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This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
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%.[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.
Diagnostic Evaluation
Every patient with newly diagnosed medulloblastoma should be evaluated with diagnostic imaging of the entire neuraxis and, when possible and safe, lumbar cerebrospinal fluid analysis.
Predictors of Outcome
Patients with disseminated disease at diagnosis are clearly at highest risk for disease relapse.[4,5,6] Other factors that portend an unfavorable outcome include younger age at diagnosis (in the absence of extensive nodularity) and possibly, a subtotal resection; however, the amount of residual disease after surgery has not been found to be a robust predictor of outcome, especially when chemotherapy was added to radiation therapy as part of postoperative treatment.[7,8] Similarly, the presence of brain stem involvement at diagnosis has not been shown to be predictive of outcome.[8,9]
In addition, histopathologic features such as large cell variant, anaplasia, and desmoplasia have been shown in retrospective analyses to correlate with outcome.[10,11] These molecular genetic immunohistochemical and histopathologic findings have not been shown to be predictive of outcome in prospective studies and with the exception of anaplasia/large cell variant, are not yet incorporated into stratification schema. A host of biological tumor cell characteristics have also been associated with prognosis, including DNA ploidy,[12,13]MYC expression and amplification,[14,15,16] chromosomal 17p loss,[17,18,19] p53 mutation status,[20,21] and chromosome 6q status.[22]
As a result of integrated molecular characterization of medulloblastoma, multiple medulloblastoma subtypes with distinct genetic profiles, pathway signatures, and clinicopathological features have been identified.[20,22,23,24,25,26,27,28,29,30] These subtypes themselves have prognostic associations, and it is clear that predictors of outcome can best be understood within the context of individual biological subtypes. The following four core subtypes have been identified:[31,32,33]
Optimal ways of identifying the four core medulloblastoma subtypes for clinical use is not clear, and both immunohistochemical methods and methods based on gene expression analysis are under development and evaluation.[34,35]
DNA sequencing studies have demonstrated fewer mutations in medulloblastoma than in adult carcinomas and a positive correlation between patient age and the number of mutations found. The relatively low numbers of mutations suggest that fewer driver mutations are required for medulloblastoma tumorigenesis. In addition, genome-wide sequencing studies have identified mutated genes previously not implicated in medulloblastoma pathogenesis, such as the tumor suppressors MLL2 and MLL3, from the family of genes affecting histone methylation.[36] These findings add an additional layer of complexity to the biologic understanding of medulloblastoma.
The classification of a childhood brain tumor is based on both the histopathologic characteristics of the tumor and its location in the brain.[1,2,3] The histopathological classification of childhood central nervous system (CNS) embryonal tumors remains somewhat controversial. These tumors all develop on the background of an undifferentiated round cell tumor but show a variety of divergent patterns of differentiation. Although it has been proposed that these tumors be merged under the term primitive neuroectodermal tumor, histologically similar tumors in different locations in the CNS demonstrate different genetic alterations.[4,5,6,7,8] In the 2007 World Health Organization (WHO) classification, embryonal tumors include the following:[2,9]
Pineoblastoma, a tumor histologically similar to CNS embryonal tumors, is reviewed in this summary, although pineoblastoma is grouped with tumors of the pineal region in the WHO classification.
By definition, medulloblastomas must arise in the posterior fossa.[1,2,3] Five different subtypes of medulloblastoma are recognized by the WHO classification and includes the following:
Significant attention has been focused on medulloblastomas that display anaplastic features, including increased nuclear size, marked cytological pleomorphism, numerous mitoses, and apoptotic bodies.[10,11] Classification is a complicated matter because most medulloblastomas have some degree of anaplasia, foci of anaplasia may appear in tumors with histologic features of both classic and large cell medulloblastomas, and there is significant overlap between the anaplastic and large cell variant.[10,11,12,13] The incidence of medulloblastoma with desmoplastic variant is higher in infants, is less common in children, and increases again in adolescents and adults. The desmoplastic variant subtype is different from medulloblastoma with extensive nodularity; the nodular variant having an expanded lobular architecture. The nodular subtype occurs almost exclusively in infants and carries an excellent prognosis.[13]
CNS PNETs generally arise in the cerebrum or suprasellar region, but may arise in the brain stem and spinal cord.[14] According to the 2007 WHO classification, tumors demonstrating areas of distinct neuronal differentiation are termed cerebral neuroblastomas and, if ganglion cells are also present, ganglioneuroblastomas. The pineoblastoma is histologically similar to the medulloblastoma; however, according to the WHO, its histogenesis is linked to a pineal cell, the pineocyte. Histologically different from the pineocyte, a pineal parenchymal tumor of intermediate differentiation showing elements of pineoblastoma and pineocytoma is recognized, although its natural history is variable and poorly characterized.[1,2] Genome-wide characterization of PNETs and pineoblastomas has demonstrated substantial molecular heterogeneity among these tumors.[8]
Both medulloepithelioma and ependymoblastoma are identified as histologically discrete tumors within the WHO classification system.[9,15] Medulloepithelioma and ependymoblastoma tumors are rare and tend to arise most commonly in infants and young children. Medulloepitheliomas, which histologically recapitulate the embryonal neural tube, tend to arise supratentorially, primarily intraventricularly, but may arise infratentorially, in the cauda, and even extraneural, along nerve roots.[9,15]
The existence of ependymoblastomas as a discrete entity has been questioned, although it remains in the most recent WHO classification. Ependymoblastoma is characterized by the presence of true multilayered (or ependymoblastic) rosettes.[16,17] The tumor has a supratentorial predilection, but like medulloepithelioma, it may occur in the spine, especially in the sacrococcygeal region. Histologically, the tumor shares features with other embryonal tumors and with a rare tumor type, the "embyronal tumor with abundant neuropil and true rosettes" (ETANTR).[16,17,18,19] The latter entity is characterized by young age at diagnosis (median age approximately 2 years), primarily supratentorial presentation, poor prognosis, and tumors showing true multilayered/ependymoblastic rosettes within a background of abundant neuropil-like areas.[17,19,20] In addition to sharing clinical characteristics (i.e., age, primary site, and prognosis), ependymoblastoma and ETANTR show common genomic alterations, including chromosome 2 gain and focal amplification at chromosome band 19q13.42. The latter chromosome region contains a cluster of microRNA coding genes,[21] and its amplification appears to be present in virtually all pediatric embryonal tumors with true multilayered rosettes (i.e., ependymoblastoma and ETANTR).[20,21,22] By contrast, 19q13.42 amplification has not been detected in more than 300 other pediatric brain tumors, suggesting that it may be a useful diagnostic marker for ependymoblastoma and ETANTR.[20]
The pathologic classification of pediatric brain tumors is a specialized area that is evolving. Immunohistochemical staining is now a routine component of evaluation.[10,11] Molecular genetic profiles are also being incorporated into evaluation and may radically alter classification in the future.[23,24,25,26] For example, gene expression profiling divides medulloblastoma into distinctive biological subtypes that differ in their clinical presentation, their underlying genomic abnormalities, and their immunohistochemical staining pattern.[25,26,27]
Subgroups include the following:
Patients with desmoplastic tumors with extensive nodularity should be carefully evaluated for stigmata of Gorlin syndrome, which is generally associated with mutations in PTCH1. One report observed that medulloblastoma with extensive nodularity (MBEN) was associated with Gorlin syndrome in 5 of 12 cases.[13] Gorlin syndrome is an autosomal dominant disorder, also known as the nevoid basal cell carcinoma syndrome, in which those affected are predisposed to the development of basal cell carcinomas later in life, especially in the radiation portal after radiation therapy. The syndrome can be diagnosed early in life by characteristic dermatological and skeletal features such as keratocysts of the jaw, bifid or fused ribs, macrocephaly, and calcifications of the falx.[13] Germline SUFU mutations have been observed among children younger than 3 years with the desmoplastic/nodular histology and may be most common among young children with MBEN.[28] While SUFU germline mutations may also be associated with Gorlin syndrome, young children with such mutations who develop medulloblastoma appear to often lack stigmata of Gorlin syndrome.[28,29]
Staging of Medulloblastoma
Evidence suggests that medulloblastomas originate from two different germinal zones within the cerebellum. The ventricular zone gives rise to the more common classic midline medulloblastomas, whereas granule neuron precursor cells of the external granule layer are believed to give rise to the lateral cerebellar hemispheric desmoplastic medulloblastomas. The tumors may spread contiguously to the cerebellar peduncle, along the floor of the fourth ventricle, into the cervical spine, or above the tentorium. At the time of diagnosis there is spread via the cerebrospinal fluid (CSF) to other intracranial sites, the spinal cord, or both in 10% to 30% of patients.[1,2,3]
Magnetic resonance imaging (MRI) is the method of choice to evaluate for intracranial or spinal cord subarachnoid metastases. To avoid postoperative artifacts, such imaging is best performed preoperatively, but postoperative evaluation is also useful when obtained at least 10 days following the operative procedure. The entire spine must be imaged in at least two planes, with contiguous magnetic resonance slices performed before and after gadolinium enhancement. The significance of positive CSF cytology in samples obtained within the first 7 to 10 days of diagnosis is unclear, as is the significance of tumor cells in cisternal fluid obtained at the time of surgery. However, CSF tumor cells found 2 to 3 weeks after diagnosis portends a poorer prognosis.[1,2,3] Extracranial spread of medulloblastoma at the time of diagnosis is less than 1%. Although bone scans and bone marrows have been routinely obtained in some older prospective studies, their yield was low and they are primarily recommended for infants or those with widespread intracranial disease, intraspinal disease, or those with symptoms and signs consistent with possible dissemination.[2,3] CSF shunts placed at the time of surgery have not been shown to increase the risk of leptomeningeal relapse.[2]
Historically, staging has been primarily based on an intraoperative evaluation of both the size and extent of the tumor, coupled with postoperative neuroimaging of the brain and spine and cytological evaluation of CSF. MRI of the brain and spine (often done preoperatively), postoperative MRI of the brain to determine the amount of residual disease, and lumbar CSF analysis are now used to determine staging.[1,2,3] Surgical impressions, including direct observation of dissemination at the time of diagnosis, extent of residual disease following surgery, and involvement of the brain stem, are still incorporated into staging systems.
Staging of Pineoblastoma
Staging for children with pineoblastomas is the same as that performed for children with medulloblastoma.[4] Dissemination at the time of diagnosis occurs in 10% to 30% of patients.[4] Because of the location of the tumor, total resections are uncommon, and most patients have only a biopsy or a subtotal resection before postsurgical treatment.[4,5] Similar to other central nervous system (CNS) primitive neuroectodermal tumors (PNETs), all pineoblastomas are treated as high-risk embryonal tumors. Prognosis is worse for patients with disseminated disease at the time of diagnosis.[4,5]
Staging of CNS PNETs
Patients with CNS PNETs are staged in a fashion similar to that used for children with medulloblastoma. CNS PNETs may be disseminated at the time of diagnosis, although the incidence of dissemination may be somewhat less than that of medulloblastomas or pineoblastomas, with dissemination at diagnosis being documented in approximately 10% to 20% of patients.[6,7] CNS PNETs are often amenable to resection; in series, 50% to 60% of patients were totally or near-totally resected.[6,7]
Staging of Other CNS Embryonal Tumors
Dissemination of both medulloepitheliomas and ependymoblastomas may occur, and the tumors are staged in the same way as medulloblastoma.
Risk Stratification for Medulloblastoma
On the basis of neuroradiographic evaluation for disseminated disease, cerebrospinal fluid (CSF) cytological examination, postoperative neuroimaging evaluation for the amount of residual disease, age of the patient, and impression of the surgeon at the time of surgery, patients with medulloblastoma have been historically stratified into the following two risk groups:
The 1.5 cm standard was arbitrarily chosen for evaluation in prospective studies. Metastatic disease includes neuroradiographic evidence of disseminated disease, positive cytology in lumbar or ventricular CSF obtained more than 7 days postsurgery, or extraneural disease.[2]
An intense area of study is the use of molecular and immunohistochemical analysis for disease stratification. In a large, multi-institution, retrospective biologic study, 397 medulloblastoma specimens were analyzed by transcriptional profiling (103 specimens) and immunohistochemical analysis.[3] Four unique clusters of medulloblastomas were identified. The following two subgroups clearly stood out:
Patients from both of these subgroups had excellent prognoses; 80% or greater 5-year progression-free survival (PFS) and overall survival (OS). The remainder of medulloblastomas, which comprise the majority of the study cohort, were separable into two other subgroups, which had greater overlap and shared a poorer prognosis, including a 30% to 45% chance of dissemination. The latter two subsets (termed Group C and Group D) differed in the following ways:
PFS for patients with Group C and D tumors ranged between 32% and 63%.[3] Other studies have confirmed the excellent prognosis of children with WNT tumors and poor prognosis of those with tumors with MYC amplification.[4,5] If this type of molecular and immunohistochemical separation can be confirmed in a homogeneously treated population of patients, preferably studied prospectively, it will dramatically alter disease stratification and likely therapy offered.[6]
Surgery is usually the initial treatment for children with medulloblastoma, both to confirm diagnosis and to remove as much tumor as is safely possible. Evidence suggests that more extensive surgical resections are related to an improved rate of survival, primarily in children with nondisseminated disease at the time of diagnosis.[7,8] One study in high-risk patients utilized presurgical chemotherapy (after tumor biopsy) to reduce tumor bulk and make subsequent resection of the tumor easier.[9] This small study did not demonstrate a high rate of survival, and postchemotherapy surgery did not seem easier and was not related to a reduced incidence of postoperative complications.
Postoperatively, children may have significant neurologic deficits caused by preoperative tumor-related brain injury, hydrocephalus, or surgery-related brain injury.[10][Level of evidence: 3iC] In addition, a significant number of patients with medulloblastoma will develop delayed onset of mutism, suprabulbar palsies, ataxia, hypotonia, and emotional lability. This constellation of findings has been termed the cerebellar mutism syndrome, and its etiology remains unclear, although cerebellar vermian damage has been postulated as a possible cause for the mutism.[11,12]; [13][Level of evidence: 3iC] In two Children's Cancer Group studies evaluating children with both average-risk and poor-risk medulloblastoma, the syndrome has been identified in nearly 25% of patients.[12,13,14]; [15][Level of evidence: 3iiiC] Many patients with this syndrome may manifest neurologic and neurocognitive sequelae posttreatment.[13,15]
Radiation Therapy
Radiation therapy is usually initiated after surgery with or without concomitant chemotherapy.[16,17,18] To date, the best survival results for children with medulloblastoma have been obtained when radiation therapy is begun within 4 to 6 weeks postsurgery.[16,17,18,19]; [20][Level of evidence: 1iA]
Prospective randomized trials and single-arm trials suggest that adjuvant chemotherapy given during and after radiation therapy improves overall survival for children with both average-risk and poor-risk medulloblastoma.[15,16,17,18,19,20] Although medulloblastoma is often sensitive to chemotherapy, preradiation chemotherapy has not been shown to improve survival compared with treatment with radiation therapy and subsequent chemotherapy. In some prospective studies, preradiation chemotherapy has been related to a poorer rate of survival.[17,18,19,20]
Children of all ages are susceptible to the adverse effects of radiation on brain development. Debilitating effects on growth and neurologic/cognitive development have been frequently observed, especially in younger children.[21,22,23,24] For this reason, the role of chemotherapy in allowing a delay in the administration of radiation therapy has been and is being studied. Results suggest that chemotherapy can be used to delay and sometimes obviate the need for radiation therapy in 20% to 40% of children younger than 3 years with nondisseminated medulloblastoma.[25,26]; [27][Level of evidence: 3iiiC] Children are also at risk for long-term endocrine dysfunction.[27]
Surveillance Testing
Surveillance testing is a part of all ongoing medulloblastoma studies.[28,29,30] Although most treatment failures in patients newly diagnosed with medulloblastoma will occur within the first 18 months postdiagnosis, relapses many years after diagnosis have been noted.[31] In addition, secondary tumors have been increasingly diagnosed in long-term survivors.[30,31]; [32][Level of evidence: 2A] As with initial management, long-term management is complex and requires a multidisciplinary approach.
Children with medulloblastoma are stratified into average-risk and poor-risk subsets. Owing to concerns about the long-term neurocognitive sequelae of whole-brain radiation therapy on the developing brain, radiation therapy for younger children has often been delayed or eliminated. Children younger than 3 years and sometimes as old as 5 years have not received the same treatment as older patients.
In all subgroups of patients, surgery is the initial means of therapy, and maximal tumor resection is the goal of treatment. Postsurgical treatment has diverged, to some degree, on the basis of risk stratification and age of the patient.
Average Risk
Standard treatment options
The traditional postsurgical treatment for patients with average-risk medulloblastoma has been 54 Gy to 55 Gy of radiation therapy to the posterior fossa and 36 Gy to the entire neuraxis (i.e., the whole brain and spine).[1,2,3,4] With radiation therapy alone, 5-year event-free survival (EFS) ranges between 50% and 65% in those with nondisseminated disease.[2,3] While the standard boost in medulloblastoma is the entire posterior fossa, patterns of failure data suggest that radiation therapy to the tumor bed instead of the entire posterior fossa would be equally effective and possibly associated with reduced toxicity.[5,6] The minimal dose of craniospinal radiation needed for disease control is unknown. Attempts to lower the dose of craniospinal radiation therapy to 23.4 Gy without chemotherapy have resulted in an increased incidence of isolated leptomeningeal relapse.[4]
Chemotherapy is now a standard component of the treatment of children with average-risk medulloblastoma; a variety of chemotherapeutic regimens have been successfully used, including the combination of cisplatin, lomustine, and vincristine or the combination of cisplatin, cyclophosphamide, and vincristine.[1,2,7] Radiation therapy and chemotherapy given during and after radiation therapy has demonstrated 5-year EFS rates of 70% to 85%.[1,2,3]; [8][Level of evidence: 2A] A lower radiation dose of 23.4 Gy to the neuraxis when coupled with chemotherapy has been shown to result in disease control in up to 85% of patients and may decrease the severity of long-term neurocognitive sequelae.[7,9,10,11]
Long-term survivors who were prepubertal at the time of diagnosis are at high risk for growth failure due to radiation-related hypothalamic failure as well as effects of radiation on spinal growth. Lower doses of craniospinal radiation therapy may decrease the incidence of hypothalamic dysfunction, but this has not yet been proven. Growth hormone replacement therapy has not been shown to increase the likelihood of disease relapse.[12]
Treatment options under clinical evaluation
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.
High Risk
In high-risk patients, numerous studies have demonstrated that multimodality therapy improves the duration of disease control and overall disease-free survival (DFS).[13,14] In contrast to standard-risk treatment, the craniospinal radiation dose is generally 36 Gy. Studies show that approximately 50% to 60% of patients with high-risk disease will experience long-term disease control.[1,13,14,15,16] The drugs that have been found to be useful in children with average-risk disease are the same drugs that have been used extensively in children with poor-risk disease, including cisplatin, lomustine, cyclophosphamide, etoposide, and vincristine.
Children Aged 3 Years and Younger
The treatment of children younger than 3 years with newly diagnosed medulloblastoma continues to evolve. Due to concerns over the likely deleterious effects of craniospinal radiation on the immature nervous system, therapeutic approaches have attempted to delay and, in some cases, avoid the use of craniospinal radiation therapy. Results have been variable, and comparison across studies has been difficult because of differences in drug regimens used and the utilization of craniospinal and local boost radiotherapy at the end of chemotherapy or when children reached age 3 years in some studies.
Five-year DFS rates for young children with medulloblastoma have ranged between 30% and 70%, with most long-term survivors successfully treated with chemotherapy alone, having nondisseminated, totally resected tumors.[17,18,19] Surgical resectability is associated with histology, as patients with desmoplastic medulloblastoma or medulloblastoma with extensive nodularity (MBEN) have a higher rate of complete resection than do patients with classic medulloblastoma.[20,21]
Several studies have observed that the histologic finding of desmoplasia, seen in patients with desmoplastic medulloblastoma or MBEN, connotes a significantly better prognosis compared with outcome for patients with classic or large cell anaplastic medulloblastoma.[20,21,22,23,24]; [25][Level of evidence: 2A] For example, desmoplasia was an independent predictor of favorable EFS rates in the German HIT 2000 multicenter trial in which 19 patients with desmoplastic medulloblastoma or MBEN had 5-year EFS rates of 90% ± 7% and OS rates of 100% ± 0%, with all patients being treated with chemotherapy alone (including intraventricular methotrexate) prior to progression.[21] By contrast, EFS and OS rates for children with classic medulloblastoma in the HIT 2000 trial were significantly lower (EFS, 30% ± 11%; OS, 68% ± 10%).[21] The COG clinical trial CCG-9921 also observed a favorable outcome for children with desmoplastic medulloblastoma (including MBEN), with an EFS of 77% ± 9% and an OS of 85% ± 8% for the desmoplastic group compared with an EFS of 17% ± 5% and OS of 29% ± 6% for patients in the nondesmoplastic group (P < .0001 for both EFS and OS comparisons).[17] In this study, patients with desmoplastic tumors did not receive radiation prior to progression. The United Kingdom Children's Cancer Study Group and International Society of Paediatric Oncology used less-intensive chemotherapy and did not observe a difference in outcome for young children with desmoplastic versus nondesmoplastic medulloblastoma (both with an EFS of approximately 40%), suggesting the potential importance of intensive chemotherapy for favorable outcome for young children with desmoplastic tumors.[26]
Therapies for younger children with medulloblastoma have included the use of multiagent chemotherapeutic approaches, including drugs such as cyclophosphamide, etoposide, cisplatin, and vincristine, with or without concomitant high-dose intravenous methotrexate and/or intrathecal methotrexate or mafosfamide, and/or intraventricular methotrexate..[17,18,19,21,27,28,29]; [26][Level of evidence: 2A] Results of trials utilizing higher-dose, marrow-ablative chemotherapeutic regimens supported by autologous stem cell rescue or peripheral stem cell rescue have also demonstrated that a subgroup of patients with medulloblastoma who are younger than 3 years at the time of diagnosis can be treated with chemotherapy alone.[30,31][Level of evidence: 2A]
Patients with desmoplastic tumors with extensive nodularity should be carefully evaluated for stigmata of Gorlin syndrome. One report observed that MBEN was associated with Gorlin syndrome in 5 of 12 cases.[24] Gorlin syndrome is an autosomal dominant disorder, also known as the nevoid basal cell carcinoma syndrome, in which those affected are predisposed to the development of basal cell carcinomas later in life, especially in the radiation portal after radiation therapy. The syndrome can be diagnosed early in life by characteristic dermatological and skeletal features such as keratocysts of the jaw, bifid or fused ribs, macrocephaly, and calcifications of the falx.[24]
In contrast to children with desmoplastic medulloblastoma or MBEN treated with current intensive chemotherapy regimens, children with other histologic subtypes fare less well, with EFS rates below 40% despite the use of intensive chemotherapy supplemented with methotrexate (intravenous, intrathecal, and intraventricular) and the use of high-dose chemotherapeutic regimens supported with stem cell rescue.[17,21] Outcome is particularly poor when these patients have disseminated disease, and there is no consensus on when and how much radiation therapy should be given and at what age radiation therapy should be instituted in patients with disseminated disease.[17,18,19]
The following are examples of national and/or institutional clinical trials that are currently being conducted. 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 medulloblastoma. 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.
Children Older Than 3 Years
The usual postsurgical treatment for pineoblastomas begins with radiation therapy, although some trials have utilized preradiation chemotherapy. The total dose of radiation therapy to the tumor site is 54 Gy to 55.8 Gy using conventional fractionation.[1,2] Craniospinal irradiation with doses ranging between 23.4 Gy and 36 Gy are also recommended because of the propensity of this tumor to disseminate throughout the subarachnoid space.[1,2] Chemotherapy is usually utilized in the same way as outlined for poor-risk medulloblastomas in children with nondisseminated disease at the time of diagnosis. Five-year disease-free survival is approximately 50%.[1,2,3] For patients with disseminated disease at the time of diagnosis, survival is considerably poorer.[1,2] Similar treatment is given for pineal parenchymal tumors of intermediate differentiation; however, there are no data on response to therapy or outcome.
For patients with pineoblastoma, a variety of different treatment approaches are under evaluation, including the use of higher doses of chemotherapy following radiation supported by peripheral stem cell rescue and the use of chemotherapy during radiation.
Children 3 years and younger with pineoblastoma are usually treated initially with chemotherapy in the hope of delaying, if not obviating, the need for radiation therapy.[4] High-dose, marrow ablative, chemotherapy with autologous bone marrow rescue or peripheral stem cell rescue has been used with some success in young children.[5][Level of evidence: 2Di] The timing and amount of radiation therapy required following chemotherapy in children responding to chemotherapy is unclear.
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with untreated childhood pineoblastoma and childhood pineal parenchymal tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
Attempting aggressive surgical resection is the first step in the management of newly diagnosed central nervous system primitive neuroectodermal tumors (CNS PNETs), although studies have yet to demonstrate that the extent of resection is predictive of outcome.[1,2,3] After surgery, children with CNS PNETs usually receive treatment similar to that received by children with poor-risk medulloblastoma. Best results have been obtained after radiation to the entire neuraxis with local boost radiation therapy, as given for medulloblastoma.[3] However, the local boost radiation therapy may be problematic because of the size of the tumor and its location in the cerebral cortex. The chemotherapeutic approaches during and after radiation therapy are similar to those used for children with poor-risk medulloblastoma. Three- to 5-year overall survival (OS) rates of 40% to 50% have been noted.[1,2,3]; [4][Level of evidence: 2A]; [5][Level of evidence: 3iiiB] Patients with disseminated disease at the time of diagnosis have poorer OS, with reported survival rates at 5 years ranging from 20% to 30%.[1,2,3]
Treatment of children aged younger than 3 years with CNS PNETs is similar to that outlined for children with medulloblastoma. With the use of chemotherapy alone, outcome has been variable, with survival rates at 5 years ranging between 0% and 50%.[6,7,8]; [9][Level of evidence: 2Di]
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood supratentorial primitive neuroectodermal tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
There are few data on which to base treatment of medulloepithelioma and ependymoblastoma tumors. Treatment considerations are usually the same as those for children with poor-risk medulloblastoma and for children 3 years and younger at diagnosis with other embryonal tumors. Prognosis is poor, with 5-year survival rates ranging between 0% and 30%.[1,2,3,4]
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood ependymoblastoma and childhood medulloepithelioma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
Recurrence of all forms of central nervous system embryonal tumors is not uncommon, usually occurring within 18 months of treatment; however, recurrent tumors may develop many years after initial treatment.[1,2] Disease may recur at the primary site or may be disseminated at the time of relapse. Sites of noncontiguous relapse may include the spinal leptomeninges, intracranial sites, and cerebrospinal fluid, in isolation or in any combination, and is variably associated with primary tumor relapse.[1,2,3] One series has found that, independent of the dose of radiation therapy employed or the type of chemotherapy utilized, approximately one-third of patients will relapse at the primary tumor site alone, one-third will relapse at the primary tumor site plus distant sites, and one-third will relapse at distant sites without relapse at the primary site.[1,2,3] At the time of relapse, a complete evaluation for extent of recurrence is indicated for all embryonal tumors. Biopsy or surgical resection may be necessary for confirmation of relapse because other entities such as secondary tumors 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 lesion, and clinical symptomatology. Extraneural disease relapse may occur but is rare and is seen primarily in patients treated with radiation therapy alone.[4][Level of evidence: 3iiiA]
Patients with recurrent embryonal tumors who have already received radiation therapy and chemotherapy may be candidates for salvage chemotherapy and/or stereotactic radiation therapy.[5] These tumors can be responsive to chemotherapeutic agents used singularly or in combination, including cyclophosphamide, cisplatin, carboplatin, lomustine, etoposide, and topotecan.[6,7,8,9,10,11,12,13,14]; [15][Level of evidence: 2A] Approximately 30% to 50% of these patients will have objective responses to conventional chemotherapy, but long-term disease control is rare. For select patients with recurrent medulloblastoma, primarily infants and young children who were treated at the time of diagnosis with chemotherapy alone and developed local recurrence, long-term disease control may be obtained after further treatment with chemotherapy plus local radiation therapy; this potential may be greatest in patients who are able to undergo complete resection of the recurrent disease.[16][Level of evidence: 2A]; [17][Level of evidence: 3iiiA]
For patients who have previously received radiation therapy, higher-dose chemotherapeutic regimens, supported with autologous bone marrow rescue or peripheral stem cell support, have been used with variable results.[18,19,20,21,22,23][Level of evidence: 2A]; [24][Level of evidence: 3iiB]; [25,26][Level of evidence: 3iiiA] With such regimens, objective response is frequent, occurring in 50% to 75% of patients; however, long-term disease control is obtained in fewer than 30% of patients and is primarily seen in patients in first relapse and in those with only localized disease at the time of relapse.[20]; [23][Level of evidence: 2A]; [24][Level of evidence: 3iiB] Additionally, results from national trials for relapsed medulloblastoma that specified intent to transplant as part of their treatment plan showed that only approximately 5% of patients initiating retrieval therapy achieve long-term disease-free survival with this strategy.[23,27] Thus, studies that report from the time of transplant overestimate the benefit of transplant-based approaches for the total population of relapsing patients. Long-term disease control for patients with disseminated disease is infrequent.[28][Level of evidence: 3iA]
Treatment Options Under Clinical Evaluation
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood pineal parenchymal tumor, recurrent childhood pineoblastoma, childhood ependymoblastoma, recurrent childhood medulloblastoma and recurrent childhood supratentorial primitive neuroectodermal tumor. 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.
General Information
Added Louis et al. as reference 2.
Revised text to state that 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.
The Predictors of Outcome subsection was extensively revised.
Cellular Classification of Central Nervous System (CNS) Embryonal Tumors
Added Taylor et al. as reference 27.
Added text about the characteristics of Gorlin syndrome, including the associated mutations and diseases, predisposition to basal cell carcinomas, and the diagnostic features (cited Brugières et al. and Pastorino et al. as references 28 and 29, respectively).
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 central nervous system embryonal tumors. 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.
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text:
Results tagged ' Denver '
The not-so-all-American game of baseball
Although as a player Ken has experienced three All-Star games (1977, 1979, 1981), he had the unique opportunity to broadcast the 1998 game in Denver for Major League Baseball International.
I tagged along on the excursion, sucked into the city's energy as it pumped out baseball adrenaline. Every nook and cranny was filled with souvenirs, activities and keyed-up baseball fans in full celebration mode, clearly thrilled to be in such close proximity to their favorite Major Leaguers, and to taste the flavor of Denver.
I met Derek Jeter for the first time during the enormous outside/inside All-Star gala sponsored the evening before by the Colorado Rockies and Major League Baseball. Quite impressive that gala (and Derek, who had brought along his sister).
Being the host of an All-Star game gives a city a chance to strut its stuff, so you can envision how many bells and whistles were included that night … an evening to celebrate Major League Baseball's finest and most popular players and their families, and a chance for the host team to throw the party of the year.
"It's not only about the game," says Ken. "Cities want to put on a good show. They want people to come back."
On game day, working in the booth alongside Gary Thorne (now a Baltimore Orioles play-by-play announcer), Ken's challenge was to deliver the All-Star game to listeners in more than 200 countries around the world, most of whom are not familiar with the sport.
"We had to explain things well," said Ken. "We couldn't take for granted that people knew what we were talking about. When doing regular games, we know that fans are more aware of what's going on."
E-mails flowed in during the telecast for Gary and Ken to address as they announced the 69th All-Star Game from Denver's Coors Field.
"We received a lot of questions about strategy," remembers Ken. "Such as, 'Why does a player sometimes bunt and sometimes not?'" The duo would address questions on-air as thoroughly as they could in between plays, to explain the American game to foreigners in New Zealand, Australia, China and around the world.
Ken had the special opportunity to further announce for MLB International, a championship game in 1997 between the Atlanta Braves and the Florida Marlins; the World Series the same year between the Marlins and the Cleveland Indians; and in 1998 the World Series between the Yankees and the San Diego Padres (which the Yanks of course won in four consecutive games).
Since Minor and Major League players come from far and wide (Argentina, Brazil, Germany, Korea, Netherlands, Italy, South Africa, to name a few) and baseball's popularity continues to grow around the globe, the role of Major League Baseball International (formed in 1989) focuses on worldwide growth of the sport through broadcasting, special events, sponsorship, licensing, etc. They have offices in New York, London, Sydney and Tokyo.
"It was a very rewarding experience," said Ken, "to know that people around the world were enjoying and learning the game."

subset: commoncrawl


text:
[dropcap]T[/dropcap]he Savora Contour Series Oil Mister is a neat product, and a great gift idea for our 2013 Father's Day Gift List. For that budding gourmet dad who puts on the apron and makes the most amazing tasting (insert his favorite thing he does so well) while simultaneously creating the largest mess in the history of kitchen messes!
Seriously though, this is a really neat device. So in a nut shell it replaces those spray can oils you buy at the store. You know the cans you don't really know… what is _actually_ in there… but you spray some non-stick spray in the pan hoping it is better for you than the slab of butter you really want to use…
This is drop dead easy to use, you just open it up, pour your oil (whatever you want, I like extra virgin olive oil). The idea is you pour your oil, then pump in with the top to push air inside the bottle, and presto you get a nice fine mist just like you would with the can of oil you buy at the store… except there is no propellant going into your food :p
The best part is you can use fresh herbs and infuse the oil, just toss them inside the bottle with the oil and let it sit for a few days / weeks / whatever you want. The bottom of the feeder tube has a special no clog filtering system that prevents the herbs from going up the tube. It won't get clogged, it's easy to clean (we put it in the dishwasher without an issue) and absolutely simple to use. Once you have one you will want 3 or 4 more to do different types of oil infusions.
Out of the box it feels a little cheap (light weight contributes most of that feeling) but once you put the oil in the bottle it takes care of that feeling as it has more heft. I like it and I'm going to give it 4 out of 5 stars. It's an excellent kitchen helper and is definitely healthier than buying the can of spray oil at the store. They run about $25 or so and come in various colors to match your kitchen. It also comes with a limited lifetime warranty.


text:
There is a survey floating around the vegan blog world, and since I am being lazy today I thought it would be fun to fill it out.
1. What is one food you thought you'd miss when you went vegan, but don't?
2. What is a food or dish you wouldn't touch as a child, but enjoy now?
3. What vegan dish or food you feel like you should like, but don't?
4. What beverage do you consume the most of on any given day?
9. What ingredient or food is worth spending the extra money to get the good stuff?
10. Are you much of a snacker? What are your favorite snacks?
11. What are your favorite vegan pizza toppings?
12. What is your favorite vegetable? Fruit?
13. What is the best salad dressing?
15. What kind of soup do you most often turn to on a chilly day or when you aren't feeling your best?
16. What is your favorite cupcake flavor? Frosting flavor?
17. What is your favorite kind of cookie?
18. What is your most-loved weeknight meal?
19. What is one dish or food you enjoy, but can't get anyone else in your household to eat?
20. Favorite non-dairy milk?
21. Most disastrous recipe/meal failure?
22. Favorite pickled item?
23. If you were stranded on an island and could only bring 3 foods…what would they be (don't worry about how you'll cook them)?
24. Most loved kitchen appliance?
26. Favorite flavor of jam/jelly?
27. Seitan, tofu, or tempeh?
28. Favorite meal to cook (or time of day to cook)?
30. Name a recipe you'd love to veganize, but haven't yet.


text: Malaysia's Obedient Wives Club aims to solve all the problems of the world by getting wives to sex their husbands more frequently. But their efforts were stymied recently when Malaysian authorities banned their book, a compendium of offensiveness titled, Islamic Sex: Fighting Jews to Return Islamic Sex to the World. The Club teaches that most wives fulfill just 10% of their husbands sexual needs (it's unclear how they arrived at this figure), and that wives should act like "first-class whores" in the bedroom to keep their husbands satisfied. In the wake of the ban, they say a planned followup book may be released as "an internal newsletter, or an internal bulletin" instead.


text:
A slow-moving Isaac brings flooding to Gulf states
(Phys.org)—Isaac - once a Category 1 hurricane and now a strong tropical storm with maximum sustained winds of 70 miles per hour (60 knots) - continues to create havoc across the Gulf Coast, from eastern Texas to Florida. While "only" reaching Category 1 on the Saffir-Simpson hurricane wind scale upon landfall on Aug. 28, Isaac is a slow mover, crawling along at only about six miles (10 kilometers) per hour. This slow movement is forecast to continue over the next 24 to 36 hours, bringing a prolonged threat of flooding to the northern Gulf Coast and south-central United States.
As seen in this infrared image from the Atmospheric Infrared Sounder (AIRS) instrument on NASA's Aqua spacecraft, acquired at 2:41 p.m. CDT on Aug. 29, 2012, the large storm is still relatively well organized and is producing strong bands of thunderstorms. The broad area of purple in the image represents cloud-top temperatures colder than minus 63 degrees Fahrenheit (minus 52 degrees Celsius) around the center of the storm's circulation. It is here that Isaac's strongest storms and heaviest rainfall are now occurring.
According to the National Oceanic and Atmospheric Administration's National Hurricane Center, strong bands of thunderstorms continue to develop over water in the storm's eastern semicircle and southwest of the center. These strong rain bands are forecast to spread gradually to the west tonight across coastal southeastern Louisiana and southern Mississippi, including the New Orleans metropolitan area. The storm is expected to weaken to a tropical depression by Thursday night and a post-tropical remnant low-pressure system by Friday.
Explore further


text:
Motorists driving for holiday may be giving thanks for the recent downtrend in gasoline prices, but history will be broken as the national average will be the highest its ever been on Thanksgiving.
GasBuddy.com Senior Petroleum Analyst Patrick DeHaan is estimating that the national average will sit at $3.43 per gallon on Thanksgiving, some 10 cents higher than it was in 2011. In the Charlotte region, gasoline prices currently stand at an average of $3.28, compared to last Thanksgiving, when prices stood at an average of $3.33.
"Gasoline prices have continued their slow decline in the last week across a solid majority of the United States, with the national average sagging to its lowest level since this early summer," according to DeHaan. "Even though consumers are seeing gasoline prices decline in most parts of the country, and we're certainly thankful for that, the national average will remain higher than where it was a year ago."
As pump prices have fallen, GasBuddy has asked surveyed motorists about their travel plans. Results from the poll of over 15,000 GasBuddy households showed some surprises with some driving fewer miles or not at all, but overall, 8% of those surveyed said they would be driving slightly or significantly more than last year, down from 9% a year ago. The results of the poll indicate that drivers drove more last year, and are planning similar travels this year, as gasoline prices have trended lower.
"Overall, we believe more Americans will be hitting the road for this Thanksgiving Day compared to last year. Gasoline prices have come down over the last month, dramatically in some states, leading motorists to feel better about things- including driving the car to get to their destinations, " added Gregg Laskoski, a GasBuddy.com analyst.


text:
Thanks to Roger Shipp for hosting.
(Hello! Just noting this piece had a mind of its own and is somewhat longer than the usual 200 words. Cheers!)
"Closing time / One last call for alcohol so finish your whiskey or beer." The mellow lines Semisonic floated into Tyrelle's ears.
It was 2:00 a.m. and his friends, Jordan and Simone, were trying to shut their house party down, arranging places for closest friends to sleep and for others to catch a cab home. Tyrelle nursed his last drink for the night. As per usual, he was upset these days.
His beautiful Cleo should've been with him here tonight, ensuring he didn't feel like such a recluse at his friends' party. He hadn't been in the mood for a party but since Cleo had ended things three-months ago, he knew he needed to move on.
More Semisonic lyrics played through from an IPad:"Closing time / Every new beginning comes from some other beginnings end."
Tyrelle watched as Simone finally locked the front door. She peered at at him and moved to give him a short friendly back rub. "You still miss Cleo, huh?"
"Yeah, everyday. Does it get easier?" Tyrelle asked her.
Simone sighed, "Before Jordan, I was with Blake and I thought he was it. Then he broke my heart and for months after, I didn't function well."
"After a while I stopped thinking about Blake as much. I realized I resented the hold he had had on me. Then I chose to become involved in life. I volunteered and I saw more friends and family. Not long after, I met Jordan," Simone said smiling.
Tyrelle smirked. As if what Simone said could ever be possible for him. Then he remembered the last line in the Semisonic song. About how other things had to end for better and new things to begin. So that's what he decided to do — to begin anew.
He picked up his phone and blocked Cleo's number. Tyrelle unfriended and blocked her on every social media. Tomorrow he would start going to a different gym location then Cleo to workout and he would go to a different grocery store by his condo to shop as well. Finally, he grinned, he would get a new haircut.
Yes, it was time to live again.
"Closing Time" by Semisonic
©Mandibelle16. (2017) All Rights Reserved.


text:
I have the following APP Design
- key store (contains 1:n user payload as 1:n key store entries)
- key store salt (is used to extend to key store password to 256 bits, stored in clear text)
- key store entry (what the user wants to encrypt)
own entry IV (payload is encrypted with AES256 MODE OFB, IV stored in clear text )
own entry SALT (64bytes random appended to payload before encryption, SALT stored in clear text)
encrypted entry is stored base64 encoded
model a) only passwords are allowed
model b) additional data is allowed
(eg. some comments / remarks in the users language / links / email addresses)
Is it secure to allow multiple keys on the key store if the key store SALT is shared on all keys? (the key store SALT is used for apple crypt function CCKeyDerivationPBKDF which extends the user password to 256bits to be used for AES256)
Can an attacker use the shared SALT for some attack ? (The number of used passwords is not detectable as the application accepts every entry as valid. You must decide on the decrypted information if the key is valid or not. This is also true for the user who should know the correct password).
Is there a security risk when I use model b) which allows the attacker to guess, that there is user language (or links/email addresses) in the encrypted entry?


text:
Farmington Sports Hall of Fame on Nov. 10
FARMINGTON — The sixth Farmington 500 Boys & Girls Club Sports Hall of Fame will be held Nov. 10 at the Henry Wilson Memorial School gym.
Tickets are $20 and can be purchased until Oct. 31 at Mills Market and Farmington High School.
The 2012 inductees include athletes Steve Mosher, Tim Mucher, Casey Howard and Marshall Gibbs, and contributors Reggie Charette, Jim Black, Dave Hagar, Dave Vachon and Cheryl Peabody.
The Thayer family will receive the Ellison Award and the 1952 youth baseball teams will be honored on the 60th anniversary of the first youth baseball season in Farmington.
Senior Citizens Indoor Tennis
ROCHESTER — Tuesdays and Thursdays from 12:00-1:00 pm in the Community Center gym. Free and all the equipment is provided. This program offers light weight
rackets and low compression balls for low-impact play. No experienced needed. So easy to play. If you have any questions, please call Rochester Rec at 332-4120 (ext 0) or visit www.rochesterrec.com.
Learn to Skate – Ages 3+
ROCHESTER — Introduction, beginner, intermediate and advanced skating offered. The Rochester Arena staff takes great care in teaching each child the basic skills of skating and allowing them to increase their skill each week. Sunday lessons are going on now through November 18 at 1:30pm. You can join anytime for $12 per lesson. Friday lessons start Oct 26-Nov 16 at 6:00pm. 4-weeks for $48. All skaters need is warm clothes and a helmet (bike helmet ok). Skate rentals available for $3 per lesson. To sign up, please stop by the Rec Office, call 332-4120 or email email@example.com.
Preschool Sports Class
ROCHESTER — Children ages 3-5 are welcome to sign up for our fun filled preschool sports class with Coach Dan. Takes place on Sundays, November 18-Dec 9 from 11:00-11:45am for $35 residents / $45 non res. Parents and their children will play different sport activities each week in an organized class. Great way for everyone to get some exercise and socialize with other families. For more information, please call the Rec Office at at 332-4120 or email firstname.lastname@example.com.
Figure Skating Lessons
ROCHESTER — Have you ever wanted to learn how to figure skate? Whether you are a child or an adult, Coach Beth will teach you the beautiful movement of figure skating. Lessons take place on Saturdays at 5:00pm through Dec 6. $14 per lesson. Skate rentals available. For more information, please call the Rec Office at 332-4120 or email email@example.com.
Roger N. Allen Baseball meeting
ROCHESTER — Roger N. Allen Baseball will hold its end-of-the-year meeting on Nov. 3, 11 a.m., in the Rochester Community Center's Conference Room 1.
Parents, coaches, league officials and the general public are invited.
Sports shorts
Farmington Sports Hall of Fame on Nov. 10


text:
Astronaut Central is your #1 source for historic, investment quality astronaut autographs, space memorabilia and artifacts. Quality, authenticity, and expertise are what we are known for. We've been in business 35 years, and were one of the very first websites on the Net in 1995 (as Novaspace Galleries) even before Amazon or eBay!
As control freaks, we assure quality by doing it all here--from obtaining authentic in-person autographs, to professional custom framing, to our prompt, secure and damage-free shipping, your item will meet or exceed your highest expectations. Read some of our unsolicited testimonials and money-back guarantee.


text:
By Eric Benson
It was late on a Friday night last July, and Jeremy Barfield, a corner outfielder for the Sacramento River Cats, was getting ready to celebrate his 25th birthday when he was summoned into a postgame meeting with his manager, Steve Scarsone, and his hitting coach, Todd Steverson. Barfield steeled himself for bad news.
For the last five years, Barfield had been rising methodically through the Oakland A's organization, and after 605 minor league games and a pair of minor-league all-star selections, he'd finally earned a promotion to Triple-A Sacramento. But in his two months with the River Cats, Barfield had seen limited time and little success at the plate, hitting only .188. As Barfield sat down in front of Scarsone and Steverson, he figured he'd soon be on his way back to west Texas. Midland. Double-A ball.
Steverson, who was hitting coordinator for the entire A's farm system, told Barfield that the organization had another idea. The A's didn't see Barfield advancing to the majors as an outfielder anytime soon, but they were intrigued by his powerful left arm. Steverson presented Barfield with the kind of choice that Don Corleone would have admired: Either Barfield could accept a demotion to Midland, where he would be assigned to the phantom DL (meaning that, although uninjured, he would ineligible to play), or he could report to Arizona, where he would begin training for a new position. The A's wanted Jeremy Barfield to become a pitcher.
Barfield was shellshocked. He bolted from the ballpark without packing up his locker. Early the next day, Barfield asked a clubhouse attendant to open up the locker room so he could gather his things before the other players showed up. "I was trying to avoid having the same conversation 24 times," Barfield said.
Nine months later, I was standing with Barfield in the shade of a sprawling mesquite tree at the A's player-development facility in Phoenix's Papago Park, a serene stretch of Sonoran desert punctuated by sandstone buttes, immaculately groomed ball fields, and a crystalline view of the iconic Four Peaks looming to the east. Barfield -- a towering 6-foot-5 and 220 pounds, with bounteous enthusiasm for Xbox, Twitter (where he has over forty-five-thousand followers), and down-home cooking ("if it's on Diners, Drive-Ins and Dives, I'm there") -- had been working out in Arizona more or less nonstop since last July. And while he hadn't picked up a bat since the previous summer, at times he still sounded like he was waiting to be woken up from a bad dream.
"I had heard it my whole career no matter how well I was hitting," Barfield told me. "Coaches, scouts, experts -- just everybody who has an opinion in this game -- it was 'you gotta use that arm, you should pitch.' Didn't matter how well I would hit, that's what they saw the most."
Barfield had long known that baseball careers often don't go according to plan. And the morning after his meeting in Sacramento, he reached out to a group of people who were happy to remind him of that fact. First, he called his dad, Jesse, a retired Toronto Blue Jays and New York Yankees right fielder who, in 1986, led the majors in home runs. The elder Barfield, who ended his big-league career in 1992 as an injury-plagued 32-year-old, advised his son to swallow his pride and take the deal: "Jeremy said, 'Dad, I don't understand, I'm an All-Star.' I said, 'Son, they have All-Stars in the big leagues on the bench -- an All-Star in Double A means nothing. You have a chance to make it to the big leagues as a left-handed pitcher. I would take that opportunity.'"
Next, Barfield called his older brother, Josh, a former big-league second baseman. Josh had taken the majors by storm in 2006, at age 23, starting for the San Diego Padres and hitting .280. But Josh hadn't seen a big-league pitch since 2009 and was spending the 2013 season with the independent Atlantic League's Long Island Ducks. He told his younger brother that he was lucky to have a job and reminded him that being a lefty pitcher was a pretty good route to a long and lucrative career.
Then Barfield called the man who would oversee his transformation, A's special assistant and rehab pitching coordinator Garvin Alston. Alston, a former pitcher who threw six big-league innings during his 11-year professional career, was a satellite member of the Barfield baseball family and had known the young slugger since he was a kid. Alston told Barfield to take a few days off, get his mind right, and then show up at Papago Park to start the next phase of his career. Within the week, they were together -- sensei and grasshopper in the Arizona heat.
"When we first talked, I asked him, 'What do you know about pitching?'" Alston told me. "He said, 'I know how to hit it.' And I was like, 'First things first: we got to change your mentality. You got to think the other way now.' He said, 'Gee, it's going to be hard for me. I'm a hitter.' And I said, 'I know you are, but this is where we at.'"
* * *
When I arrived at A's facility at the end of March, on what qualified as a lazy Sunday in no-days-off spring training, Barfield was throwing long toss, going through defensive drills, and practicing pick-off moves, much of the time with Alston watching nearby. Barfield wasn't scheduled to pitch for another two days, and his team officially had the afternoon off. But as a member of the lowly Stockton Ports, he was obligated to stay on the premises to watch a mixed squad of more advanced A's minor leaguers take on the Langley Blaze, a youth team from British Columbia. Barfield looked on half-heartedly. This was his sixth year in the organization. He'd been through a lot. He didn't want to spend his Sunday afternoon watching a bunch of Canadian high school kids.
When Barfield began his conversion to the mound in 2013, it was the height of the Arizona summer. For the first few weeks, in triple-digit heat, he spent his time running, building up his arm strength, lifting weights, and explaining to a bunch of just-drafted 18-year-olds why the Triple-A home-run hitter was now performing beginners' pitching drills. In early August, Barfield got to the mound. He was wild, and his body was stiff. He stretched out his hamstrings and hips, and squatted until his quadriceps were bursting through his jeans. His command slowly improved. It was time to build up his repertoire.
Alston had tried to teach Barfield a circle change-up, but Barfield, with the hands of a basketball power forward, couldn't get a feel for the pitch. Barfield suggested that they try a split-fingered fastball instead. The A's organization has a policy against the splitter, due to the stress it places on a pitcher's elbow, but Alston told Barfield he could give it a try. Barfield fired the pitch and watched as it dived dramatically below Alston's glove and hit him in the knee. "He was laughing," Alston remembers. "I said, 'OK, we'll work with it.'"
As the months progressed in Arizona, Barfield would seek out the advice of the wise men in the Barfield baseball family, not just his dad and brother, but his godfather, former Indians closer Mike Jackson, and another close family friend, Hall of Fame outfielder Rickey Henderson. Standing under the mesquite tree, Barfield recalled their conversations, imitating the distinctive voices of both men with unabashed glee.
"Mike Jackson, he was so intense on the mound, but he's so laid back in person," Barfield laughed. "He calls me, 'Hey, what's up six-five? He calls me six-five, because I'm 6-foot-5. He goes, What's up, six-five. You chunking it?"
"You chunking it?" I asked.
"Yeah," Barfield said. "'You chunkin' it?' That means, 'How you throwing? 'You breakin' 'em off? Good! You better use that slider!'"
When it came to Henderson, the conversations were less about slider grips or mound strategy than savory food and old-fashioned banter.
"Me and Rickey, he'll text me all the time, see how things are going," Barfield told me. "We used to have a deal when I was hitting. Whenever he was in town, if I would hit a home run he would order me a chicken pot pie from this place in Oakland, have them shipped out -- best pot pies ever. It got to the point that if Rickey would be in town for five days, I'm hitting two, three home runs just because I want the pot pies. Last year, he came to Midland, and I homered in three straight games. I said, 'You owe me three pot pies!'"
Barfield, smiling ear to ear, paused before breaking into Henderson's gravely inflection, "He said, 'I'll get em to ya. I'll get em to ya.'"
Henderson, Barfield continued, had three daughters but no sons, and he had taken it upon himself to craft his buddy Jesse's kid into little Rickey.
"He used to always dress me up like him and drive me around, and it's funny because I ended up batting right-handed and throwing left-handed like he did. When I was starting to play catch, my dad gave me two gloves: a left-handed glove and a right-handed glove. Rickey hid the right-handed glove and so I just picked the left-handed glove. That's how I ended up throwing lefty."
That turned out well for your pitching career, I said.
"Absolutely," Barfield said. "I just wish I would have hit left-handed too. Then this whole thing wouldn't be happening."
* * *
The A's minor leaguers were now clobbering the Langley Blaze in Papago Park (the final score was 15-3), and as Barfield looked on at the hapless Canadians, I asked him about the travels of his baseball life. He'd begun his minor-league career in Vancouver, had lived for a summer in Japan when his father played for the Yomiuri Giants, and had spent two weeks in 2012 playing for the Cardenales de Lara in the Venezuelan fall league.
"And actually after the instructional league here, I had to go down to the Dominican and live in our complex down there," Barfield said.
"How was that?" I asked.
"That was the longest three weeks of my entire life," he laughed. "You're in the middle of the jungle. It's hot and humid every day -- bugs crawling everywhere. The electricity would go out for four, five, six hours. The running water would stop. You're waking up at 6 a.m. every day. It's 17-, 18-, 19-year-old guys that barely speak English. There's no real communication with the outside world. And you're eating really sketchy food -- they got this stuff called mangú. Then we're talking salami for breakfast, room-temperature hot dogs, mystery meats. You couldn't drink the milk cause it's unpasteurized and would turn your stomach inside and out. Baseball-wise, pitching-wise, it went really well. I had six outings. I got a lot better. I was feeling comfortable on the mound. But it really put things in perspective for me."
Back in Arizona, Barfield segued back into a cushier baseball life. To make money in the winter, he got a job installing high-end Christmas tree light displays on ballplayers' houses, and suddenly Dontrelle Willis, the former Marlins ace, was helping him out with his slider, and Braves outfielder Justin Upton was inviting him to parties. "They don't care that I'm a minor leaguer," Barfield said. "When I'm hanging lights on their 12,000 square-foot houses, it gives me something to look forward to."
* * *
Does Jeremy Barfield have a 12,000 square-foot mansion to look forward to? Will he ever make it to the promised land and have the kind of eternal career that made lefties like Darren Oliver and John Franco rich men? A month into his minor-league pitching career, he has 18 strike outs in 12 innings and a 3.75 ERA -- promising enough numbers, particularly the strikeouts -- but he's pitching in Class A ball. There are a lot of coach buses and grueling practice sessions and maybe plates of mangú ahead of him.
Still, he can look for inspiration to a number of position players who became successful pitchers. In late summer 2011, an oft-injured A's first-base prospect named Sean Doolittle made the transition to the mound. Less than a year later, he was promoted to the majors, where he has become a dominant reliever. In 2009, a light-hitting Dodgers minor league catcher named Kenley Jansen was encouraged to take up pitching. He debuted for the big league club in 2010, and over the past five seasons he has an ERA of 2.17 and has struck out batters at a rate of more than 14 per nine innings. Trevor Hoffman, a seven-time all-star with 601 career saves, began his professional career as an infielder in the Reds organization. Even Barfield's godfather, Mike Jackson, had barely pitched until he signed a professional contract after college.
As I was making my way around Papago Park, I stopped Keith Liepmann, the A's director of player development, to talk with him about Barfield's progress. "The adjustment is going to take a little while, but he certainly has been able to get a lot of swings and misses," Liepmann said. "He throws strikes, there's a lot of movement on his throws, everything looks good so far."
But, Liepmann continued, Barfield was going to have to work harder than Doolittle and Jansen to get to the majors: Doolittle had been a star pitcher in college and he could throw in the high 90s. Jansen's cut fastball is almost unhittable, and his velocity can approach 100 mph. Before last summer, Barfield hadn't thrown a pitch since his sophomore year of high school, and while he was known for his cannon arm in right field, that power hadn't yet translated to an overpowering fastball.
"We had thought just because of the way he was as an outfielder -- he always led the league in assists -- that the velocity would flash right away," Liepmann said. "But it really didn't. He's throwing 90, 91. He's just not going to be a dominating guy like some of the pitchers who are throwing 98. He's going to have to be able to pitch: to changes speeds, and to do all the other things that have taken other pitchers years to acquire. So it is a daunting task."
* * *
Two days later, Barfield made one of his final spring training appearances, taking the mound in the bottom of the 8th inning against the San Jose Giants with the score tied 3-3. Barfield challenged hitters with his fastball. He got swings and misses on his slider. And then with two runners on and two outs, Barfield unleashed what is now his best pitch, his splitter, inducing a harmless flare to the shortstop to end the inning. He'd faced five hitters, and thrown 22 pitches -- sweat-inducing work. But he'd preserved the tie. He was learning how to pitch.
That night Barfield, wearing a black t-shirt that read "work hard, play hard," was chowing down on a full-rack of Bali Hai barbecue ribs at a high-end Polynesian-fusion restaurant in Scottsdale, surrounded by a group that included his agent, Greg Maroni, and another Maroni client, Dutch minor-league outfielder Kalian Sams. In a few days, Barfield would head back to northern California, where he would suit up for the Stockton Ports and live in the guest room of Maroni's house in nearby Sacramento.
Barfield and Maroni had a buddy-comedy rapport. Barfield had complained that his agent was taking too long primping at the W Hotel and had left in a mock-huff to meet me at the restaurant. When Barfield learned that a friend of Maroni's with a dog was currently occupying his room, he flew into a comic display of operatic rage. Maroni, playing the straight man, assured him all would be fine. "You will have a non-soiled living space in Sacramento!" the agent decreed.
"I actually know a guy in reality TV who joked that it would make a great show," Maroni said of their roommate arrangement. "You have this little nerdy white guy and this big angry black man -- it would be perfect!"
Sams, 27, although buddies with both Maroni and Barfield, wasn't quite so fortunate. He was a minor celebrity in his home country -- a documentary film crew from the Netherlands had shadowed him during spring training, and the Dutch baseball magazine Fastball had put him on its March cover -- but the Texas Rangers had released him two days earlier. Sams was now looking for a job. (He was since been picked up by the Atlantic League's Camden Riversharks.)
The comings and goings, the uncertainty, the tumble-wash of baseball got Barfield and Sams reminiscing. They laughed about Bull Durham-like antics in fourth-tier minor-league towns: "You guys ever play in Visalia? There was that host mom there…" "Bakersfield is bad, man! That's where I got a staph infection in my knee…" "So we're in Beloit in 2009…" But soon the talk turned more sober.
Barfield brought up the story of Vinnie Catricala, a Seattle Mariners minor leaguer who in 2011 had torn through Single and Double A, hitting .349 with 25 home runs and 106 RBIs. Sixteen months later, he retired from baseball.
"He just lost it," Barfield said. "He quit to become a cop."
Barfield and Sams then puzzled over the even more curious case of the former A's prospect Grant Desme. In 2009, the then 23-year-old Desme had demolished single-A pitching, hitting 31 home runs, then followed up his breakout season by winning MVP honors in the Arizona Fall League. Two months later, in January 2010, Desme announced he was leaving baseball to become a Catholic priest.
"We had another guy, Adrian Cardenas," Barfield said. "He didn't like baseball anymore. He wrote an article for the New Yorker about it. Now he's at NYU getting a degree in liberal studies or something."
Cardenas had gone all the way to the big leagues, making 67 plate appearances in 2012 as a pinch hitter for the Chicago Cubs, but had turned down an invitation to major-league spring training in 2013 and quietly retired. In the New Yorker piece, he writes, "To put it simply, other players were much better than I was at separating the game of baseball from the job of baseball … These players, at once the objects of my envy and my admiration, are the resilient ones, still in the game. I am no longer one of them."
"How do you feel about guys like that?" I asked Barfield. "Someone who gets so close and then gives it up?"
"It's not for everybody," he said. "Most people would be happier without baseball in their lives."
Back in Papago Park, I'd asked Barfield if he'd ever thought about quitting. When the A's told him they wanted him to convert to pitching, did part of him want to walk away?
"Nah," he said. "For me, it was really a pride thing. It's like, man, I pride myself on being a good hitter and a great outfielder. And just to hang that all up? It still hurts. But at the end of the day I want to be a major leaguer. If that's me hitting, if that's me catching, if that's me pitching -- I want to be a major leaguer. It's funny, I was feeling good about my career. I'm 24, and I'm in Triple A! And then, boom! I'm 25, and I'm in rookie ball."
Photos via Jeremy Barfield and California Sports Management
* * *
Eric Benson is a journalist whose work has appeared in the New York Times Magazine, Grantland, and The Oxford American. He lives in Austin, Tex.


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Cranberry Apple Oatmeal Crisp
This recipe is a riff on a classic apple crisp. If you've been reading my posts lately, you'll know that I've been on a bit of a quest to find creative ways to utilize our Thanksgiving leftovers. A cranberry apple crisp seemed like the perfect destiny for the leftover cranberries the fridge.
It's an incredibly easy recipe to make. If you have cranberry sauce, then all you really need to do is to add a sweetener, prepare the topping and bake the individual servings in the oven. They are great for intimate holiday parties.
Yields: 14 mini-ramekins2 red delicious apples, (10 ounces)
1 tablespoon lemon juice, freshly squeezed
2 tablespoons honey
1/2 vanilla bean, slit lengthwise
3/4 cup fresh cranberries, (3 ounces)
1/3 cup guava nectar, as needed
1/2 cinnamon stick
2 tablespoons frozen guava pulp (optional)
1/2 cup granulated sugar
1/2 teaspoon cinnamon, freshly ground
1/2 cup rolled oats
1/4 cup whole wheat flour
3/4 cup all-purpose flour
1/4 teaspoon salt
1/4 cup granulated sugar
1/3 cup brown sugar
9 tablespoons unsalted butter
1/2 cup whipped cream (optional)
For the compote de pomme à la vanille (vanilla-flavored apple sauce):
Using a paring knife, scrape and gather all the grains of the vanilla bean.
Peel, core and dice the apple. Coat the diced apples in lemon juice to prevent oxidation (turning brown) of the fruit. Place the apples, honey, grains of vanilla bean and 2 tablespoons of guava nectar in a small saucepan. Bring to a boil, then lower the heat to a gentle simmer for about 6-7 minutes until the apples are tender. Stir frequently. Allow to cool, then blend the mixture in a mini-blender (or a regular blender if you don't have a mini).
For the cranberry filling:
Wash the cranberries. Pick out and discard any bad ones (discolored, shriveled or bruised). Place the cranberries in a saucepan; add 1/4 cup of sugar, cinnamon stick, and 1/8 teaspoon of salt. Add the remaining guava nectar. Bring to a boil, then lower the heat to a gentle simmer. Skim off any foam that develops on the top. Cover and cook for about 25 minutes, until the cranberries have burst. Using a wooden spoon, stir frequently to prevent the cranberries from sticking to the bottom of the pan. Add the guava pulp (if used). Stirring constantly, bring back to a boil over medium-high heat and let it boil for about 20 seconds. Turn off the heat. Remove and discard the cinnamon stick. Allow to cool for at least 30 minutes. Mix in the apple sauce.
For the crisp topping:
Preheat the oven to 350°F.
Grease 14 2.75-ounce mini-ramekins with a thin layer of butter. Melt the remaining butter in the microwave (or over the stove) for 20 seconds.
In a bowl, combine the flours, ground cinnamon and 1/8 teaspoon of salt. Sift the dry ingredients. Add 1/4 cup of sugar, the brown sugar and the rolled oats. Add the melted butter and mix using a pastry blender or the back of fork until it forms sandy crumbs of butter, oats and flour. Do NOT over-mix. Set aside.
Assembly time:
Place about 2 tablespoons of the cranberry filling into each ramekin. Evenly spoon the crumbly topping over the cranberry filling.
Bake for 25-30 minutes, then broil (if necessary) for 2 minutes until the top is crisp and golden.
Allow to cool for about 15 minutes.
Serve warm with a dollop of whipped cream or a scoop of vanilla ice cream.
Bon appétit!
If you host a buffet-style dinner, this is the ideal way to run a stress free party as this dish can be prepared in advance. Just bake the cranberry crisps when the guests start the meal.
After scraping the grains of vanilla, do NOT discard the remaining vanilla bean. Just place the vanilla bean in a jar and cover it with regular granulated sugar. Let it sit for a few weeks and you'll get a nice, fragrant vanilla sugar.
When washing and soaking the cranberries, also discard the ones that sink.
I used Kern's guava juice but you can use any other juices you prefer.
Remember, the cranberry filling should be slightly sweeter to your taste before placing in the ramekins. When the cranberry filling cooks down in the oven, the flavor will get a little more intense; you want to make sure the result won't be too tart because of the cranberries. I think the amount of honey, the guava pulp and the addition of apple sauce balance out the tartness of the cranberries. But again, you can make an unlimited number of variations of this cranberry crisp.
I usually get a bag of cinnamon sticks at a more reasonable price at the Indian market, compared to the regular local chain stores and grated it using a microplane. You can use ready-made ground cinnamon but I think the flavors are more intense when freshly grated.
Don't have cranberries? No worries. Fruit crisp is a very versatile dessert. The base is just your average crisp topping, but you can add your own twist to it by using different fruit flavor combination. I used cranberry, apple and guava but rhubarb, pear, apricot or other berries sound as delicious. It is a true culinary chameleon.
I get all sorts of frozen pure pulp of fruit at Crossroads World Market -720 San Antonio Rd -Palo Alto, CA 94303. I love this place. It's a sweet little store. Crossroads market carries a wide range of European products. I use the fruit pulp (lemon, passion fruit, guava and different other flavors) to make ganaches, verrines, parfaits and very soon... macarons.
If you want a crispier topping, you can add a paper-thin slice of butter to each ramekin prior to baking in the oven.
Published By: on November 30, 2009.


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European Aeronautic, Defence & Space Co. and BAE Systems Plc are reviving a decade-old plan to build an equal to Boeing Co. that would balance civil and defense operations in an era of shrinking military budgets.
EADS stock slumped as much as 10 percent in Paris, while BAE declined as much as 9.2 percent in London on concern that a combined company will struggle to achieve savings and penetrate the U.S. defense market.
EADS, the parent of Airbus SAS, would control 60 percent of the new entity, with London-based BAE owning the rest, the companies said Wednesday.
�This will be a very complex organization and there is a risk of synergies coming only much later,� said Yan Derocles, an analyst at Oddo Securities in Paris. �Airbus is a big growth story and will be heavily diluted in the new company. And there�s also the problem of significant constraints on the defense business in the U.S.�
The new company would have a combined market value of about $45 billion, sales nudging $100 billion and 220,000 employees, with assets spanning civil jets, Eurofighter warplanes and nuclear submarines. A merger would revive plans for a single European aerospace business that were abandoned more than a decade ago when the formation of EADS and BAE split the industry in the region along civil and defense lines.
�Significant Benefits�
BAE slumped as much as 33.6 pence to 330 pence Thursday, reversing an 11 percent surge yesterday after the companies confirmed that they are in talks. Thursday�s drop, which stood at 5 percent as of 8:41 a.m. in London, clipped BAE�s market value to about 11.3 billion pounds ($18.2 billion). EADS dropped as much as 2.89 euros to 25.11 euros in Paris, valuing it at 21 billion euros ($27 billion).
The deal would add Toulouse, France-based EADS�s revenue of about 49 billion euros last year to BAE�s 17.7 billion pounds. That compares with $68.7 billion at Chicago-based Boeing and $46.5 billion at Bethesda, Maryland-based Lockheed Martin Corp., the world�s biggest defense company.
�BAE Systems and EADS believe that the potential combination of their two businesses offers the prospect of significant benefits for customers and shareholders,� the companies said in a statement after markets closed.
EADS Chief Executive Officer Tom Enders, who took over in June, has been revamping senior management positions and switched the leader of the Cassidian defense business this month. Enders, a German reserve army officer, previously ran the Airbus business, which is EADS�s biggest sales contributor and the world�s largest maker of civil aircraft ahead of Boeing.
Airbus Dependence
The companies, who cooperate on the Eurofighter warplane, first explored scenarios for a combination in early June, followed by the first outlines of a combination a month later in Munich that included the 60-40 split, a person familiar with the talks said. Besides Enders, EADS chief strategist Marwan Lahoud has been a driving force behind a deal, said the person, who asked to remain anonymous because the information isn�t public.
The companies didn�t say where the combined group would be based, or who would lead it. EADS is moving its headquarters from Paris and Munich to Toulouse in order to be on the same location as Airbus. Besides Airbus, EADS also has helicopter, space and defense operations.
�EADS has been seeking to reduce its dependence on Airbus and achieve a better balance between commercial aerospace and defense,� said Zafar Khan, an analyst at Societe Generale in London. �A combination with BAE would certainly achieve that.�
No Threat
BAE is a supplier to Boeing on military and commercial aircraft, including automatic flight control systems and belly- mounted guns for the V-22 Osprey, a touch-screen attendant control panel on the 737 airliner and engine-control systems on 787 Dreamliner jets, according to Michel Merluzeau, a consultant with G2 Solutions in Kirkland, Washington.
Boeing CEO Jim McNerney told reporters in Washington yesterday that a combination of EADS and BAE wouldn�t �threaten us fundamentally.�
�I have a pretty deep and abiding faith in our company�s strength,� he said at the Council on Foreign Relations office. �It does reflect a global consolidation that is beginning to happen.�
A combination of EADS and BAE would be larger than Boeing�s purchase of McDonnell Douglas in 1997 that was valued at $16.3 billion. That deal brought together two civil aviation manufacturers, two years after Lockheed�s defense-focused combination with Martin Marietta Corp.
U.S. Strength
BAE, led by CEO Ian King, was the U.S. government�s ninth- largest contractor in fiscal 2011, with $7.3 billion in direct, or prime, contracts, while EADS was its 100th, with $684 million in contracts, according to a Bloomberg Government study ranking the top 200 contractors.
The two companies employ about 45,000 workers in the U.S., 90 percent of them at BAE, and operate under special security agreements with the government. BAE supplies the U.S. military with combat vehicles and artillery such as the Bradley fighting vehicle, the self-propelled Paladin howitzer and naval guns.
EADS makes UH-72 Lakota light-utility helicopters for the U.S. Army. The company in 2011 lost a bid to Boeing to develop a new refueling tanker for the Air Force as part of an estimated $35 billion program.
Given the �highly secure and sensitive� nature of the defense business involved, BAE and EADS plan to ring-fence certain activities, particularly relating to the U.S., the world�s biggest defense market, they said.
U.K. Shortfall
Weapons makers worldwide have been struggling with shrinking defense budgets as austerity-minded administrations rein in spending. BAE has suffered as Britain seeks to eliminate a 38 billion-pound defense shortfall, while governments across Europe have cut commitments for Eurofighter combat jets and armored-vehicle sales have fallen following the end of the war in Iraq and a wind-down of troop numbers in Afghanistan.
Governments in Germany, France and the U.K. would be issued with special shares in the new business, BAE said. EADS has also agreed to pay shareholders 200 million pounds before completion to help harmonize the companies� dividend payouts.
Among EADS�s biggest shareholders is the French government, which owns 15 percent. German carmaker Daimler AG controls 22.5 percent, of which 7.5 percent is owned by German federal states and some banks. The Spanish government owns 5.4 percent. Daimler said it still intends to reduce its stake in EADS this year.
European Schism
The British government�s Department of Business, Innovation and Skills said it was aware of the merger proposal and that while any business benefits are �a matter for the companies,� it will ensure that the public interest is protected in any deal.
BAE was created in 1999 when British Aerospace Plc, which had been exploring a merger with Daimler�s Dasa unit in Germany, opted instead for an all-U.K. combination with the Marconi Electronic Systems unit of GEC in 1999.
That prompted Dasa first to acquire Construcciones Aeronauticas SA of Spain and then to combine with France�s Aerospatiale Matra SA to form EADS. The sequence of events gave EADS control of 80 percent of airliner manufacturer Airbus, which BAE exited in 2006, while allowing the U.K. company to dominate the European defense sector.
Morgan Stanley, Goldman Sachs Group Inc. and Gleacher Shacklock LLP are advising BAE, with Freshfields Bruckhaus Deringer LP as legal counsel. UBS AG is serving as BAE�s corporate broker on the deal. EADS is being advised by Evercore Partners Inc., Perella Weinberg Partners LP, Lazard Ltd. and BNP Paribas SA, and Clifford Chance LLP is acting as counsel, according to two people familiar with the matter.
Credit Suisse Group AG will probably be asked to compile a fairness opinion, said one of the people, who asked to remain anonymous because the advisers have not been publicly announced.