging , one usually sees homogeneous hypointensities in the T1 sequence and homogeneous hyperintensities in the T2 sequence . In general there is no necrosis, no bleeding and no contrast enhancement. Occasionally, pathologically structured isointense formations can be seen in the T1 weighting.

In the PET scan of the glucose metabolism (FDG-PET), the astrocytoma is shown as hypometabolic (“cold nodule”, which means it is tissue with reduced metabolic rate and energy consumption). Dedifferentiations within the tumor occasionally lead to malignant intermediate stages, which can then appear in the PET image as “hot spots” (tissue with increased substance and energy turnover) within the “cold node”.

pathology

Pathologists distinguish three forms of low-grade astrocytoma WHO grade II: the protoplasmic astrocytoma , the fibrillar astrocytoma and the gemistocytic astrocytoma .

When viewed with the naked eye ( macroscopically ) , the protoplasmic astrocytoma appears as a soft gray expansion of the cortex. The tumor passes into the cortex and medullary bed without a precise border and sometimes shows cystic formations in the sectional image. In contrast, the fibrillar astrocytomas appear to be of firmer tissue consistency.

On microscopic assessment, the very rare, cell-poor protoplasmic astrocytomas show an even distribution of tumor cells in a matrix that can be stained with eosin . The tumor cells are delicate to plump and have few processes. Microcysts occur. There are few blood vessels that are inconspicuously configured. The most common fibrillary astrocytoma show a rather loose penetration of the tissue with glial fibers . These can be shown with antibodies against the acidic glial fiber protein ( GFAP ). Most neuropathologies meanwhile no longer differentiate between protoplasmic and fibrillar astrocytomas WHO grade II, since they are probably the same tumor entity. The gemocytic or branch-cell astrocytoma has tumor cells with large cytoplasm and sometimes several eccentrically located nuclei. No mitoses are seen in WHO grade II astrocytomas. However, the detection of a single mitosis does not justify the diagnosis of an anaplastic astrocytoma WHO grade III. The general microscopic picture of an astrocytoma can be described as follows: Pre-existing blood vessels are displaced, the infiltrated tissue in the marginal area is well preserved, the meninges can be infiltrated and the tumor can, for example, form a tissue bridge through the Sylvian fissure . A Liquoraussaat of tumor cells is rare. There are seldom degenerative changes within microcysts with calcifications.

The most important immunohistochemical finding is the GFA protein , which is formed by tumor cells and their appendages. Furthermore, the rate of proliferation should be determined using Mib1-specific antibodies.

The electron has no significance in the diagnosis of glial tumors. In electron microscopy, intermediate filaments with a size of 7 to 11 nm can be seen in the cell plasma . Microtubules are found in some cell processes.

Malignant transformation of the tumor

The question of transformation into a malignant form is important as it affects the classification and prognosis of these cancers. It is not uncommon to find small anaplastic foci in tissue samples of resected astrocytomas , areas with higher-grade tumor cell populations. The most important clinical studies are briefly presented below:

• In 1940, Scherer was the first author to find anaplasia in 13 of 18 cases.
• Russell and Rubinstein described 50% anaplastic foci in 55 autopsies in 1989. In 129 autopsies of glioblastoma multiforme, the same authors found evidence of astrocytoma genesis in about 30% of cases.
• Muller et al. examined 72 patients with the initial diagnosis of astrocytoma in 1977. At the time of relapse , 15% of patients showed unchanged pathology, 55% anaplastic astrocytomas, and 30% multiformed glioblastomas. The mean time between initial diagnosis and relapse was 2.5 years.
• Laws et al. found in 1984 in 79 patients with recurrent tumor growth a dedifferentiation to higher grade astrocytoma forms in 50% of the cases.
• Piepmeier, on the other hand, only found a malignant transformation in 13% of the patients examined after a tumor recurrence or autopsy. However, the average follow-up time was short at 5 years.

In summary, one can say that the detection of anaplastic foci at the time of a second resection does not necessarily represent the result of an initial negative selection. Or, to put it simply, benign astrocytomas are very likely to turn into malignant tumors over time.

The following findings are available on the question of the causes of the malignant transformation. In the transition from low-grade astrocytoma via anaplastic astrocytoma to glioblastoma , the astrocytoma does not show p53 mutations in any of the cases examined , the anaplastic astrocytoma 36% p53 mutations and glioblastoma 28% p53 mutations. There is also a marked increase in chromosome 10 abnormalities : no abnormalities in grade I astrocytoma, 23% abnormalities in anaplastic astrocytoma and 61% abnormalities in glioblastoma.

Guidelines for making the diagnosis

The diagnosis of astrocytoma cannot be made clinically or through technical examination procedures. The only way to diagnose an astrocytoma is to examine the suspicious tissue with a fine tissue. When in doubt, an astrocytoma does not differ from an area of ​​a cerebral infarction when it comes to imaging . From the point of view of neurology, it is therefore considered advantageous that doctors judge not on the basis of the technical findings, but on the basis of the anamnesis : a young person with an astrocytoma does not have a cerebral infarction-like event that precedes paralysis, for example. The paralysis did not come suddenly, but slowly. So if the technical findings ( CCT , MRI , etc.) look like a cerebral infarction, but the patient's description does not match and there are no vascular risk factors, the neurologist will think of a tumor and recommend a brain biopsy.

therapy

In the treatment of astrocytomas, the surgical removal of the tumor is in the foreground. The general concept for a therapy plan for astrocytoma patients is, however, controversial. The first rule for any tumor surgery is to operate as early as possible. However, since improved imaging techniques are increasingly making diagnoses before patients have suffered neurological failures, it has been suggested that surgery should be postponed until the tumor shows radiological changes in cases where it would result in a postoperative neurological deficit. This recommendation was made in light of the fact that early surgery has not been proven to extend the life expectancy of astrocytoma patients.

In 1992, Recht compared 26 patients with astrocytomas and subsequent delayed surgery with 20 patients with the following surgery immediately after diagnosis. There was no significant difference, either in the extent of tumor dedifferentiation or in life expectancy. In the final summary it was said: "deferring surgery will not make worse outcome" - "waiting does not worsen the prognosis".

According to Guthrie and Laws (1990), the tumor center should be searched for and then resected peripherally. This can be done stereotactically using CT or MRI . Stereotactic resections of small tumors or stereotactic biopsies are now practically performed on an outpatient basis.

There is no randomized, controlled and prospective clinical study on the question of postoperative radiation therapy in astrocytoma patients. Hardly two of the published studies are even comparable in terms of individual aspects of patient selection, age, extent or location of the tumor, pathological classification, radiation dose of the irradiated patient, etc.

• In 1960 Bouchard and Peirce showed that in 81 astrocytoma patients with postoperative radiation versus 71 astrocytoma patients without radiation, the 3-year survival rate was the same (62% versus 59%), but the 5-year survival rate of the irradiated group was improved (49% versus 38%).
• Gol reported something similar in a study of 194 astrocytoma patients.
• Uihlein et al. documented the opposite in a 1966 study by the Mayo Clinic.
• Garcia et al. retrospectively report on 86 patients over a period from 1950 to 1979: 3-year rate irradiated / non-irradiated: 61% / 35%. 5-year rate irradiated / non-irradiated 40% / 22%. 10-year rate irradiated / non-irradiated 9% / 9%.

Despite the fundamentally significant shortcomings of all studies carried out, the majority of the studies published in English-speaking countries benefit from postoperative irradiation of astrocytoma patients. Complications arise from radiation necrosis of the brain tissue. This occurs especially with full head irradiation.

There are no studies that demonstrate a benefit for patients from chemotherapy for astrocytoma. In general, chemotherapy for low-grade astrocytomas is of no great importance or is rarely indicated.

The main cause of therapy failure is local relapse . If re-therapy is needed, the first step is a biopsy. If the astrocytoma persists, radiological controls are carried out. If the tumor continues to grow, a resection will be necessary. In the case of malignant transformation, more aggressive therapy is necessary. The second irradiation of a relapsed astrocytoma has so far been an experimental procedure.

forecast

The 5-year survival rate for patients with astrocytoma is 40 to 50%. The 10-year survival rate is 20 to 30%. The latest data on this question show a slight improvement in the prognosis: the 5-year survival rate increased to 65% and the 10-year survival rate to 40%.

Astrocytomas in children

Astrocytomas are the most common tumor with hemispheric localization (cerebral cortex) in childhood. They make up 8% of all pediatric intracranial neoplasms . The maximum age of their occurrence is between 8 and 12 years. Gender is irrelevant: boys and girls are affected roughly equally. In addition to being located in the cerebrum, astrocytomas can also occur in the spinal cord and along the cranial nerves. Astrocytomas on the optic nerve (nervus opticus) are particularly common, often in patients with neurofibromatosis . The occurrence of astrocytomas is also increased in other phakomatoses (see above).

The most common brain tumor in childhood is medulloblastoma .

Clinical symptoms are headache, dizziness, vomiting, seizures, and visual disturbances such as: B. Spontaneous squint, occasionally a focal neurological deficit ( e.g. hemiparesis ). Diagnosis is carried out using the same means as in adulthood: an ophthalmological examination (evidence of papillary edema as a sign of increased intracranial pressure) and, above all, an MRI of the skull. In the context of the multicenter treatment studies, an MRI of the entire neuraxis (brain and spinal cord) is now required in children in order to detect or exclude drip metastases in the spinal cord (spinal sowing). The only exceptions to this standard are optic gliomas (astrocytomas of the optic nerve), although - extremely rarely - optic gliomas can metastasize into the spinal cord. A lumbar puncture should always be performed during diagnosis : this is used to detect tumor cells in the liquor (nerve fluid ) and to determine tumor markers in the liquor. This is intended to distinguish other childhood brain tumors (intracranial germ cell tumors , medulloblastoma , ependymoma ) from astrocytoma preoperatively. In the case of germ cell tumors, surgical intervention is at best allowed to obtain a histological diagnosis by means of a sample biopsy: these tumors respond very well to radio and chemotherapy and are therefore primarily to be treated with these methods.

50% of the surgical resections of the radiologically diagnosed hemispheric astrocytomas are low-grade grade I astrocytomas. The cystic juvenile pilocystic astrocytoma is an occasional subtype . The rest are astrocytomas grade II, III and IV according to WHO. In the case of optic gliomas (astrocytoma I optic nerve), an operation is initially not indicated due to the threat of serious damage to the eyesight. Treatment here primarily involves a combination of chemotherapy and radiation therapy. Proton therapy has become established in recent years , especially for young children , as this is particularly gentle on children and can thus reduce long-term side effects of radiation therapy.

The treatment is carried out with maximally total resection, as far as possible. Patients with astrocytoma WHO grade I and total resection receive radiological controls at regular intervals after the operation, mostly by means of magnetic resonance imaging. Astrocytoma patients with significant residuals (remnants of the tumor) after the operation are irradiated. Patients with higher-grade astrocytomas (WHO grade III and IV) receive radiation and chemotherapy regardless of the residual tumor. Astrocytomas WHO I and II in children have a high 10-year survival rate. The prognosis of an astrocytoma WHO III (anaplastic astrocytoma) is significantly worse, the prognosis of an astrocytoma WHO IV (glioblastoma) is very bad.

Individual evidence

1. ↑ H. Yan, DW Parsons, et al .: IDH1 and IDH2 mutations in gliomas. In: The New England Journal of Medicine . Volume 360, Number 8, February 2009, ISSN  1533-4406 , pp. 765-773, doi : 10.1056 / NEJMoa0808710 , PMID 19228619 , PMC 2820383 (free full text). Page 1, Results: "... mutations ... of IDH1 in more than 70% of WHO grade II and III astrocytomas", p. 5, Discussion: "... IDH1 mutations in 10 of 10 oligoastrocytomas and anaplastic oligoastrocytomas ..."
2. ↑ L. Dang et al .: Cancer-associated IDH1 mutations produce 2-hydroxyglutarate. In: Nature . 2009; 462 (7274), pp. 739-744.
3. ↑ CL Yu et al .: No association between residential exposure to petrochemicals and brain tumor risk. In: Cancer Epidemiol Biomarkers Prev . 2005; 14 (12), pp. 3007-3009.
4. ↑ I. Deltour et al .: Time trends in brain tumor incidence rates in Denmark, Finland, Norway, and Sweden, 1974-2003. In: J Natl Cancer Inst . 2009; 101 (24), pp. 1721-1724.
5. ↑ Hartmann, Wiestler: The new WHO brain tumor classification from 2007 . In: brainstorm. 1/2008, p. 24. ISSN  1619-0750
6. ↑ S. Feiden, W. Feidenr: WHO classification of CNS tumors . In: Pathologist. 2008, 29, pp. 411-421. PMID 18820922
7. ↑ KJ Zülch: Histologic Typing of Tumors of the Central Nervous System. International Histological Classification of Tumors, no.21. World Health Organization, Geneva 1979. (not found via PubMed, possibly this article: PMID 6245388 )
8. ↑ P. Varlet et al .: Criteria of diagnosis and grading of oligodendrogliomas or oligo-astrocytomas according to the WHO and Sainte-Anne classifications. In: Neurosurgery. 2005. 51 (3-4 Pt.1), pp. 239-246. PMID 16292167 .
9. ↑ PC Burger et al .: Glioblastoma Multiforme and Anaplastic Astrocytoma: Pathologic Criteria and Prognostic Implications. In: Cancer . 1985; 56, pp. 1106-1111. PMID 2990664
10. ^ C. Daumas-Duport et al .: Grading of astrocytomas. A simple and reproducible method. Cancer 1988. 62 (10), pp. 2152-2165. PMID 3179928
11. ↑ C. Daumas-Duport et al .: Oligodendrogliomas. Part I: Patterns of growth, histological diagnosis, clinical and imaging correlations: a study of 153 cases. In: Journal of Neurooncology. 1997; 34 (1), pp. 37-59. PMID 9210052
12. ↑ C. Daumas-Duport et al .: Oligodendrogliomas. Part II: A new grading system based on morphological and imaging criteria. In: Journal of Neurooncology. 1997; 34 (1), pp. 61-78. PMID 9210053
13. ^ S. Cha et al .: Differentiation of low-grade oligodendrogliomas from low-grade astrocytomas by using quantitative blood-volume measurements derived from dynamic susceptibility contrast-enhanced MR imaging. In: American Journal of Neuroradiology. 2005; 26 (2), pp. 266-273. PMID 15709123
14. ↑ V. Barbashina et al .: Allelic losses at 1p36 and 19q13 in gliomas: correlation with histologic classification, definition of a 150-kb minimal deleted region on 1p36, and evaluation of CAMTA1 as a candidate tumor suppressor gene. In: Clinical Cancer Research . 2005; 11 (3), pp. 1119-1128. PMID 15709179
15. ↑ DJ Brat at al .: Molecular genetic alterations in radioation-induced astrocytomas. In: The American Journal of Pathology . 1999; 154 (5), pp. 1431-1438. PMID 10329596
16. ↑ P. Kleihues, WK Cavenee: . Pathology and genetics of Tumors of the nervous system IARC Press, Lyon 2000th
17. ^ JW Kernohan, RF Mabon: A simplified classification of the gliomas. In: Proceedings of the staff meetings. In: Mayo Clinic. Volume 24, Number 3, February 1949, pp. 71-75, ISSN  0092-699X . PMID 18111063 .
18. ↑ JH Scherer et al .: In: American Journal of Cancer. 1940; 40, pp. 159-198. (no Pubmed entry)
19. ^ DS Russel, LJ Rubinstein (Ed.): Pathology of Tumors of the Nervous System. Baltimore 1989.
20. ^ W. Muller et al .: In: Acta Neurochirurgica . 1977; 37, pp. 75-91. PMID 195444
21. ^ ER Laws Jr. et al .: In: Journal of Neurosurgery . 1984; 61, pp. 665-673. PMID 6470776
22. ↑ JM Piepmeier et al .: In: Journal of Neurosurgery. 67: 177-181. PMID 3598677
23. ^ LD Recht et al .: In: Annals of Neurology. 1992; 31, pp. 431-436. PMID 1586143
24. ↑ J. Bouchard et al .: In: American Journal of Radiology. 1960; 84, pp. 610-628. (no Pubmed Hit, perhaps: PMID 13472594 )
25. ^ A. Gol: In: Journal of Neurosurgery. 1961; 18, pp. 501-506. (no Pubmed Hit, perhaps: PMID 13655110 )
26. ↑ A. Uihlein et al .: Acta Radiologica. 1966; 5, pp. 67-78. PMID 5954310
27. ^ DM Garcia et al .: In: Cancer. 1985; 55, pp. 919-927. PMID 3967199
28. ↑ L. Stephen: Hauser. In: Harrison's Neurology. 17th edition. 2010, p. 502.
29. ↑ Werner Hacke: Neurology. 13th edition. Springer Verlag, 2010, p. 311.
30. ↑ Proton therapy for brain tumors at the WPE. In: WPE-UK.de. West German Proton Therapy Center Essen (WPE), accessed on August 5, 2019 . 
31. ↑ Medulloblastoma (brief information). Retrieved August 5, 2019 . 
32. ↑ B. Timmermann: Radiation therapy for cancer in childhood - effect, opportunities and possible risks. (PDF) German Children's Cancer Foundation, August 29, 2018, accessed on August 5, 2019 . 

Unproven information mainly relates to:

• Andrew H. Kaye, Edward R. Laws Jr. (Eds.): Brain Tumors. Churchill Livingston, Edinburgh 1995, ISBN 0-443-04840-1 .

This article is about a health issue. It is not used for self-diagnosis and does not replace a diagnosis by a doctor. Please note the information on health issues !

This version was added to the list of articles worth reading on June 7, 2006 .