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The PDQ childhood brain tumor treatment summaries are organized primarily according to the World Health Organization classification of nervous system tumors.[1,2] For a full description of the classification of nervous system tumors and a link to the corresponding treatment summary for each type of brain tumor, refer to the PDQ summary on Childhood Brain and Spinal Cord Tumors Treatment Overview.
Dramatic improvements in survival have been achieved for children and adolescents with cancer. Between 1975 and 2002, childhood cancer mortality has decreased by more than 50%. Childhood and adolescent cancer survivors require close follow-up because cancer therapy side effects may persist or develop months or years after treatment. Refer to the PDQ summary on Late Effects of Treatment for Childhood Cancer for specific information about the incidence, type, and monitoring of late effects in childhood and adolescent cancer survivors.
Primary brain tumors are a diverse group of diseases that together constitute the most common solid tumor of childhood. Brain tumors are classified according to histology, but tumor location and extent of spread are important factors that affect treatment and prognosis. Immunohistochemical analysis, cytogenetic and molecular genetic findings, and measures of mitotic activity are increasingly used in tumor diagnosis and classification.
Clinicopathologic Classification of Childhood Astrocytomas and Other Tumors of Glial Origin
The pathologic classification of pediatric brain tumors is a specialized area that is undergoing evolution; review of the diagnostic tissue by a neuropathologist who has particular expertise in this area is strongly recommended.
Childhood astrocytomas and other tumors of glial origin are classified according to clinicopathologic and histologic subtype and are histologically graded from grade I to IV according to the World Health Organization's (WHO) histologic typing of central nervous system (CNS) tumors. Tumor types are based on the glial cell type of origin: astrocytomas (astrocytes), oligodendroglial tumors (oligodendrocytes), mixed gliomas (cell types of origin include oligodendrocytes, astrocytes, and ependymal cells) and neuronal tumors (with or without an astrocytic component).
WHO histologic grades are commonly referred to as low-grade gliomas or high-grade gliomas (see Table 1).
In 2007, the WHO further categorized astrocytomas, oligodendroglial tumors, and mixed gliomas according to histopathologic features and biologic behavior. It was determined that the pilomyxoid variant of pilocytic astrocytoma may be a more aggressive variant and may be more likely to disseminate, and it was reclassified by the WHO as a grade II tumor (see Table 2).[1,2,4]
Childhood astrocytomas and other tumors of glial origin can occur anywhere in the CNS, although each tumor type tends to have preferential CNS locations (see Table 3).
More than 80% of astrocytomas located in the cerebellum are low-grade (pilocytic grade I) and often cystic; most of the remainder are diffuse grade II astrocytomas. Malignant astrocytomas in the cerebellum are rare.[1,2] The presence of certain histologic features has been used retrospectively to predict event-free survival for pilocytic astrocytomas arising in the cerebellum or other location.[5,6,7]
Astrocytomas arising in the brain stem may be either high-grade or low-grade, with the frequency of either type being highly dependent on the location of the tumor within the brain stem.[8,9] Tumors not involving the pons are overwhelmingly low-grade gliomas (e.g., tectal gliomas of the midbrain), whereas tumors located exclusively in the pons without exophytic components are largely high-grade gliomas (e.g., diffuse intrinsic pontine gliomas).[8,9]
Children with neurofibromatosis type 1 (NF1) have an increased propensity to develop WHO grade I and II astrocytomas in the visual pathway; approximately 20% of all patients with NF1 will develop a visual pathway glioma. In these patients, the tumor may be found on screening evaluations when the child is asymptomatic or has apparent static neurologic and/or visual deficits. Pathologic confirmation is frequently not obtained in asymptomatic patients, and when biopsies have been performed, these tumors have been found to be predominantly pilocytic (grade I) rather than fibrillary (grade II) astrocytomas.[2,4,10,11,12] In general, treatment is not required for incidental tumors found with surveillance scans. Symptomatic lesions or those that have radiographically progressed may require treatment.
Genomic alterations involving BRAF are very common in sporadic cases of pilocytic astrocytoma, resulting in activation of the ERK/MAPK pathway. BRAF activation in pilocytic astrocytoma occurs most commonly through a gene fusion between KIAA1549 and BRAF, producing a fusion protein that lacks the BRAF regulatory domain.[14,15,16,17,18] This fusion is seen in the majority of infratentorial and midline pilocytic astrocytomas, but is present at lower frequency in supratentorial (hemispheric) tumors.[14,15,19,20,21,22,23] Other genomic alterations in pilocytic astrocytomas that can also activate the ERK/MAPK pathway (e.g., alternative BRAF gene fusions, RAF1 rearrangements, RAS mutations, and BRAF V600E point mutations) are less commonly observed.[15,17,18,24] As expected, given the role of NF1 deficiency in activating the ERK/MAPK pathway, activating BRAF genomic alterations are uncommon in pilocytic astrocytoma associated with NF1. Presence of the BRAF-KIAA1549 fusion predicted for better clinical outcome (progression-free survival [PFS] and overall survival) in one report that described children with incompletely resected low-grade gliomas. However, other factors such as p16 deletion and tumor location may modify the impact of BRAF mutation on outcome.BRAF activation through the KIAA1549-BRAF fusion has also been described in other pediatric low-grade gliomas (e.g., pilomyxoid astrocytoma).[22,23]BRAF point mutations (V600E) are observed in nonpilocytic pediatric low-grade gliomas as well, including approximately two-thirds of pleomorphic xanthoastrocytoma cases and in ganglioglioma and desmoplastic infantile ganglioglioma.[26,27,28]
Molecular features of pediatric high-grade astrocytomas show some similarities to the genetic aberrations seen in adult glioblastomas that arise from pre-existing lower-grade gliomas (so-called secondary glioblastoma).[29,30,31] These include a high incidence of TP53 mutations, a low incidence of PTEN and P16INK4A mutations, and the presence of PDGF/PDGFR overexpression. However, the IDH1 mutations that have been identified in a high proportion of adults with secondary glioblastoma are rarely seen in pediatric glioblastoma.[32,33] While the incidence of IDH1 mutations is low in children, it increases with age in the adolescent and young adult population. Mutations in histone H3.3 (H3F3A) are present in approximately one-third of non–brain stem pediatric high-grade astrocytomas,[33,34] and most of these cases also have TP53 mutations. Pediatric high-grade astrocytomas with H3F3A mutations often additionally have somatic mutations in ATRX, a gene coding for a protein involved in chromatin remodeling. Diffuse intrinsic pontine gliomas show an even higher frequency of H3F3A mutations than do non–brain stem pediatric high-grade astrocytomas, with approximately three-fourths of cases showing mutations.[34,35] Diffuse intrinsic pontine gliomas show a comparably high frequency of TP53 mutations, but IDH1 and IDH2 mutations are rare. These findings suggest that a substantial proportion of pediatric high-grade astrocytomas are associated with processes required for establishing normal chromatin architecture.
The molecular profile of pediatric patients with oligodendroglioma does not demonstrate deletions of 1p or 19q, as found in 40% to 80% of adult cases. Pediatric oligodendroglioma harbors MGMT gene promoter methylation in the majority of tumors.
Gliomatosis cerebri is a diffuse glioma that involves widespread involvement of the cerebral hemispheres in which it may be confined, but it often extends caudally to affect the brain stem, cerebellum, and/or spinal cord. It rarely arises in the cerebellum and spreads rostrally. The neoplastic cells are most commonly astrocytes, but in some cases, they are oligodendroglia. They may respond to treatment initially, but overall have a poor prognosis.
Low-grade astrocytomas (grade I [pilocytic] and grade II) have a relatively favorable prognosis, particularly for circumscribed, grade I lesions where complete excision may be possible.[39,40,41,42,43,44] Tumor spread, when it occurs, is usually by contiguous extension; dissemination to other CNS sites is uncommon, but does occur.[45,46] Although metastasis is uncommon, tumors may be of multifocal origin, especially when associated with NF1.
Unfavorable prognostic features include young age, fibrillary histology, and inability to obtain a complete resection. Elevated MIB-1 labeling index, a marker of cellular proliferative activity, is associated with shortened PFS in patients with pilocytic astrocytoma. A BRAF-KIAA fusion, found in pilocytic tumors, confers a better clinical outcome.
Oligodendrogliomas are rare in children and have a relatively favorable prognosis, with the exception of children younger than 3 years who have less than a gross total resection.
High-grade astrocytomas are often locally invasive and extensive and tend to occur above the tentorium.[39,42] Spread via the subarachnoid space may occur. Metastasis outside of the CNS has been reported but is extremely infrequent until multiple local relapses have occurred. Biologic markers, such as p53 overexpression and mutation status, may be useful predictors of outcome in patients with high-grade gliomas.[4,49,50] MIB-1 labeling index is predictive of outcome in childhood malignant brain tumors. Both histologic classification and proliferative activity evaluation have been shown to be independently associated with survival. Although high-grade astrocytoma carries a generally poor prognosis in younger patients, those with anaplastic astrocytoma and those in whom a gross total resection is possible may fare better.[43,52,53]
Presenting symptoms for childhood astrocytomas depend not only on CNS location, but also size of tumor, rate of growth, and chronologic and developmental age of the child.
There is no generally recognized staging system for childhood astrocytomas. For the purposes of this summary, childhood astrocytomas will be described as low-grade astrocytoma (pilocytic astrocytomas and diffuse fibrillary astrocytomas) or high-grade astrocytoma (anaplastic astrocytomas and glioblastoma) and as untreated or recurrent.
Many of the improvements in survival in childhood cancer have been made as a result of clinical trials that have attempted to improve on the best available, accepted therapy. Clinical trials in pediatrics are designed to compare new therapy with therapy that is currently accepted as standard. This comparison may be done in a randomized study of two treatment arms or by evaluating a single new treatment and comparing the results with those that were previously obtained with existing therapy.
Because of the relative rarity of cancer in children, all patients with brain tumors should be considered for entry into a clinical trial. To determine and implement optimum treatment, treatment planning by a multidisciplinary team of cancer specialists who have experience treating childhood brain tumors is required. Radiation therapy of pediatric brain tumors is technically very demanding and should be carried out in centers that have experience in that area in order to ensure optimal results.
Debilitating effects on growth and neurologic development have frequently been observed following radiation therapy, especially in younger children.[1,2,3] There are also other less-common complications of radiation therapy, including cerebrovascular accidents. For this reason, the role of chemotherapy in allowing a delay in the administration of radiation therapy is under study, and preliminary results suggest that chemotherapy can be used to delay, and sometimes obviate, the need for radiation therapy in children with benign and malignant lesions. Long-term management of these patients is complex and requires a multidisciplinary approach.
To determine and implement optimum management, treatment is often guided by a multidisciplinary team of cancer specialists who have experience treating childhood brain tumors.
In infants and young children, low-grade astrocytomas presenting in the hypothalamus may result in the diencephalic syndrome, which is manifested by failure to thrive in an emaciated, seemingly euphoric child. Such children may have little in the way of other neurologic findings, but can have macrocephaly, intermittent lethargy, and visual impairment. Because the location of these tumors makes a surgical approach difficult, biopsies are not always done. This is especially true in patients with neurofibromatosis type 1 (NF1). When associated with NF1, tumors may be of multifocal origin.
For children with low-grade optic pathway astrocytomas, treatment options should be considered not only to improve survival but also to stabilize visual function.[3,4] Children with isolated optic nerve tumors have a better prognosis than those with lesions that involve the chiasm or that extend along the visual pathway.[1,2,5,6]; [Level of evidence: 3iiC] Children with NF1 also have a better prognosis, especially when the tumor is found in asymptomatic patients at the time of screening.[5,8] Observation is an option for patients with NF1 or nonprogressive masses.[1,5,9,10] Spontaneous regressions of optic pathway gliomas have been reported in children with and without NF1.[11,12,13]
Surgical resection is the primary treatment for childhood low-grade astrocytoma [1,2,5,14] and surgical feasibility is determined by tumor location. For example, complete or near complete removal can be obtained in 90% to 95% of patients with pilocytic tumors that occur in the cerebellum. Similarly, circumscribed, grade I hemispheric tumors are often amenable to complete surgical resection.[14,15,16] For children with isolated optic nerve lesions and progressive symptoms, complete surgical resection or local radiation therapy may result in prolonged progression-free survival (PFS).
Factors related to outcome for children with low-grade gliomas treated with surgery followed by observation were identified in a Children's Oncology Group study that included 518 evaluable patients. Overall outcome for the entire group was 78% PFS at 8 years and 96% overall survival (OS) at 8 years. The following factors were related to prognosis:
Diffuse astrocytomas may be less amenable to total resection, and this may account for the poorer outcome. The extent of resection necessary for cure, as noted above, is unknown because patients with microscopic and even gross residual tumor after surgery may experience long-term PFS without postoperative therapy.[2,9,14] The long-term functional outcome of cerebellar pilocytic astrocytomas is relatively favorable. Full-scale mean IQs of patients with low-grade gliomas treated with surgery alone are close to the normative population. However, long-term medical, psychological, and educational deficits may be present in these patients.[18,19][Level of evidence: 3iiiC]
Low-grade astrocytomas that occur in midline structures (e.g., hypothalamus, thalamus, brain stem, and spinal cord) can also be aggressively resected, with resultant long-term disease control;[11,12,20]; [Level of evidence: 3iiiA] however, such resection may result in significant neurologic sequelae, especially in children younger than 2 years at diagnosis.; [Level of evidence: 3iC] Because of the infiltrative nature of some deep-seated lesions, extensive surgical resection may not be appropriate and biopsy only should be considered.[Level of evidence: 3iiiDiii] Treatment options for patients with incompletely resected tumor must be individualized and may include observation, a second resection, chemotherapy, and/or radiation. A shunt or other cerebrospinal fluid diversion procedure may be needed.
Following resection, immediate (within 48 hours of resection per Children's Oncology Group [COG] criteria) postoperative magnetic resonance imaging is obtained. Surveillance scans are then obtained periodically for completely resected tumors, although the value following the initial 3- to 6-month postoperative period is uncertain.; [Level of evidence: 3iiDiii] In selected patients in whom a portion of the tumor has been resected, the patient may also be observed without further disease-directed treatment, particularly if the pace of tumor regrowth is anticipated to be very slow. Approximately 50% of patients with less-than-gross total resection may have disease that remains progression-free at 5 to 8 years, supporting the observation strategy in selected patients.
Radiation therapy is usually reserved until progressive disease is documented,[16,26] and its use may be further delayed through the use of chemotherapy, a strategy that is commonly employed in young children.[27,28] Radiation therapy results in long-term disease control for most children with chiasmatic and posterior pathway chiasmatic gliomas, but may also result in substantial intellectual and endocrinologic sequelae, cerebrovascular damage, and possibly an increased risk of secondary tumors.[11,17,29,30]; [Level of evidence: 2C] An alternative to immediate radiation therapy is subtotal surgical resection, but it is unclear how many patients will have stable disease and for how long. Radiation therapy and alkylating agents are used as a last resort for patients with NF1, given the theoretically heightened risk of inducing neurologic toxic effects and second malignancy in this population. Children with NF1 may be at higher risk for radiation-associated secondary tumors and morbidity due to vascular changes.
For children with low-grade glioma for whom radiation therapy is indicated, conformal radiation therapy or stereotactic radiosurgery approaches appear effective and offer the potential for reducing the acute and long-term toxicities associated with this modality. Care must be taken in separating radiation-induced imaging changes from disease progression during the first year after radiation, especially in patients with pilocytic astrocytomas.[33,34,35]; [Level of evidence: 2A]; [Level of evidence: 2C]; [Level of evidence: 3iiiDi]; [Level of evidence: 3iiiDii]; [23,39][Level of evidence: 3iiiDiii]
Given the side effects associated with radiation therapy, chemotherapy may be particularly appropriate for patients with NF1 and for younger children.
Chemotherapy may result in objective tumor shrinkage and will delay the need for radiation therapy in most patients.[27,28,40,41] Chemotherapy has been shown to shrink tumors in children with hypothalamic gliomas and the diencephalic syndrome, resulting in weight gain in those who respond to treatment.
The most widely used regimens to treat progression or symptomatic nonresectable, low-grade gliomas are carboplatin with or without vincristine [27,28,43] or a combination of thioguanine, procarbazine, lomustine, and vincristine.; [Level of evidence: 1iiA] Other chemotherapy approaches have been employed to treat children with progressive low-grade astrocytomas, including multiagent platinum-based regimens [28,40,45]; [Level of evidence: 2Diii] and temozolomide.[47,48]
Reported 5-year PFS rates have ranged from approximately 35% to 60% for children receiving platinum-based chemotherapy for optic pathway gliomas,[28,40] but most patients ultimately require further treatment. This is particularly true for children who initially present with hypothalamic/chiasmatic gliomas that have neuraxis dissemination.[Level of evidence: 3iiiDiii]
Among children receiving chemotherapy for optic pathway gliomas, those without NF1 have higher rates of disease progression than those with NF1, and infants have higher rates of disease progression than do children older than 1 year.[28,40,45] Whether vision is improved with chemotherapy is unclear.[50,51][Level of evidence: 3iiiC]
The COG completed a randomized phase III trial (COG-A9952) that treated children younger than 10 years with low-grade chiasmatic/hypothalamic gliomas on one of two regimens: carboplatin and vincristine or thioguanine (6-thioguanine), lomustine, and procarbazine hydrochloride given with vincristine. Children with NF1 were treated only on the carboplatin and vincristine arm. Study results are pending.
Most children with tuberous sclerosis have a mutation in one of two tuberous sclerosis genes (TSC1/hamartin or TSC2/tuberin). Either of these mutations results in an overexpression of the mTOR complex 1. These children are at risk for the development of subependymal giant cell astrocytomas (SEGA), in addition to cortical tubers and subependymal nodules. For children with symptomatic SEGAs, agents that inhibit mTOR (e.g., everolimus and sirolimus) have been shown in small series to cause significant reductions in the size of these tumors, often eliminating the need for surgery.[Level of evidence: 2C]; [Level of evidence: 3iiiC] Whether reduction in size of the mass is durable, obviating the need for future surgery, is currently unknown.
Treatment Options Under Clinical Evaluation
Early-phase therapeutic trials may be available for selected patients. These trials may be available via Children's Oncology Group phase I institutions, the Pediatric Brain Tumor Consortium, or other entities. Information about ongoing clinical trials is available from the NCI Web site.
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood low-grade untreated astrocytoma or other tumor of glial origin. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
Childhood low-grade astrocytomas may recur many years after initial treatment. Recurrent disease is usually at the primary tumor site, though multifocal or widely disseminated disease to other intracranial sites and to the spinal leptomeninges has been documented.[1,2] Most children whose low-grade fibrillary astrocytomas recur will harbor low-grade lesions; however, malignant transformation is possible.
At the time of recurrence, a complete evaluation to determine the extent of the relapse is indicated. Biopsy or surgical resection may be necessary for confirmation of relapse because other entities, such as secondary tumor and treatment-related brain necrosis, may be clinically indistinguishable from tumor recurrence. The need for surgical intervention must be individualized on the basis of the initial tumor type, the length of time between initial treatment and the reappearance of the mass lesion, and the clinical picture.
An individual plan needs to be tailored based on patient age, tumor location, and prior treatment. If patients have not received radiation therapy, local radiation therapy is the usual treatment, although further chemotherapy in lieu of radiation may be considered, depending on the child's age and the extent and location of the tumor.[Level of evidence: 3iA]; [Level of evidence: 3iiiDi] For children with low-grade glioma for whom radiation therapy is indicated, conformal radiation therapy approaches appear effective and offer the potential for reducing the acute and long-term toxicities associated with this modality.[7,8] In patients treated with surgery alone whose disease progresses, chemotherapy and/or radiation therapy are options. If recurrence takes place after irradiation, chemotherapy should be considered. Chemotherapy may result in relatively long-term disease control.[9,10] Vinblastine alone, temozolomide alone, or temozolomide in combination with carboplatin and vincristine may be useful at the time of recurrence for children with low-grade gliomas.[9,10,11]; [Level of evidence: 3iiDi]
Patients with low-grade astrocytomas who relapse after being treated with surgery alone should be considered for another surgical resection. If this is not feasible, local radiation therapy is the usual treatment. If there is recurrence in an unresectable site after irradiation, chemotherapy should be considered.
Entry into studies of novel therapeutic approaches should be considered for patients with recurrent brain tumors.[15,16] Information about ongoing clinical trials is available from the NCI Web site.
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with recurrent childhood astrocytoma or other tumor of glial origin. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
The therapy for both children and adults with supratentorial high-grade astrocytoma includes surgery, radiation therapy, and chemotherapy. Outcome in high-grade gliomas occurring in childhood may be more favorable than that in adults, but it is not clear if this difference is caused by biologic variations in tumor characteristics, therapies used, tumor resectability, or other factors that are presently not understood. The ability to obtain a complete resection is associated with a better prognosis. Radiation therapy is administered to a field that widely encompasses the entire tumor. The radiation therapy dose to the tumor bed is usually at least 54 Gy. Despite such therapy, overall survival rates remain poor. Similarly poor survival is seen in children with spinal cord primaries and children with thalamic high-grade gliomas.[3,4]; [Level of evidence: 3iiiA] In one trial, children with glioblastoma who were treated on a prospective randomized trial with adjuvant lomustine, vincristine, and prednisone fared better than children treated with radiation therapy alone. Among patients treated with surgery, radiation therapy, and nitrosourea (lomustine)-based chemotherapy, 5-year progression-free survival was 19% ± 3%; survival was 40% in those who had total resections. Similarly, in a trial of multiagent chemoradiotherapy and adjuvant chemotherapy in addition to valproic acid, 5-year event-free survival (EFS) was 13%, but for children with a complete resection of their tumor, the EFS was 48%.[Level of evidence: 2A] In adults, the addition of temozolomide during and after radiation therapy resulted in improved 2-year EFS as compared with treatment with radiation therapy alone. Adult patients with glioblastoma with a methylated O6-methylguanine-DNA-methyltransferase (MGMT) promoter benefited from temozolomide, whereas those who did not have a methylated MGMT promoter did not benefit from temozolomide.[9,10] The role of temozolomide given concurrently with radiation therapy for children with supratentorial high-grade glioma appears comparable to the outcome seen in children treated with nitrosourea-based therapy  and again demonstrated a survival advantage for those children with a methylated MGMT promoter. Younger children may benefit from chemotherapy to delay, modify, or, in selected cases, obviate the need for radiation therapy.[12,13,14] Clinical trials that evaluate chemotherapy with or without radiation therapy are ongoing. Information about ongoing clinical trials is available from the NCI Web site.
The following is an example of a national and/or institutional clinical trial that is currently being conducted or is under analysis. Information about ongoing clinical trials is available from the NCI Web site.
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood high-grade untreated astrocytoma or other tumor of glial origin. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
Most patients with high-grade astrocytomas or gliomas will eventually have tumor recurrence, usually within 3 years of original diagnosis but perhaps many years after initial treatment. Disease may recur at the primary tumor site, at the margin of the resection/radiation bed, or at noncontiguous central nervous system sites. Systemic relapse is rare but may occur. At the time of recurrence, a complete evaluation for extent of relapse is indicated for all malignant tumors. Biopsy or surgical resection may be necessary for confirmation of relapse because other entities, such as secondary tumor and treatment-related brain necrosis, may be clinically indistinguishable from tumor recurrence. The need for surgical intervention must be individualized on the basis of the initial tumor type, the length of time between initial treatment and the reappearance of the mass lesion, and the clinical picture.
Patients for whom initial treatment fails may benefit from additional treatment. High-dose, marrow-ablative chemotherapy with hematopoietic stem cell transplant may be effective in a subset of patients with minimal residual disease at time of treatment.; [Level of evidence: 3iiiA] Such patients should also be considered for entry into trials of novel therapeutic approaches. Information about ongoing clinical trials is available from the NCI Web site.
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with . The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Added text to state that other factors such as p16 deletion and tumor location may modify the impact of BRAF mutation on outcome (cited Horbinski et al. as reference 25).
Treatment of Childhood Low-Grade Astrocytomas
Added Ater et al. as reference 44 and level of evidence 1iiA.
This summary is written and maintained by the PDQ Pediatric Treatment Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ NCI's Comprehensive Cancer Database pages.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of childhood astrocytomas. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Pediatric Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
The lead reviewers for Childhood Astrocytomas Treatment are:
Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Levels of Evidence
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Pediatric Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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National Cancer Institute: PDQ® Childhood Astrocytomas Treatment. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://cancer.gov/cancertopics/pdq/treatment/child-astrocytomas/HealthProfessional. Accessed <MM/DD/YYYY>.
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Last Revised: 2013-01-30
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