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This group of tumors includes most astrocytomas in the cerebellum, a region in the lower back portion of the brain that controls movement and balance; optic nerve gliomas, tumors that arise from the supporting cells in the optic nerve; and several other types of benign tumors. Learn about pilocytic astrocytomas and find information on how we support and care for children with pilocytic astrocytomas before, during, and after treatment.
The Brain Tumor Center at Dana-Farber/Boston Children's Cancer and Blood Disorders Center cares for children with many different types of common and rare brain and spinal tumors, including astrocytomas, medulloblastomas, ependymoma, glioblastomas, and primitive neuroectodermal tumors (PNET).
Your child will receive care from some of the world's most experienced pediatric brain tumor doctors and internationally recognized pediatric subspecialists.
Our team works closely together to develop a care plan that offers your child the highest possible quality of life after treatment, and takes the needs of your child and your family into account.
Children treated at the Brain Tumor Center have access to some of the most advanced diagnostics and therapies, including:
Thanks to refined surgical techniques and improved chemotherapy and radiation therapy, the majority of children with brain and spinal cord tumors are now long-term survivors. However, they may face physical, social, and intellectual challenges that require specialized care.
Learn more about our Brain Tumor Center.
A pilocytic astrocytoma is a brain tumor that originates from star-shaped cells called astrocytes. Astrocytes are a kind of glial cell, cells that support and nourish neurons in the brain. An astrocytoma is a type of glioma, and pilocytic astrocytomas are low-grade gliomas — a family of slow-growing tumors that arise from glial cells. They are the most benign and most treatable of the gliomas, with a cure rate of over 90 percent.
Children with pilocytic astrocytomas are treated at Dana-Farber/Boston Children's through our Brain Tumor Center's Glioma Program, one of the largest and most experienced pediatric glioma programs in the world. Our glioma specialists — a team of neuro-oncologists, surgeons, pathologists and radiation oncologists — focus solely on the care of children diagnosed with gliomas.
Find in-depth information on pilocytic astroctyomas on the Dana-Farber/Boston Children's website, including answers to:
The PDQ childhood brain tumor treatment summaries are organized primarily according to the World Health Organization (WHO) 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 decreased by more than 50%.[3] 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.
Gliomas arise from glial cells that are present in the brain and spinal cord. Gliomas are named according to their clinicopathologic and histologic subtype. For example, astrocytomas originate from astrocytes, oligodendroglial tumors from oligodendrocytes, and mixed gliomas from a mix of oligodendrocytes, astrocytes, and ependymal cells. Astrocytoma is the most commonly diagnosed type of glioma in children. According to the WHO classification of brain tumors, gliomas are further classified as low-grade (grades I and II) and high-grade (grades III and IV) tumors. Children with low-grade tumors have a relatively favorable prognosis, especially when the tumors can be completely resected. Children with high-grade tumors generally have a poor prognosis, unless the tumor is an anaplastic astrocytoma that can be completely resected.
Childhood astrocytomas can occur anywhere in the central nervous system (CNS). Refer to Table 3 for the preferential CNS location for each tumor type.
Presenting symptoms for childhood astrocytomas depend on the following:
In infants and young children, low-grade astrocytomas presenting in the hypothalamus may result in 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.[4]
The diagnostic evaluation for astrocytoma is often limited to a magnetic resonance imaging (MRI) of the brain or spine. Additional imaging, when clinically indicated, would consist of an MRI of the remainder of the neuraxis.
The pathologic classification of pediatric brain tumors is a specialized area that is evolving. Examination of the diagnostic tissue by a neuropathologist who has particular expertise in this area is strongly recommended.
Tumor types are based on the glial cell type of origin:
According to the WHO histologic typing of CNS tumors, childhood astrocytomas and other tumors of glial origin are classified according to clinicopathologic and histologic subtype and are graded (grade I to IV).[1]
WHO histologic grades are commonly referred to as low-grade gliomas or high-grade gliomas (refer to Table 1).
WHO Histologic Grade
Grade Classification
Low grade
High grade
Astrocytic Tumors:
Pilocytic astrocytoma
Pilomyxoid astrocytomaa
Pleomorphic xanthoastrocytoma
Subependymal giant cell astrocytoma
Diffuse astrocytoma:
Gemistocytic astrocytoma
Protoplasmic astrocytoma
Fibrillary astrocytoma
Anaplastic astrocytoma
Oligodendroglial Tumors:
Anaplastic oligodendroglioma
Mixed Gliomas:
Anaplastic oligoastrocytoma
aIn 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 an aggressive variant that is more likely to disseminate, and it was reclassified as a grade II tumor.[1][2][5]
Childhood astrocytomas and other tumors of glial origin can occur anywhere in the CNS, although each tumor type tends to have preferential CNS locations (refer to Table 3).
Tumor Type
Preferential CNS Location
Pilocytic astrocytoma
Optic nerve, optic chiasm/hypothalamus, thalamus and basal ganglia, cerebral hemispheres, cerebellum, and brain stem; and spinal cord (rare)
Pleomorphic xanthoastrocytoma
Superficial location in cerebrum (temporal lobe preferentially)
Diffuse astrocytoma (including fibrillary)
Cerebrum (frontal and temporal lobes), brain stem, spinal cord, optic nerve, optic chiasm, optic pathway, hypothalamus, and thalamus
Anaplastic astrocytoma, glioblastoma
Cerebrum; occasionally cerebellum, brain stem, and spinal cord
Cerebrum (frontal lobe preferentially followed by temporal, parietal, and occipital lobes), cerebellum, brain stem, and spinal cord
Cerebral hemispheres (frontal lobe preferentially followed by the temporal lobe)
Gliomatosis cerebri
Cerebrum with or without brain stem involvement, cerebellum, and spinal cord
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 (e.g., MIB-1 rate, anaplasia) has been used retrospectively to predict event-free survival for pilocytic astrocytomas arising in the cerebellum or other location.[6][7][8]
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.[9][10] 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).[9][10] (Refer to the PDQ summary on Childhood Brain Stem Glioma Treatment for more information.)
High-grade astrocytomas are often locally invasive and extensive and tend to occur above the tentorium in the cerebrum.[11][12] 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.
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.[1] It rarely arises in the cerebellum and spreads rostrally.[13] 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.[14]
Children with NF1 have an increased propensity to develop WHO grade I and grade II astrocytomas in the visual (optic) pathway; approximately 20% of all patients with NF1 will develop an optic 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; when biopsies have been performed, these tumors have been found to be predominantly pilocytic (grade I) rather than fibrillary (grade II) astrocytomas.[2][5][15][16][17]
In general, treatment is not required for incidental tumors found with surveillance scans. Symptomatic lesions or those that have radiographically progressed may require treatment.[18]
Genomic alterations involving BRAF activation 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 KIAA1549-BRAF gene fusion, producing a fusion protein that lacks the BRAF regulatory domain.[19][20][21][22][23] This fusion is seen in most infratentorial and midline pilocytic astrocytomas, but is present at lower frequency in supratentorial (hemispheric) tumors.[19][20][24][25][26][27][28]
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.[28] However, other factors such as p16 deletion and tumor location may modify the impact of BRAF mutation on outcome.[29]
BRAF activation through the KIAA1549-BRAF fusion has also been described in other pediatric low-grade gliomas (e.g., pilomyxoid astrocytoma).[27][28]
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.[20][22][23][30]BRAF (V600E) point mutations 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.[31][32][33] One retrospective study of 53 children with gangliogliomas demonstrated BRAF V600E staining in approximately 40% of tumors. Five-year recurrence-free survival was worse in the V600E-mutated tumors (about 60%) than in the tumors that did not stain for V600E (about 80%).[34]
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.[26]
Activating mutations in FGFR1 and PTPN11, as well as NTRK2 fusion genes, have also been identified in noncerebellar pilocytic astrocytomas.[35] In pediatric grade II diffuse astrocytomas, the most common alterations reported are rearrangements in the MYB family of transcription factors in up to 53% of tumors.[36][37]
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 of developing subependymal giant cell astrocytomas, in addition to cortical tubers and subependymal nodules.
Pediatric high-grade gliomas, especially glioblastoma multiforme, are biologically distinct from those arising in adults.[38][39][40][41] Pediatric high-grade gliomas, compared with adult tumors, less frequently have PTEN and EGFR genomic alterations, and more frequently have PDGF/PDGFR genomic alterations and mutations in histone H3.3 genes. Although it was believed that pediatric glioblastoma multiforme tumors were more closely related to adult secondary glioblastoma multiforme tumors in which there is stepwise transformation from lower-grade into higher-grade gliomas and in which most tumors have IDH1 and IDH2 mutations, the latter mutations are rarely observed in childhood glioblastoma multiforme tumors.[42][43][44]
Based on epigenetic patterns (DNA methylation), pediatric glioblastoma multiforme tumors are separated into relatively distinct subgroups with distinctive chromosome copy number gains/losses and gene mutations.[44]
Two subgroups have identifiable recurrent H3F3A mutations, suggesting disrupted epigenetic regulatory mechanisms, with one subgroup having mutations at K27 (lysine 27) and the other group having mutations at G34 (glycine 34). The subgroups are the following:
The H3F3A K27 and G34 mutations appear to be unique to high-grade gliomas and have not been observed in other pediatric brain tumors.[45] Both mutations induce distinctive DNA methylation patterns compared with the patterns observed in IDH-mutated tumors, which occur in young adults.[42][43][44][45][46]
Other pediatric glioblastoma multiforme subgroups include the RTK PDGFRA and mesenchymal clusters, both of which occur over a wide age range, affecting both children and adults. The RTK PDGFRA and mesenchymal subtypes are comprised predominantly of cortical tumors, with cerebellar glioblastoma multiforme tumors being rarely observed; they both carry a poor prognosis.[44]
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 oligodendrogliomas harbor MGMT gene promoter methylation in the majority of tumors.[47]
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.[11][12][48][49][50][51] Tumor spread, when it occurs, is usually by contiguous extension; dissemination to other CNS sites is uncommon, but does occur.[52][53] Although metastasis is uncommon, tumors may be of multifocal origin, especially when associated with NF1.
Unfavorable prognostic features for childhood low-grade astrocytomas include the following:[54]
In patients with pilocytic astrocytoma, elevated MIB-1 labeling index, a marker of cellular proliferative activity, is associated with shortened PFS.[8] A BRAF-KIAA fusion, found in pilocytic tumors, confers a better clinical outcome.[28]
Children with isolated optic nerve tumors have a better prognosis than those with lesions that involve the chiasm or that extend along the optic pathway.[55][56][57][58]; [59][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.[55][60]
Biologic markers, such as p53 overexpression and mutation status, may be useful predictors of outcome in patients with high-grade gliomas.[5][61][62] 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.[63]
Although high-grade astrocytomas generally carry a poor prognosis in younger patients, those with anaplastic astrocytomas in whom a gross-total resection is possible may fare better.[50][64][65]
Oligodendrogliomas are rare in children and have a relatively favorable prognosis; however, children younger than 3 years who have less than a gross-total resection have a less favorable prognosis.[66]
This summary does not address the treatment of children with oligodendrogliomas.
Louis DN, Ohgaki H, Wiestler OD, et al., eds.: WHO Classification of Tumours of the Central Nervous System. 4th ed. Lyon, France: IARC Press, 2007.
Louis DN, Ohgaki H, Wiestler OD, et al.: The 2007 WHO classification of tumours of the central nervous system. Acta Neuropathol 114 (2): 97-109, 2007.
Smith MA, Seibel NL, Altekruse SF, et al.: Outcomes for children and adolescents with cancer: challenges for the twenty-first century. J Clin Oncol 28 (15): 2625-34, 2010.
Kilday JP, Bartels U, Huang A, et al.: Favorable survival and metabolic outcome for children with diencephalic syndrome using a radiation-sparing approach. J Neurooncol 116 (1): 195-204, 2014.
Komotar RJ, Burger PC, Carson BS, et al.: Pilocytic and pilomyxoid hypothalamic/chiasmatic astrocytomas. Neurosurgery 54 (1): 72-9; discussion 79-80, 2004.
Tibbetts KM, Emnett RJ, Gao F, et al.: Histopathologic predictors of pilocytic astrocytoma event-free survival. Acta Neuropathol 117 (6): 657-65, 2009.
Rodriguez FJ, Scheithauer BW, Burger PC, et al.: Anaplasia in pilocytic astrocytoma predicts aggressive behavior. Am J Surg Pathol 34 (2): 147-60, 2010.
Margraf LR, Gargan L, Butt Y, et al.: Proliferative and metabolic markers in incompletely excised pediatric pilocytic astrocytomas--an assessment of 3 new variables in predicting clinical outcome. Neuro Oncol 13 (7): 767-74, 2011.
Fried I, Hawkins C, Scheinemann K, et al.: Favorable outcome with conservative treatment for children with low grade brainstem tumors. Pediatr Blood Cancer 58 (4): 556-60, 2012.
Fisher PG, Breiter SN, Carson BS, et al.: A clinicopathologic reappraisal of brain stem tumor classification. Identification of pilocystic astrocytoma and fibrillary astrocytoma as distinct entities. Cancer 89 (7): 1569-76, 2000.
Pollack IF: Brain tumors in children. N Engl J Med 331 (22): 1500-7, 1994.
Pfister S, Witt O: Pediatric gliomas. Recent Results Cancer Res 171: 67-81, 2009.
Rorke-Adams LB, Portnoy H: Long-term survival of an infant with gliomatosis cerebelli. J Neurosurg Pediatr 2 (5): 346-50, 2008.
Armstrong GT, Phillips PC, Rorke-Adams LB, et al.: Gliomatosis cerebri: 20 years of experience at the Children's Hospital of Philadelphia. Cancer 107 (7): 1597-606, 2006.
Listernick R, Darling C, Greenwald M, et al.: Optic pathway tumors in children: the effect of neurofibromatosis type 1 on clinical manifestations and natural history. J Pediatr 127 (5): 718-22, 1995.
Rosai J, Sobin LH, eds.: Dysgenetic syndromes. In: Rosai J, Sobin LH, eds.: Atlas of Tumor Pathology. Third Series. Washington, DC : Armed Forces Institute of Pathology, 1994., pp 379-90.
Allen JC: Initial management of children with hypothalamic and thalamic tumors and the modifying role of neurofibromatosis-1. Pediatr Neurosurg 32 (3): 154-62, 2000.
Molloy PT, Bilaniuk LT, Vaughan SN, et al.: Brainstem tumors in patients with neurofibromatosis type 1: a distinct clinical entity. Neurology 45 (10): 1897-902, 1995.
Bar EE, Lin A, Tihan T, et al.: Frequent gains at chromosome 7q34 involving BRAF in pilocytic astrocytoma. J Neuropathol Exp Neurol 67 (9): 878-87, 2008.
Forshew T, Tatevossian RG, Lawson AR, et al.: Activation of the ERK/MAPK pathway: a signature genetic defect in posterior fossa pilocytic astrocytomas. J Pathol 218 (2): 172-81, 2009.
Jones DT, Kocialkowski S, Liu L, et al.: Tandem duplication producing a novel oncogenic BRAF fusion gene defines the majority of pilocytic astrocytomas. Cancer Res 68 (21): 8673-7, 2008.
Jones DT, Kocialkowski S, Liu L, et al.: Oncogenic RAF1 rearrangement and a novel BRAF mutation as alternatives to KIAA1549:BRAF fusion in activating the MAPK pathway in pilocytic astrocytoma. Oncogene 28 (20): 2119-23, 2009.
Pfister S, Janzarik WG, Remke M, et al.: BRAF gene duplication constitutes a mechanism of MAPK pathway activation in low-grade astrocytomas. J Clin Invest 118 (5): 1739-49, 2008.
Korshunov A, Meyer J, Capper D, et al.: Combined molecular analysis of BRAF and IDH1 distinguishes pilocytic astrocytoma from diffuse astrocytoma. Acta Neuropathol 118 (3): 401-5, 2009.
Horbinski C, Hamilton RL, Nikiforov Y, et al.: Association of molecular alterations, including BRAF, with biology and outcome in pilocytic astrocytomas. Acta Neuropathol 119 (5): 641-9, 2010.
Yu J, Deshmukh H, Gutmann RJ, et al.: Alterations of BRAF and HIPK2 loci predominate in sporadic pilocytic astrocytoma. Neurology 73 (19): 1526-31, 2009.
Lin A, Rodriguez FJ, Karajannis MA, et al.: BRAF alterations in primary glial and glioneuronal neoplasms of the central nervous system with identification of 2 novel KIAA1549:BRAF fusion variants. J Neuropathol Exp Neurol 71 (1): 66-72, 2012.
Hawkins C, Walker E, Mohamed N, et al.: BRAF-KIAA1549 fusion predicts better clinical outcome in pediatric low-grade astrocytoma. Clin Cancer Res 17 (14): 4790-8, 2011.
Horbinski C, Nikiforova MN, Hagenkord JM, et al.: Interplay among BRAF, p16, p53, and MIB1 in pediatric low-grade gliomas. Neuro Oncol 14 (6): 777-89, 2012.
Janzarik WG, Kratz CP, Loges NT, et al.: Further evidence for a somatic KRAS mutation in a pilocytic astrocytoma. Neuropediatrics 38 (2): 61-3, 2007.
Dougherty MJ, Santi M, Brose MS, et al.: Activating mutations in BRAF characterize a spectrum of pediatric low-grade gliomas. Neuro Oncol 12 (7): 621-30, 2010.
Dias-Santagata D, Lam Q, Vernovsky K, et al.: BRAF V600E mutations are common in pleomorphic xanthoastrocytoma: diagnostic and therapeutic implications. PLoS One 6 (3): e17948, 2011.
Schindler G, Capper D, Meyer J, et al.: Analysis of BRAF V600E mutation in 1,320 nervous system tumors reveals high mutation frequencies in pleomorphic xanthoastrocytoma, ganglioglioma and extra-cerebellar pilocytic astrocytoma. Acta Neuropathol 121 (3): 397-405, 2011.
Dahiya S, Haydon DH, Alvarado D, et al.: BRAF(V600E) mutation is a negative prognosticator in pediatric ganglioglioma. Acta Neuropathol 125 (6): 901-10, 2013.
Jones DT, Hutter B, Jäger N, et al.: Recurrent somatic alterations of FGFR1 and NTRK2 in pilocytic astrocytoma. Nat Genet 45 (8): 927-32, 2013.
Zhang J, Wu G, Miller CP, et al.: Whole-genome sequencing identifies genetic alterations in pediatric low-grade gliomas. Nat Genet 45 (6): 602-12, 2013.
Ramkissoon LA, Horowitz PM, Craig JM, et al.: Genomic analysis of diffuse pediatric low-grade gliomas identifies recurrent oncogenic truncating rearrangements in the transcription factor MYBL1. Proc Natl Acad Sci U S A 110 (20): 8188-93, 2013.
Paugh BS, Qu C, Jones C, et al.: Integrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease. J Clin Oncol 28 (18): 3061-8, 2010.
Bax DA, Mackay A, Little SE, et al.: A distinct spectrum of copy number aberrations in pediatric high-grade gliomas. Clin Cancer Res 16 (13): 3368-77, 2010.
Ward SJ, Karakoula K, Phipps KP, et al.: Cytogenetic analysis of paediatric astrocytoma using comparative genomic hybridisation and fluorescence in-situ hybridisation. J Neurooncol 98 (3): 305-18, 2010.
Pollack IF, Hamilton RL, Sobol RW, et al.: IDH1 mutations are common in malignant gliomas arising in adolescents: a report from the Children's Oncology Group. Childs Nerv Syst 27 (1): 87-94, 2011.
Schwartzentruber J, Korshunov A, Liu XY, et al.: Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma. Nature 482 (7384): 226-31, 2012.
Wu G, Broniscer A, McEachron TA, et al.: Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas. Nat Genet 44 (3): 251-3, 2012.
Sturm D, Witt H, Hovestadt V, et al.: Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma. Cancer Cell 22 (4): 425-37, 2012.
Gielen GH, Gessi M, Hammes J, et al.: H3F3A K27M mutation in pediatric CNS tumors: a marker for diffuse high-grade astrocytomas. Am J Clin Pathol 139 (3): 345-9, 2013.
Khuong-Quang DA, Buczkowicz P, Rakopoulos P, et al.: K27M mutation in histone H3.3 defines clinically and biologically distinct subgroups of pediatric diffuse intrinsic pontine gliomas. Acta Neuropathol 124 (3): 439-47, 2012.
Suri V, Jha P, Agarwal S, et al.: Molecular profile of oligodendrogliomas in young patients. Neuro Oncol 13 (10): 1099-106, 2011.
Hoffman HJ, Berger MS, Becker LE: Cerebellar astrocytomas. In: Deutsch M, ed.: Management of Childhood Brain Tumors. Boston: Kluwer Academic Publishers, 1990, pp 441-56.
Fisher PG, Tihan T, Goldthwaite PT, et al.: Outcome analysis of childhood low-grade astrocytomas. Pediatr Blood Cancer 51 (2): 245-50, 2008.
Qaddoumi I, Sultan I, Gajjar A: Outcome and prognostic features in pediatric gliomas: a review of 6212 cases from the Surveillance, Epidemiology, and End Results database. Cancer 115 (24): 5761-70, 2009.
Wisoff JH, Sanford RA, Heier LA, et al.: Primary neurosurgery for pediatric low-grade gliomas: a prospective multi-institutional study from the Children's Oncology Group. Neurosurgery 68 (6): 1548-54; discussion 1554-5, 2011.
von Hornstein S, Kortmann RD, Pietsch T, et al.: Impact of chemotherapy on disseminated low-grade glioma in children and adolescents: report from the HIT-LGG 1996 trial. Pediatr Blood Cancer 56 (7): 1046-54, 2011.
Mazloom A, Hodges JC, Teh BS, et al.: Outcome of patients with pilocytic astrocytoma and leptomeningeal dissemination. Int J Radiat Oncol Biol Phys 84 (2): 350-4, 2012.
Stokland T, Liu JF, Ironside JW, et al.: A multivariate analysis of factors determining tumor progression in childhood low-grade glioma: a population-based cohort study (CCLG CNS9702). Neuro Oncol 12 (12): 1257-68, 2010.
Campbell JW, Pollack IF: Cerebellar astrocytomas in children. J Neurooncol 28 (2-3): 223-31, 1996 May-Jun.
Schneider JH Jr, Raffel C, McComb JG: Benign cerebellar astrocytomas of childhood. Neurosurgery 30 (1): 58-62; discussion 62-3, 1992.
Due-Tønnessen BJ, Helseth E, Scheie D, et al.: Long-term outcome after resection of benign cerebellar astrocytomas in children and young adults (0-19 years): report of 110 consecutive cases. Pediatr Neurosurg 37 (2): 71-80, 2002.
Massimi L, Tufo T, Di Rocco C: Management of optic-hypothalamic gliomas in children: still a challenging problem. Expert Rev Anticancer Ther 7 (11): 1591-610, 2007.
Campagna M, Opocher E, Viscardi E, et al.: Optic pathway glioma: long-term visual outcome in children without neurofibromatosis type-1. Pediatr Blood Cancer 55 (6): 1083-8, 2010.
Hernáiz Driever P, von Hornstein S, Pietsch T, et al.: Natural history and management of low-grade glioma in NF-1 children. J Neurooncol 100 (2): 199-207, 2010.
Pollack IF, Finkelstein SD, Woods J, et al.: Expression of p53 and prognosis in children with malignant gliomas. N Engl J Med 346 (6): 420-7, 2002.
Rood BR, MacDonald TJ: Pediatric high-grade glioma: molecular genetic clues for innovative therapeutic approaches. J Neurooncol 75 (3): 267-72, 2005.
Pollack IF, Hamilton RL, Burnham J, et al.: Impact of proliferation index on outcome in childhood malignant gliomas: results in a multi-institutional cohort. Neurosurgery 50 (6): 1238-44; discussion 1244-5, 2002.
Finlay JL, Boyett JM, Yates AJ, et al.: Randomized phase III trial in childhood high-grade astrocytoma comparing vincristine, lomustine, and prednisone with the eight-drugs-in-1-day regimen. Childrens Cancer Group. J Clin Oncol 13 (1): 112-23, 1995.
Villano JL, Seery TE, Bressler LR: Temozolomide in malignant gliomas: current use and future targets. Cancer Chemother Pharmacol 64 (4): 647-55, 2009.
Creach KM, Rubin JB, Leonard JR, et al.: Oligodendrogliomas in children. J Neurooncol 106 (2): 377-82, 2012.
There is no generally recognized staging system for childhood astrocytomas. For the purposes of this summary, childhood astrocytomas will be described as follows:
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 previously obtained results that assessed an 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, 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 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] Also, there are other less-common complications of radiation therapy, including cerebrovascular accidents.[4] 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.[5] Long-term management of these patients is complex and requires a multidisciplinary approach.
Standard Treatment Options
Childhood low-grade astrocytomas:
Newly diagnosed childhood low-grade astrocytomas
Adjuvant therapy (for tumors that are incompletely resected):
Radiation therapy
Second surgery
Targeted therapy (for subependymal giant cell astrocytomas)
Recurrent childhood low-grade astrocytomas
Childhood high-grade astrocytomas:
Newly diagnosed childhood high-grade astrocytomas
Adjuvant therapy:
Recurrent childhood high-grade astrocytomas
High-dose, marrow-ablative chemotherapy with hematopoietic stem cell transplant (not considered standard treatment)
Novel therapeutic approaches (not considered standard treatment)
Packer RJ, Sutton LN, Atkins TE, et al.: A prospective study of cognitive function in children receiving whole-brain radiotherapy and chemotherapy: 2-year results. J Neurosurg 70 (5): 707-13, 1989.
Johnson DL, McCabe MA, Nicholson HS, et al.: Quality of long-term survival in young children with medulloblastoma. J Neurosurg 80 (6): 1004-10, 1994.
Packer RJ, Sutton LN, Goldwein JW, et al.: Improved survival with the use of adjuvant chemotherapy in the treatment of medulloblastoma. J Neurosurg 74 (3): 433-40, 1991.
Bowers DC, Mulne AF, Reisch JS, et al.: Nonperioperative strokes in children with central nervous system tumors. Cancer 94 (4): 1094-101, 2002.
Duffner PK, Horowitz ME, Krischer JP, et al.: Postoperative chemotherapy and delayed radiation in children less than three years of age with malignant brain tumors. N Engl J Med 328 (24): 1725-31, 1993.
To determine and implement optimal 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 make surgery difficult; consequently, biopsies are not always done. This is especially true in patients with neurofibromatosis type 1 (NF1).[1] 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.[2][3]
Standard treatment options for newly diagnosed childhood low-grade astrocytomas include the following:
Observation is an option for patients with NF1 or nonprogressive masses.[4][5][6][7] Spontaneous regressions of optic pathway gliomas have been reported in children with and without NF1.[8][9][10]
Surgical resection is the primary treatment for childhood low-grade astrocytoma [1][4][5][11] and surgical feasibility is determined by tumor location.
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.[17]; [18][Level of evidence: 3iiDiii]
Factors related to outcome for children with low-grade gliomas treated with surgery followed by observation were identified in a COG study that included 518 evaluable patients.[11] Overall outcome for the entire group was 78% progression-free survival (PFS) at 8 years and 96% overall survival (OS) at 8 years. The following factors were related to prognosis:[11]
The extent of resection necessary for cure is unknown because patients with microscopic and even gross residual tumor after surgery may experience long-term PFS without postoperative therapy.[1][6][11]
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.[19][20][Level of evidence: 3iiiC]
Adjuvant therapy following complete resection of a low-grade glioma is generally not required unless there is a subsequent recurrence of disease. Treatment options for patients with incompletely resected tumor must be individualized and may include one or more of the following:
A shunt or other cerebrospinal fluid diversion procedure may be needed.
In selected patients in whom a portion of the tumor has been resected, the patient may 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.[11]
Radiation therapy is usually reserved until progressive disease is documented [16][21] and may be further delayed through the use of chemotherapy, a strategy that is commonly employed in young children.[22][23] For children with low-grade gliomas for whom radiation therapy is indicated, conformal radiation therapy, intensity-modulated radiation therapy, or stereotactic radiation therapy approaches appear effective and offer the potential for reducing the acute and long-term toxicities associated with these modalities.[24]; [25][Level of evidence: 3iDiii] 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.[26][27][28]; [29][Level of evidence: 2A]; [30][Level of evidence: 2C]; [31][Level of evidence: 3iiiDi]; [32][Level of evidence: 3iiiDii]; [15][33][Level of evidence: 3iiiDiii]
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.[8][34][35][36]; [30][Level of evidence: 2C]
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.[37] Children with NF1 may be at higher risk for radiation-associated secondary tumors and morbidity due to vascular changes.
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.[8]
Given the side effects associated with radiation therapy, postoperative chemotherapy may be initially recommended.
Chemotherapy may result in objective tumor shrinkage and delay the need for radiation therapy in most patients.[22][23][38][39] Chemotherapy is also an option that may delay or avoid radiation therapy in adolescents with optic nerve pathway gliomas.[40][Level of evidence: 3iiDii] 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.[41]
The most widely used regimens to treat tumor progression or symptomatic nonresectable, low-grade gliomas are the following:
The COG reported the results of a randomized phase III trial (COG-A9952) that treated children younger than 10 years with low-grade chiasmatic/hypothalamic gliomas using one of two regimens: carboplatin and vincristine (CV) or TPCV. The 5-year event-free survival rate was 39% ± 4% for the CV regimen and 52% ± 5% for the TPCV regimen.[43]
Other chemotherapy approaches have been employed to treat children with progressive low-grade astrocytomas, including multiagent, platinum-based regimens [23][38][44]; [45][Level of evidence: 2Diii] and temozolomide.[46][47] Reported 5-year PFS rates have ranged from approximately 35% to 60% for children receiving platinum-based chemotherapy for optic pathway gliomas,[23][38] but most patients ultimately require further treatment. This is particularly true for children who initially present with hypothalamic/chiasmatic gliomas that have neuraxis dissemination.[48][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.[23][38][44] Whether vision is improved with chemotherapy is unclear.[49][50][Level of evidence: 3iiiC]
For children with symptomatic subependymal giant cell astrocytomas (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.[51]; [52][Level of evidence: 2C]; [53][Level of evidence: 3iiiC] A multicenter, phase III, placebo-controlled trial of 117 patients confirmed these earlier findings; 35% of the patients in the everolimus group had at least a 50% reduction in the size of the SEGA, versus no reduction in the placebo group.[54][Level of evidence: 1iDiv] Whether reduction in size of the mass is durable, obviating the need for future surgery, is unknown.
The following is an example of a national and/or institutional clinical trial that is currently being conducted. 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 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.
An individual plan needs to be tailored based on the following:
Recurrent disease is usually at the primary tumor site, although multifocal or widely disseminated disease to other intracranial sites and to the spinal leptomeninges has been documented.[55][56] Most children whose low-grade fibrillary astrocytomas recur will harbor low-grade lesions; however, transformation into a higher grade tumor is possible.[57] Surveillance imaging will frequently identify asymptomatic recurrences.[58]
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 following:
Standard treatment options for recurrent childhood low-grade astrocytomas include the following:
Patients with low-grade astrocytomas who relapse after being treated with surgery alone should be considered for another surgical resection.[59]
The rationale for the use of radiation therapy is essentially the same when utilized as first-line therapy or at the time of recurrence (refer to the Radiation therapy subsection of the Treatment of Newly Diagnosed Childhood Low-Grade Astrocytomas section of this summary). If the child has never received radiation therapy, local radiation therapy may be a treatment option, although chemotherapy in lieu of radiation may be considered, depending on the child's age and the extent and location of the tumor.[60][Level of evidence: 3iA]; [61][Level of evidence: 3iiiDi]
For children with low-grade gliomas 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.[27][30]
If there is recurrence at an unresectable site that has been previously irradiated, chemotherapy should be considered.[62]
In patients previously treated with surgery and radiation therapy, chemotherapy should be considered. Chemotherapy may result in relatively long-term disease control.[23][63] 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.[23][46][63]
Antitumor activity has also been observed for bevacizumab given in combination with irinotecan. In a phase II study of bevacizumab plus irinotecan for children with recurrent low-grade gliomas, sustained partial response was observed in only two patients (5.7%), but the 6-month PFS was 85.4% (standard error [SE] ± 5.96%) and the 2-year PFS was 47.8% (SE ± 9.27%).[64] A pilot study of 14 patients with recurrent low-grade gliomas also evaluated bevacizumab plus irinotecan and observed 12 patients (86%) with objective responses.[65][Level of evidence: 3iiDi]; [66][Level of evidence: 3iiiDiv] No patients progressed on therapy (median treatment duration, 12 months), but 13 of 14 progressed after stopping bevacizumab at a median of 5 months.
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.
Nicolin G, Parkin P, Mabbott D, et al.: Natural history and outcome of optic pathway gliomas in children. Pediatr Blood Cancer 53 (7): 1231-7, 2009.
Kramm CM, Butenhoff S, Rausche U, et al.: Thalamic high-grade gliomas in children: a distinct clinical subset? Neuro Oncol 13 (6): 680-9, 2011.
Hayostek CJ, Shaw EG, Scheithauer B, et al.: Astrocytomas of the cerebellum. A comparative clinicopathologic study of pilocytic and diffuse astrocytomas. Cancer 72 (3): 856-69, 1993.
Listernick R, Ferner RE, Liu GT, et al.: Optic pathway gliomas in neurofibromatosis-1: controversies and recommendations. Ann Neurol 61 (3): 189-98, 2007.
Wisoff JH, Abbott R, Epstein F: Surgical management of exophytic chiasmatic-hypothalamic tumors of childhood. J Neurosurg 73 (5): 661-7, 1990.
Albright AL: Feasibility and advisability of resections of thalamic tumors in pediatric patients. J Neurosurg 100 (5 Suppl Pediatrics): 468-72, 2004.
Piccirilli M, Lenzi J, Delfinis C, et al.: Spontaneous regression of optic pathways gliomas in three patients with neurofibromatosis type I and critical review of the literature. Childs Nerv Syst 22 (10): 1332-7, 2006.
Tseng JH, Tseng MY: Survival analysis of 81 children with primary spinal gliomas: a population-based study. Pediatr Neurosurg 42 (6): 347-53, 2006.
Milano MT, Johnson MD, Sul J, et al.: Primary spinal cord glioma: a Surveillance, Epidemiology, and End Results database study. J Neurooncol 98 (1): 83-92, 2010.
Scheinemann K, Bartels U, Huang A, et al.: Survival and functional outcome of childhood spinal cord low-grade gliomas. Clinical article. J Neurosurg Pediatr 4 (3): 254-61, 2009.
Sawamura Y, Kamada K, Kamoshima Y, et al.: Role of surgery for optic pathway/hypothalamic astrocytomas in children. Neuro Oncol 10 (5): 725-33, 2008.
Pollack IF, Claassen D, al-Shboul Q, et al.: Low-grade gliomas of the cerebral hemispheres in children: an analysis of 71 cases. J Neurosurg 82 (4): 536-47, 1995.
Sutton LN, Cnaan A, Klatt L, et al.: Postoperative surveillance imaging in children with cerebellar astrocytomas. J Neurosurg 84 (5): 721-5, 1996.
Dorward IG, Luo J, Perry A, et al.: Postoperative imaging surveillance in pediatric pilocytic astrocytomas. J Neurosurg Pediatr 6 (4): 346-52, 2010.
Turner CD, Chordas CA, Liptak CC, et al.: Medical, psychological, cognitive and educational late-effects in pediatric low-grade glioma survivors treated with surgery only. Pediatr Blood Cancer 53 (3): 417-23, 2009.
Daszkiewicz P, Maryniak A, Roszkowski M, et al.: Long-term functional outcome of surgical treatment of juvenile pilocytic astrocytoma of the cerebellum in children. Childs Nerv Syst 25 (7): 855-60, 2009.
Fisher BJ, Leighton CC, Vujovic O, et al.: Results of a policy of surveillance alone after surgical management of pediatric low grade gliomas. Int J Radiat Oncol Biol Phys 51 (3): 704-10, 2001.
Packer RJ, Ater J, Allen J, et al.: Carboplatin and vincristine chemotherapy for children with newly diagnosed progressive low-grade gliomas. J Neurosurg 86 (5): 747-54, 1997.
Gnekow AK, Falkenstein F, von Hornstein S, et al.: Long-term follow-up of the multicenter, multidisciplinary treatment study HIT-LGG-1996 for low-grade glioma in children and adolescents of the German Speaking Society of Pediatric Oncology and Hematology. Neuro Oncol 14 (10): 1265-84, 2012.
Paulino AC, Mazloom A, Terashima K, et al.: Intensity-modulated radiotherapy (IMRT) in pediatric low-grade glioma. Cancer 119 (14): 2654-9, 2013.
Müller K, Gnekow A, Falkenstein F, et al.: Radiotherapy in pediatric pilocytic astrocytomas. A subgroup analysis within the prospective multicenter study HIT-LGG 1996 by the German Society of Pediatric Oncology and Hematology (GPOH). Strahlenther Onkol 189 (8): 647-55, 2013.
Chawla S, Korones DN, Milano MT, et al.: Spurious progression in pediatric brain tumors. J Neurooncol 107 (3): 651-7, 2012.
Marcus KJ, Goumnerova L, Billett AL, et al.: Stereotactic radiotherapy for localized low-grade gliomas in children: final results of a prospective trial. Int J Radiat Oncol Biol Phys 61 (2): 374-9, 2005.
Combs SE, Schulz-Ertner D, Moschos D, et al.: Fractionated stereotactic radiotherapy of optic pathway gliomas: tolerance and long-term outcome. Int J Radiat Oncol Biol Phys 62 (3): 814-9, 2005.
Merchant TE, Kun LE, Wu S, et al.: Phase II trial of conformal radiation therapy for pediatric low-grade glioma. J Clin Oncol 27 (22): 3598-604, 2009.
Merchant TE, Conklin HM, Wu S, et al.: Late effects of conformal radiation therapy for pediatric patients with low-grade glioma: prospective evaluation of cognitive, endocrine, and hearing deficits. J Clin Oncol 27 (22): 3691-7, 2009.
Kano H, Niranjan A, Kondziolka D, et al.: Stereotactic radiosurgery for pilocytic astrocytomas part 2: outcomes in pediatric patients. J Neurooncol 95 (2): 219-29, 2009.
Hallemeier CL, Pollock BE, Schomberg PJ, et al.: Stereotactic radiosurgery for recurrent or unresectable pilocytic astrocytoma. Int J Radiat Oncol Biol Phys 83 (1): 107-12, 2012.
Mansur DB, Rubin JB, Kidd EA, et al.: Radiation therapy for pilocytic astrocytomas of childhood. Int J Radiat Oncol Biol Phys 79 (3): 829-34, 2011.
Jenkin D, Angyalfi S, Becker L, et al.: Optic glioma in children: surveillance, resection, or irradiation? Int J Radiat Oncol Biol Phys 25 (2): 215-25, 1993.
Tao ML, Barnes PD, Billett AL, et al.: Childhood optic chiasm gliomas: radiographic response following radiotherapy and long-term clinical outcome. Int J Radiat Oncol Biol Phys 39 (3): 579-87, 1997.
Khafaga Y, Hassounah M, Kandil A, et al.: Optic gliomas: a retrospective analysis of 50 cases. Int J Radiat Oncol Biol Phys 56 (3): 807-12, 2003.
Grill J, Couanet D, Cappelli C, et al.: Radiation-induced cerebral vasculopathy in children with neurofibromatosis and optic pathway glioma. Ann Neurol 45 (3): 393-6, 1999.
Laithier V, Grill J, Le Deley MC, et al.: Progression-free survival in children with optic pathway tumors: dependence on age and the quality of the response to chemotherapy--results of the first French prospective study for the French Society of Pediatric Oncology. J Clin Oncol 21 (24): 4572-8, 2003.
Prados MD, Edwards MS, Rabbitt J, et al.: Treatment of pediatric low-grade gliomas with a nitrosourea-based multiagent chemotherapy regimen. J Neurooncol 32 (3): 235-41, 1997.
Chong AL, Pole JD, Scheinemann K, et al.: Optic pathway gliomas in adolescence--time to challenge treatment choices? Neuro Oncol 15 (3): 391-400, 2013.
Gropman AL, Packer RJ, Nicholson HS, et al.: Treatment of diencephalic syndrome with chemotherapy: growth, tumor response, and long term control. Cancer 83 (1): 166-72, 1998.
Gururangan S, Cavazos CM, Ashley D, et al.: Phase II study of carboplatin in children with progressive low-grade gliomas. J Clin Oncol 20 (13): 2951-8, 2002.
Ater JL, Zhou T, Holmes E, et al.: Randomized study of two chemotherapy regimens for treatment of low-grade glioma in young children: a report from the Children's Oncology Group. J Clin Oncol 30 (21): 2641-7, 2012.
Massimino M, Spreafico F, Cefalo G, et al.: High response rate to cisplatin/etoposide regimen in childhood low-grade glioma. J Clin Oncol 20 (20): 4209-16, 2002.
Massimino M, Spreafico F, Riva D, et al.: A lower-dose, lower-toxicity cisplatin-etoposide regimen for childhood progressive low-grade glioma. J Neurooncol 100 (1): 65-71, 2010.
Gururangan S, Fisher MJ, Allen JC, et al.: Temozolomide in children with progressive low-grade glioma. Neuro Oncol 9 (2): 161-8, 2007.
Khaw SL, Coleman LT, Downie PA, et al.: Temozolomide in pediatric low-grade glioma. Pediatr Blood Cancer 49 (6): 808-11, 2007.
Moreno L, Bautista F, Ashley S, et al.: Does chemotherapy affect the visual outcome in children with optic pathway glioma? A systematic review of the evidence. Eur J Cancer 46 (12): 2253-9, 2010.
Shofty B, Ben-Sira L, Freedman S, et al.: Visual outcome following chemotherapy for progressive optic pathway gliomas. Pediatr Blood Cancer 57 (3): 481-5, 2011.
Franz DN, Agricola KD, Tudor CA, et al.: Everolimus for tumor recurrence after surgical resection for subependymal giant cell astrocytoma associated with tuberous sclerosis complex. J Child Neurol 28 (5): 602-7, 2013.
Krueger DA, Care MM, Holland K, et al.: Everolimus for subependymal giant-cell astrocytomas in tuberous sclerosis. N Engl J Med 363 (19): 1801-11, 2010.
Franz DN, Leonard J, Tudor C, et al.: Rapamycin causes regression of astrocytomas in tuberous sclerosis complex. Ann Neurol 59 (3): 490-8, 2006.
Franz DN, Belousova E, Sparagana S, et al.: Efficacy and safety of everolimus for subependymal giant cell astrocytomas associated with tuberous sclerosis complex (EXIST-1): a multicentre, randomised, placebo-controlled phase 3 trial. Lancet 381 (9861): 125-32, 2013.
Perilongo G, Carollo C, Salviati L, et al.: Diencephalic syndrome and disseminated juvenile pilocytic astrocytomas of the hypothalamic-optic chiasm region. Cancer 80 (1): 142-6, 1997.
Leibel SA, Sheline GE, Wara WM, et al.: The role of radiation therapy in the treatment of astrocytomas. Cancer 35 (6): 1551-7, 1975.
Giannini C, Scheithauer BW: Classification and grading of low-grade astrocytic tumors in children. Brain Pathol 7 (2): 785-98, 1997.
Udaka YT, Yeh-Nayre LA, Amene CS, et al.: Recurrent pediatric central nervous system low-grade gliomas: the role of surveillance neuroimaging in asymptomatic children. J Neurosurg Pediatr 11 (2): 119-26, 2013.
Austin EJ, Alvord EC Jr: Recurrences of cerebellar astrocytomas: a violation of Collins' law. J Neurosurg 68 (1): 41-7, 1988.
Scheinemann K, Bartels U, Tsangaris E, et al.: Feasibility and efficacy of repeated chemotherapy for progressive pediatric low-grade gliomas. Pediatr Blood Cancer 57 (1): 84-8, 2011.
de Haas V, Grill J, Raquin MA, et al.: Relapses of optic pathway tumors after first-line chemotherapy. Pediatr Blood Cancer 52 (5): 575-80, 2009.
Garcia DM, Marks JE, Latifi HR, et al.: Childhood cerebellar astrocytomas: is there a role for postoperative irradiation? Int J Radiat Oncol Biol Phys 18 (4): 815-8, 1990.
Packer RJ, Lange B, Ater J, et al.: Carboplatin and vincristine for recurrent and newly diagnosed low-grade gliomas of childhood. J Clin Oncol 11 (5): 850-6, 1993.
Gururangan S, Fangusaro J, Poussaint TY, et al.: Efficacy of bevacizumab plus irinotecan in children with recurrent low-grade gliomas--a Pediatric Brain Tumor Consortium study. Neuro Oncol 16 (2): 310-7, 2014.
Hwang EI, Jakacki RI, Fisher MJ, et al.: Long-term efficacy and toxicity of bevacizumab-based therapy in children with recurrent low-grade gliomas. Pediatr Blood Cancer 60 (5): 776-82, 2013.
Packer RJ, Jakacki R, Horn M, et al.: Objective response of multiply recurrent low-grade gliomas to bevacizumab and irinotecan. Pediatr Blood Cancer 52 (7): 791-5, 2009.
Warren KE, Goldman S, Pollack IF, et al.: Phase I trial of lenalidomide in pediatric patients with recurrent, refractory, or progressive primary CNS tumors: Pediatric Brain Tumor Consortium study PBTC-018. J Clin Oncol 29 (3): 324-9, 2011.
To determine and implement optimal management, treatment of childhood high-grade astrocytomas is often guided by a multidisciplinary team of cancer specialists who have experience treating childhood brain tumors.
Outcomes in high-grade gliomas occurring in childhood are more favorable than that in adults. It is not clear whether this difference is caused by biologic variations in tumor characteristics, therapies used, tumor resectability, or other factors.[1]
The therapy for both children and adults with supratentorial high-grade astrocytoma includes surgery, radiation therapy, and chemotherapy.
Standard treatment options for newly diagnosed childhood high-grade astrocytomas include the following:
The ability to obtain a complete resection is associated with a better prognosis.[2][3] 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.[4] Similarly, in a trial of multiagent chemoradiation therapy 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%.[5][Level of evidence: 2A]
Radiation therapy is routinely 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 treated with radiation therapy.[6][7]; [8][9][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.[10]
The use of temozolomide to treat glioblastoma was initially investigated in adults. 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 benefitted from temozolomide, whereas those who did not have a methylated MGMT promoter did not benefit from temozolomide.[11][12] 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 [13] 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.[14][15][16]
Clinical trials that evaluate chemotherapy with or without radiation therapy are ongoing. Information about ongoing clinical trials is available from the NCI Web site.
Early-phase therapeutic trials may be available for selected patients. These trials may be available via the Children's Oncology Group, the Pediatric Brain Tumor Consortium, or other entities. 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 some patients recur 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 rarely occurs.
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 following:
Patients for whom initial treatment fails may benefit from additional treatment.[17] 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 recurrence.[18]; [19][Level of evidence: 3iiiA] Such patients should also be considered for entry into trials of novel therapeutic approaches.
Rasheed BK, McLendon RE, Herndon JE, et al.: Alterations of the TP53 gene in human gliomas. Cancer Res 54 (5): 1324-30, 1994.
Wisoff JH, Boyett JM, Berger MS, et al.: Current neurosurgical management and the impact of the extent of resection in the treatment of malignant gliomas of childhood: a report of the Children's Cancer Group trial no. CCG-945. J Neurosurg 89 (1): 52-9, 1998.
Yang T, Temkin N, Barber J, et al.: Gross total resection correlates with long-term survival in pediatric patients with glioblastoma. World Neurosurg 79 (3-4): 537-44, 2013 Mar-Apr.
Fouladi M, Hunt DL, Pollack IF, et al.: Outcome of children with centrally reviewed low-grade gliomas treated with chemotherapy with or without radiotherapy on Children's Cancer Group high-grade glioma study CCG-945. Cancer 98 (6): 1243-52, 2003.
Wolff JE, Driever PH, Erdlenbruch B, et al.: Intensive chemotherapy improves survival in pediatric high-grade glioma after gross total resection: results of the HIT-GBM-C protocol. Cancer 116 (3): 705-12, 2010.
Tendulkar RD, Pai Panandiker AS, Wu S, et al.: Irradiation of pediatric high-grade spinal cord tumors. Int J Radiat Oncol Biol Phys 78 (5): 1451-6, 2010.
Wolff B, Ng A, Roth D, et al.: Pediatric high grade glioma of the spinal cord: results of the HIT-GBM database. J Neurooncol 107 (1): 139-46, 2012.
Ononiwu C, Mehta V, Bettegowda C, et al.: Pediatric spinal glioblastoma multiforme: current treatment strategies and possible predictors of survival. Childs Nerv Syst 28 (5): 715-20, 2012.
Sposto R, Ertel IJ, Jenkin RD, et al.: The effectiveness of chemotherapy for treatment of high grade astrocytoma in children: results of a randomized trial. A report from the Childrens Cancer Study Group. J Neurooncol 7 (2): 165-77, 1989.
Stupp R, Mason WP, van den Bent MJ, et al.: Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med 352 (10): 987-96, 2005.
Hegi ME, Diserens AC, Gorlia T, et al.: MGMT gene silencing and benefit from temozolomide in glioblastoma. N Engl J Med 352 (10): 997-1003, 2005.
Cohen KJ, Pollack IF, Zhou T, et al.: Temozolomide in the treatment of high-grade gliomas in children: a report from the Children's Oncology Group. Neuro Oncol 13 (3): 317-23, 2011.
Duffner PK, Krischer JP, Burger PC, et al.: Treatment of infants with malignant gliomas: the Pediatric Oncology Group experience. J Neurooncol 28 (2-3): 245-56, 1996 May-Jun.
Dufour C, Grill J, Lellouch-Tubiana A, et al.: High-grade glioma in children under 5 years of age: a chemotherapy only approach with the BBSFOP protocol. Eur J Cancer 42 (17): 2939-45, 2006.
Warren KE, Gururangan S, Geyer JR, et al.: A phase II study of O6-benzylguanine and temozolomide in pediatric patients with recurrent or progressive high-grade gliomas and brainstem gliomas: a Pediatric Brain Tumor Consortium study. J Neurooncol 106 (3): 643-9, 2012.
McCowage GB, Friedman HS, Moghrabi A, et al.: Activity of high-dose cyclophosphamide in the treatment of childhood malignant gliomas. Med Pediatr Oncol 30 (2): 75-80, 1998.
Finlay JL, Dhall G, Boyett JM, et al.: Myeloablative chemotherapy with autologous bone marrow rescue in children and adolescents with recurrent malignant astrocytoma: outcome compared with conventional chemotherapy: a report from the Children's Oncology Group. Pediatr Blood Cancer 51 (6): 806-11, 2008.
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.
This summary was reformatted.
General Information About Childhood Astrocytomas
Added text to state that one retrospective study of 53 children with gangliogliomas demonstrated BRAF V600E staining in approximately 40% of tumors. Five-year recurrence-free survival was worse in the V600E-mutated tumors (about 60%) than in the tumors that did not stain for V600E (about 80%) (cited Dahiya et al. as reference 34).
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.
This information is provided by the National Cancer Institute.
This information was last updated on June 20, 2014.
Many children with cancer receive treatment in the outpatient setting, which allows them to stay in school and continue to develop intellectually and socially. However, returning to school can be an emotional experience; our Back to School Program is designed to ease your child's transition back to the classroom.
Concierge Services is your one-stop place to learn about Dana-Farber programs, services and resources, as well as information on getting around Boston, finding lodging or restaurants, and activities in the area.
The Expressive Arts Therapy program, sponsored by the Leonard P. Zakim Center for Integrative Therapies, provides adult patients, family members, and caregivers with a variety of options to support well-being during cancer treatment. From live music meditation to painting technique workshops, the program offers a range of creative outlets to suit every interest.
Dana-Farber and Children's Hospital, including parking facilities, are fully accessible to people with disabilities. There are wheelchairs at the main entrance, and security staff can provide personal assistance. We also have many educational materials available in large print and audiotape formats.
The Ethics Consultation Service is available for patients and families who may be facing difficult decisions and choices regarding care. Our goal is to bring together patients, families and health care providers to talk about ethical concerns and help everyone involved arrive at a resolution that is right for all.
Find practical tips and suggestions for individuals caring for a family member or friend with cancer, including creating a caregiving plan, finding community resources, and looking after your own well-being.
Friends' Place provides personal consultations to help cancer patients of all ages cope with changes in physical appearance that result from cancer treatment. Our experienced, compassionate team provides fittings for compression garments or breast prostheses, helps with wigs and other head coverings, and offers make-up and skincare advice.
The Friends' Corner Gift Shop, located on the first floor of the Yawkey Center for Cancer Care, offers a wide selection of unique gifts and everyday items for patients, families and staff.
Every year, thousands of patients with cancer from around the world come to Dana-Farber for their care. We provide a wide array of logistical and other services for individuals who live outside the United States.
Dana-Farber provides interpreting services for patients whose first language is not English. Interpreters may be requested for any activity, including registration, booking appointments, attending treatments and exams, support groups, and meetings with doctors and other members of your health care team.
Just for Teens provides programs and activities for teens and young adults with cancer at the Jimmy Fund Clinic and Children's Hospital Boston. We offer activities and events both inside and out of the hospital so that you have creative ways to pass the time and can meet other teens who are going through similar experiences.
Our nutritionists are registered dietitians who can assist you in planning an optimal diet during any stage of your cancer journey, cope with any side effects you may experience, and answer your questions about the latest findings on cancer and nutrition.
The Eleanor and Maxwell Blum Patient and Family Resource Center and its satellite resource rooms are staffed by health care professionals and provide computer stations, books, brochures, videos, and CDs to help you find information and support on a variety of issues about cancer treatment and care.
Patients websites help friends and family members stay up-to-date on their loved ones' condition and write messages of support and encouragement.
The Dana-Farber pharmacy fills prescriptions for all pediatric and adult patients. Our pharmacists are an extension of the patient care team and work closely with your physicians to provide seamless, convenient, safe care.
More than 1,200 Dana-Farber patients and their families have enjoyed free trips to baseball games, theater shows, museums, and other attractions this year through the Recreational Resources program.
The School Liaison Program is for pediatric patients who are diagnosed with or have completed a treatment that involves the central nervous system. We provide consultation about the cognitive late effects of treatment to help parents understand and advocate for their child's learning needs.
Through all stages of cancer treatment and survivorship, our Spiritual Care staff is available 24 hours a day to provide emotional and spiritual support for adults and pediatric patients and family members.
Integrative therapies, also known as complementary therapies, range from acupuncture and massage to nutritional guidance and music therapy. Patients treated at the Zakim Center credit its services with easing nausea, improving circulation, and reducing pain, stress, and anxiety associated with cancer treatment.
Dr. Mark Kieran, Director of the Pediatric Brain Tumor Program, cares for children and teens with brain tumors. Dr. Kieran explains how explains how a multidisciplinary team of specialists come together to deliver specialized care for each child.
Learn more about how Dana-Farber/Children's Hospital Cancer Center's Pediatric Brain Tumor Program clinicians uniquely treat children and teens with brain and spinal cord tumors.
Browse clinical trials


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Shipping Rates
All orders are charged actual shipping rates. Available shipping options for each order will be calculated during the checkout process based on package dimensions and destination. You will have the opportunity to review the shipping fees for your order before finalizing and submitting your order. For full shipping details and options see our shipping page at http://www.aswexpress.com/information/shipping.html.
Oversized orders
Certain items and large orders ship via LTL (less than truckload) with reduced ground rates inside the contiguous 48 states.
Turnaround times
Most orders leave our warehouse in 24-48 hours. Orders received before 9:30 AM EST on a weekday will most likely ship the same business day contingent upon warehouse volume. Our warehouse is located in Henderson, NC. Your estimated transit time will vary based on your proximity to our warehouse. Custom sectional frames are cut-to-order so please allow additional time for delivery.

subset: commoncrawl


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all wordsany wordsphrase
n. 1) the criminal act of entering a residence or other enclosed property through the slightest amount of force (even pushing open a door), without authorization. If there is intent to commit a crime, this is burglary. If there is no such intent, the breaking and entering alone is probably at least illegal trespass, which is a misdemeanor crime. 2) the criminal charge for the above.


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March 2, 2013
Lupus is not an equal-opportunity disease! It discriminates against minorities, and according to findings of a new study, lupus discriminates against the poor. Supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the study shows the disparity in lupus and lupus nephritis incidence among the low-income population receiving Medicaid. Authors concluded that their findings indicate a need for increased resources to be allocated to this group to ensure adequate care is afforded. These results were just published in the professional publication Arthritis & Rheumatism.


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|1818 Moore Boulevard in North-East Davis
|Individual Owners
|Types of Units:
|2br/2ba, 4br/2ba
|Price Range:
The Wildhorse Condominiums feature individually owned and property-company-managed condos. It was built in 2006, so it is one of the newer housing areas in Davis. It is also one of the furthest complexes from the UC Davis campus. Luxury comes with a price: distance. Every unit has a garage in addition to regular amenities like washer and dryer, dishwasher, garbage disposal, fridge, and central heat and air. Second story units have a deck while first floor units have a small, unenclosed patio area. There is also a pool and a spa, but sadly the management does not heat the spa, nor do they clean the spider webs off of buildings, which they claim they will do, even though they apparently are very willing to hand out charges for violations of 'décor' (a.k.a. plastic chairs on porches).
The complex is generally quiet because it is populated by a mix of families, young professionals, and college students. Units on Moore Blvd. have a great view of Nugget Fields and are well within earshot of screaming soccer moms and whistles (and an ice cream truck that plays annoying music at 125 decibels - which I hope they have a noise permit for - nonstop during games), and the rear units overlook part of the Wildhorse Golf Course. There are many visitor parking spots, but be warned that management will tow cars that repeatedly park in visitor spots.
The Oak Tree Plaza and Davis Athletic Club are relatively close.
- Unitrans L-Line bus stop about 30 second walk from the door of your condo (Moore and Pole Line Stop)
- Unitrans P/Q Line stops a 10-minute walk away (Pole Line and Covell)
- Yolobus 42A/42B stops a 10-minute walk away (Pole Line and Covell)
- UC Davis Campus 3 miles away, or a 55-minute walk
- 20-minute Bike Ride to UC Davis campus
- At unannounced times, a private security guard will arrive and sit in his security car in the parking lot, which has the great side effect of deterring any creeps. This makes the condos, which would otherwise feel a little secluded, seem one of the safer places in Davis.
"Tot Lot":
To learn more about rental housing in Davis, check out our Housing Guide as well as our Apartments pages.
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Standing on the Side of Love
You never know when the moment of decision will come. Perhaps it is on the school playground, when you see the class bully picking on a new victim. Or standing in the check-out line at the grocery store behind a young mother whose screaming child has her at her wits end. Or at a staff forum at work when your pledge to take some unpaid leave days could help save a coworker's job. Or on a beautiful Minnesota weekend, such as this, when we can choose to stand proudly with our Southwestern Minnesota LGBT [lesbian, gay, bisexual and transgender] community in support of the rights and dignity of all people or to hear our President engage the debate on health care reform and the basic human rights of the over 46 million uninsured people in our country.
Such moments come in different ways to each of us, but they do come. They remind us that the decisions we make in our day to day lives do make a difference. They point out the ongoing choices we make between standing uncomfortably on the sidelines of our messy world, unsure of what to do, and acting deliberately in small but concrete ways to help create a kinder, more compassionate reality. They return us to the powerful truth that in critical times it is possible to stand on the side of love, and, in the mystic's words, "to help its mighty power to surge upward and surmount every obstacle" by defending, supporting, and advocating for each other as if we all were equals in our humanity.
Or do they? Perhaps you are sitting here on this home-coming Sunday thinking that your minister is once again waxing idealistic. After all, are we fallible human beings really that powerful? If standing on the side of love is so significant, then why isn't the world a better place already? Don't most people already think of themselves as standing for love? Or at least as much love as they can manage, given that most of us cannot live as saints?
It is a spiritual paradox. It is precisely because we live in a world which knows the evils of greed and violence and the seas of human indifference that we understand just how sacred it is when our acts of love and compassion actually triumph. And it is precisely because we live in a world which knows such triumphs that we cannot fully give up hope on our imperfect humanity.
If there is one thing that I appreciate about our Unitarian Universalist Association's invitation to stand on the side of love in these current times, it is that the invitation invites love as an active force in our lives. So much of our understanding of love can be passive—we talk of "falling" in love, or of being "helplessly" in love, or we assume love's automatic presence in a family or a home or a community and are shocked to learn otherwise. But I do believe that love is more than merely a power that claims us. It is also a power that we claim by choosing our response to the truths of our world.
This weekend in the Twin Cities, our flags stand at half-mast for Officer Richard Crittenden, who was killed providing protection to a woman and her child as he escorted her into her apartment, where her abusive estranged husband was lying in wait with a burning rag. Often in the news we hear stories of law enforcement protection orders failing to provide the protection that is so desperately needed. In this case, Officer Crittenden and his colleague helped to defend a mother and daughter's right to freedom and safety, even though it meant putting themselves in the line of fire. Perhaps Officer Crittenden, known as "Critter," would have said he was just doing his job, but I think he chose to take a stand—to stand on the side of love despite the sea of violence that can surround us.
Love is a choice. Love is a stand. Whether we are standing by the bedside of a loved one dying, or standing in support by the side of a stranger we have only just met. Whether we are standing side by side in a parade to help end discrimination, or standing up for our children by donating a day's business profit to Kids Against Hunger. The love which inspires the courage and commitment of such choices is not a sweet or sentimental kind of love. Rather it is a love which recognizes the greater good and the bonds of kinship of which we are a part.
But once we accept love as a choice, then we must also come to terms with where that choice leads us. This was the profound and radical insight of our Universalist forbears – that if Love comes from God, then there can be no exceptions. Love cannot be just for one, or some of us. If it is for any of us, it must be for all. Love cannot be just for those with loud voices, but also for the voiceless. Love cannot be just for those with power, but also for those who are marginalized. Love cannot be just for those who still hope, but also for those who despair that help and hope will ever come.
The Standing on the Side of Love campaign was born out of the tragic shootings in our sister congregation, the Tennessee Valley Unitarian Universalist Church (TVUUC) in Knoxville, TN, last summer. On July 27, 2008, Jim David Adkisson walked into the church's sanctuary during the performance of a children's musical and began firing a shotgun, killing two and injuring six. Among the fatalities were members of TVUUC and Westside Unitarian Universalist Church, also in Knoxville. In a letter later found by police, Adkisson said that he targeted the church because of its liberal values—including its openness to gays and lesbians. He wrote of his beliefs that "The UU church is the Fountainhead [sic], the veritable wellspring of anti-American organizations like Moveon.org, Code Pink, and other un-American groups Oh But after the shooting, both Knoxville congregations pledged to remain open and welcoming, and in fact chose to embrace their inclusive and loving spirit even more boldly in the days that followed, supported by their wider community and religious neighbors. In doing so, they also drew on their Unitarian Universalist heritage which consistently urges us to choose love over hate and fear.
As I thought about this homecoming Sunday, I thought of the ways in which this congregation has chosen to stand on the side of love in the almost six years that I have walked with you as your minister. I thought about how we went through the process to become a Welcoming Congregation, how we opened our doors to host the luncheon for the Reconciliation Riders last November, when the Mankato mayor issued a formal apology on behalf of the city for the tragic lynching that is part of our history, how we continue to serve hot meals at the Salvation Army and to pool our resources to make a difference through the Kiva micro-loan program, and how we will become an International Peace Site with the dedication of our Peace Pole, lovingly made by our own Dave and Nancy Allen, next week. And there is so much more that I could lift up as examples.
But I don't share this list to be "intent on vanities" in the words of Thomas a Kempis, or to pat ourselves on the back. That isn't why we choose to stand on the side of love in these ways. Instead I lift them up to point out that the love we choose is always contextual. How we act on the side of love in our own lives and in our own community will be different than the choices made by our neighbors a few towns over, or our fellow religionists several states to the south. And different times and moments in history and community call us to stand with our brothers and sisters in the world on different issues and for different needs.
So take a moment to reflect on this particular time, in your own life, in the lives of your family and friends, and in the state of our community and our world. Who needs us to stand with them on the side of love? What moral questions does our commitment to love call us to address in the coming year? Is it time to learn something from our Iowan neighbors and to make same-sex marriage legal in Minnesota, so that we don't need to organize any more Love Buses to Des Moines? Is it time to create an interfaith voice in Greater Mankato that can speak with a shared voice to the moral issues of our times, whether health care or immigration reform, hunger or homelessness? Is it time, despite the recession, to finally build that elevator to make our spiritual home fully accessible to all? I don't have the answers, nor are the choices only mine to make. But I lift up these questions to spark a conversation – as individual people who care about this world and as a community of faith, memory and hope.
Recently, reflecting on the opportunities to stand for love, a friend of mine asked, why does it have to be a side? Must there always be a side? I understand her regret. The last thing our world needs is more division. One answer might be that the call to stand on the side of love is made in the spirit of inclusion, in the hope that one day it will be the only place to stand. But I also think that we are being invited to stand in a new place, or on a new side, of understanding about what it means to live spiritually in our world. Our newly-elected Unitarian Universalist Association (UUA) President, the Rev. Peter Morales, expresses it with these words: 'There's no difference between spiritual values and social action," he observes. "They're two sides of the same coin. When we experience our connection with that which transcends us and with other people, we become compassionate. We suffer with, not separated from the other. That's a deeply spiritual experience... Standing on the Side of Love... is simply a way in which we can act upon our deepest religious passions." Love is a choice. It is a stand. It is a deep life-changing passion, not just for our hearts, but also for our souls.
In her map of the country, the poet Adrienne Rich ponders whether or not she has described a map or a mural. Her description of our troubled and difficult world reminds me of the maps of olden times, where there would be occasional warnings of danger marked with the words "here there are dragons." I always pondered that the map makers never quite seemed to create a similar tip for those places of help and safety. Where were the places that could be marked, "here there is love?" As I reflect on my own years, as a child, a youth, and an adult in this faith and I think of the friends and experiences that have shaped my own faith journey, I know that I have found those places of help and safety in the congregations that I have been blessed to know. It is you who remind me of the importance of love, you who remind me of why we are called to find love, and choose it, and act it out in the world, over and over again.
So, welcome back to your Fellowship. Welcome to this house of the spirit, to this caring community, and to this call to service. It is good to stand, here with you, on the side of love—the only place I would ever choose to be. Will you join me, once again?


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Invest in people, promote innovation
In what ways can staff development be implemented effectively?
At Waggener Edstrom, we've always believed certain things to be true - invest in people, build a culture of innovation and focus on clients' needs.
We run the company around our people and understand that they are our only asset. It is crucial to allocate a significant portion of profits to cultivating talent. It is a long-term view and the right thing to do but not always the easiest.
In the intense, dynamic environment of the public relations (PR) industry, it is easy for many agencies to under-invest in people, resulting in higher staff turnover and poor quality of work. It is a simple equation that eventually impacts the business on a larger scale. Lesser profits means less investment in people, and the vicious cycle repeats.
Right now, the PR industry is reaching a crisis point with our talent challenges. If we don't come together as an industry and actively invest in the development of our people, this problem will get worse.
Investing in people needs to start on day one and be sustained. Clients and staff will be more loyal and long-term profits will rise. Waggener Edstrom copes with this challenge in several ways. Firstly, we offer all employees who start, regardless of level, 20 days' personal leave per year, and this increases with length of tenure.
We also offer work-at-home days. In fact, our agency goal this year is to ensure a minimum of five work-from-home days for every employee. We have implemented this because we believe that our people can be more effective if they have flexibility and are empowered to plan their time and work priorities.
Because Waggener's philosophy is to let our people create the culture, we see employees in different offices adding their own local flavour to their workplace. We encourage this diversity as it creates an environment that enables everyone to contribute to their full potential.
Even though we now have offices all over the globe, we work hard to make sure that everyone still feels connected to each other. Technology plays a crucial role, offering a myriad ways to encourage interaction, from desktop video-conferencing to instant messaging and, of course, e-mail. We also give employees the experience of working in other offices through overseas assignments.
Training and development is one area where this heightened interaction yields incredible dividends. Our global learning and development team delivers courses ranging from leadership development to social media 101, oftentimes across continents.
We also have leadership development tools that we use across all countries in our agencies. Psychometric personality profiling is mandated for mid- to senior levels, and go-forward career planning for all employees twice a year.
Finally, we have an annual global exchange programme open to all employees in the agency. They tell us which overseas office they'd like to work in for two weeks and we choose the best entries. We've found it to be a great motivation, enabling them to get a global view of the business.


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Moderator: Mahavihara moderator
Asevana ca balanam
Panditananca sevana
Puja ca puja-niyanam
Etam mangalam uttamam
Oleksandr wrote:Paṇḍita - wiseAsevana ca balanam
Panditananca sevana
Puja ca puja-niyanam
Etam mangalam uttamam
Bahusaccanca sippanca,
vinayo ca susikkhito;
subhasita ca ya vaca,
etam mangalam-uttamam.
Oleksandr wrote:yathābhūtaŋ - as is
yathābhūtaŋ ñāṇadassanaŋ - seeing (dassana) as (yathā) is (bhūtaŋ) with wisdom (ñāṇa)
David N. Snyder wrote:paṇṇākara (present)
Kara [fr. kṛ] 1. (adj.) ( -- ˚) producing, causing, forming, making, doing, e. g. anta˚ putting an end to; pabhaŋ causing splendour; pāpa˚ doing evil; divā˚ & divasa the day -- maker, i. e. the sun;
http://dsal.uchicago.edu/cgi-bin/philol ... 1:332.pali
Oleksandr wrote:As far as I understand in Pali, say, bla + ablabla make together blāblabla
Oleksandr wrote:Anyway, my word is paṇṇa - leaf, writing "paper"
Dukkhanirodha wrote:my favourite one:
dukkhanirodha: destruction of suffering. (m.)
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I perform about 500 Brazilian buttlifts each year, and this procedure is the most surgeon dependent plastic surgery procedure. Find a plastic surgeon with ELITE credentials who performs hundreds of Brazilian buttlifts each year. Then look at the plastic surgeon's website before and after photo galleries to get a sense of who can deliver the results.
Kenneth Hughes, MD Los Angeles, CA