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Berlin Brandenburg

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  • 1
    Language: English
    In: Cancer, 15 July 2011, Vol.117(14), pp.3262-3267
    Description: BACKGROUND: Contemporary therapy for medulloblastoma results in adverse neurocognitive effects on young children, particularly those under the age of 3. Stratification of patients by risk group may allow toxic treatment to be avoided.METHODS: Seventy-six patients diagnosed with medulloblastoma and enrolled on CCG-9921 underwent central review of pathology, and histologic subtype was designated as desmoplastic or nondesmoplastic. Nonparametric event-free survival (EFS) and survival (OS) curves were computed using the product limit (Kaplan-Meier) estimates, and the log-rank test was used to compare survival according to histologic subtype.RESULTS: Patients with desmoplastic medulloblastoma experienced a favorable EFS of 77% ± 9% and OS of 85% ± 8% compared with EFS of 17% ± 5% and OS of 29% ± 6% for patients with tumors in the nondesmoplastic group (P 〈 .0001 for both EFS and OS comparisons). Patients without disease progression did not receive radiation therapy.CONCLUSIONS: Children less than 3 with desmoplastic histology of medulloblastoma represent a lower-risk group for whom reduction of therapy, including elimination of radiation therapy, is an appropriate strategy.
    Keywords: Medulloblastoma ; Desmoplastic ; Survival ; Brain Neoplasms
    ISSN: 0008-543X
    E-ISSN: 1097-0142
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  • 2
    In: Cancer, 15 July 2013, Vol.119(14), pp.2645-2653
    Description: Patients with relapsed osteosarcoma have a poor prognosis. Whereas surgery is essential for survival, chemotherapy may slow disease progression in patients without remission. This study provides data on prognostic factors and event‐free survival after relapse that are needed for the design of phase 2 trials of novel agents.
    Keywords: Osteosarcoma ; Relapse ; Chemotherapy ; Outcome ; Survival ; Prognostic Factors
    ISSN: 0008-543X
    E-ISSN: 1097-0142
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  • 3
    In: Nature, 2010, Vol.466(7306), p.632
    Description: Understanding the biology that underlies histologically similar but molecularly distinct subgroups of cancer has proven difficult because their defining genetic alterations are often numerous, and the cellular origins of most cancers remain unknown (1-3). We sought to decipher this heterogeneity by integrating matched genetic alterations and candidate cells of origin to generate accurate disease models. First, we identified subgroups of human ependymoma, a form of neural tumour that arises throughout the central nervous system (CNS). Subgroup-specific alterations included amplifications and homozygous deletions of genes not yet implicated in ependymoma. To select cellular compartments most likely to give rise to subgroups of ependymoma, we matched the transcriptomes of human tumours to those of mouse neural stem cells (NSCs), isolated from different regions of the CNS at different developmental stages, with an intact or deleted Ink4a/Arf locus (that encodes Cdkn2a and b). The transcriptome of human supratentorial ependymomas with amplified EPHB2 and deleted INK4A/ARF matched only that of embryonic cerebral Ink4a/[Arf.sup.-/-] NSCs. Notably, activation of Ephb2 signalling in these, but not other, NSCs generated the first mouse model of ependymoma, which is highly penetrant and accurately models the histology and transcriptome of one subgroup of human supratentorial tumour. Further, comparative analysis of matched mouse and human tumours revealed selective deregulation in the expression and copy number of genes that control synaptogenesis, pinpointing disruption of this pathway as a critical event in the production of this ependymoma subgroup. Our data demonstrate the power of cross-species genomics to meticulously match subgroup-specific driver mutations with cellular compartments to model and interrogate cancer subgroups.
    Keywords: Genomics -- Research ; Gliomas -- Genetic Aspects ; Gliomas -- Care And Treatment ; Brain Cells -- Abnormalities ; Brain Cells -- Genetic Aspects ; Stem Cells -- Abnormalities;
    ISSN: 0028-0836
    E-ISSN: 14764687
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  • 4
    Language: English
    In: Current opinion in pediatrics, February 2012, Vol.24(1), pp.33-9
    Description: Most children diagnosed with cancer today are expected to be cured. Medulloblastoma, the most common pediatric malignant brain tumor, is an example of a disease that has benefitted from advances in diagnostic imaging, surgical techniques, radiation therapy and combination chemotherapy over the past decades. It was an incurable disease 50 years ago, but approximately 70% of children with medulloblastoma are now cured of their disease. However, the pace of increasing the cure rate has slowed over the past 2 decades, and we have likely reached the maximal benefit that can be achieved with cytotoxic therapy and clinical risk stratification. Long-term toxicity of therapy also remains significant. To increase cure rates and decrease long-term toxicity, there is great interest in incorporating biologic 'targeted' therapy into treatment of medulloblastoma, but this will require a paradigm shift in how we classify and study disease. Using genome-based high-throughput analytic techniques, several groups have independently reported methods of molecular classification of medulloblastoma within the past year. This has resulted in a working consensus to view medulloblastoma as four molecular subtypes, including wingless-type murine mammary tumor virus integration site (WNT) pathway subtype, Sonic Hedgehog pathway subtype and two less well defined subtypes (groups C and D). Novel classification and risk stratification based on biologic subtypes of disease will form the basis of further study in medulloblastoma and identify specific subtypes that warrant greater research focus.
    Keywords: Brain Neoplasms -- Classification ; DNA, Neoplasm -- Genetics ; Medulloblastoma -- Classification ; RNA, Neoplasm -- Genetics
    ISSN: 10408703
    E-ISSN: 1531-698X
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  • 5
    Language: English
    In: Clinical cancer research : an official journal of the American Association for Cancer Research, 15 October 2017, Vol.23(20), pp.6062-6069
    Description: Trebananib is a first-in-class antiangiogenic peptibody (peptide-Fc fusion protein) that inhibits Angiopoietin 1 and 2. A pediatric phase 1 trial was performed to define trebananib dose-limiting toxicities (DLT), recommended phase 2 dose (RP2D), and pharmacokinetics (PK). Trebananib was administered by weekly infusion. Three dose levels (10, 15, or 30 mg/kg/dose) were evaluated using a rolling-six design. Part 2 evaluated a cohort of subjects with primary central nervous system (CNS) tumors. Pharmacokinetic sampling and analysis of peripheral blood biomarkers was performed during the first 4 weeks. Response was evaluated after 8 weeks. Correlative studies included angiogenic protein expression and DCE-MRI. Thirty-seven subjects were enrolled (31 evaluable for toxicity) with median age 12 years (range, 2 to 21). Two of 19 evaluable non-CNS subjects developed DLT at the 30 mg/kg dose level, including venous thrombosis and pleural effusion. In the CNS cohort, 3/12 subjects developed DLT, including decreased platelet count, transient ischemic attack, and cerebral edema with headache and hydrocephalus. Other grade 3 or 4 toxicities included lymphopenia ( = 4), anemia, thrombocytopenia, neutropenia, vomiting, and hypertension ( = 1 each). Response included stable disease in 7 subjects, no partial or complete responses. Two subjects continued study treatment with prolonged stable disease for 18 cycles (neuroblastoma) and 26 cycles (anaplastic astrocytoma). Pharmacokinetics appeared linear over 3 dose levels. Correlative studies demonstrated increased PlGF and sVCAM-1, but no change in endoglin or perfusion by DCE-MRI. Trebananib was well tolerated in pediatric patients with recurrent or refractory solid or CNS tumors. RP2D is 30 mg/kg. .
    Keywords: Antineoplastic Agents, Immunological -- Therapeutic Use ; Central Nervous System Neoplasms -- Drug Therapy ; Neoplasms -- Drug Therapy ; Recombinant Fusion Proteins -- Therapeutic Use
    ISSN: 1078-0432
    E-ISSN: 15573265
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  • 6
  • 7
    Language: English
    In: Nature medicine, November 2018, Vol.24(11), pp.1752-1761
    Description: Brain tumors are the leading cause of cancer-related death in children. Genomic studies have provided insights into molecular subgroups and oncogenic drivers of pediatric brain tumors that may lead to novel therapeutic strategies. To evaluate new treatments, better preclinical models adequately reflecting the biological heterogeneity are needed. Through the Children's Oncology Group ACNS02B3 study, we have generated and comprehensively characterized 30 patient-derived orthotopic xenograft models and seven cell lines representing 14 molecular subgroups of pediatric brain tumors. Patient-derived orthotopic xenograft models were found to be representative of the human tumors they were derived from in terms of histology, immunohistochemistry, gene expression, DNA methylation, copy number, and mutational profiles. In vivo drug sensitivity of targeted therapeutics was associated with distinct molecular tumor subgroups and specific genetic alterations. These models and their molecular characterization provide an unprecedented resource for the cancer community to study key oncogenic drivers and to evaluate novel treatment strategies.
    Keywords: Biological Specimen Banks ; Immunohistochemistry ; Brain Neoplasms -- Pathology ; Xenograft Model Antitumor Assays -- Methods
    ISSN: 10788956
    E-ISSN: 1546-170X
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  • 8
    Language: English
    In: Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 01 August 2013, Vol.31(22), pp.2833-4
    Keywords: Survivors ; Echocardiography, Doppler -- Methods ; Neoplasms -- Physiopathology ; Tricuspid Valve Insufficiency -- Physiopathology
    ISSN: 0732183X
    E-ISSN: 1527-7755
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  • 9
    Language: English
    In: Obstetrics and gynecology, December 2012, Vol.120(6), pp.1283-90
    Description: To explore the association between the presence of maternal heart disease and maternal, perinatal, and infant outcomes. We conducted a population-based retrospective cohort study using Washington State birth certificates linked with hospital discharge records of mothers noted to have maternal congenital heart disease, ischemic heart disease, heart failure, or pulmonary hypertension. Women who gave birth between 1987 and 2009 (n=2,171) were compared with a sample of mothers without these conditions (n=21,710). We described characteristics of pregnant women with heart disease over time. Logistic regression estimated the association between chronic maternal heart disease and small-for-gestational-age (SGA) neonates as well as perinatal, postneonatal, and maternal death. The proportion of births to women with reported heart disease increased 224% between the 1987 and 1994 and 2002 and 2009 calendar periods. Chronic maternal heart disease was associated with increased risk of SGA (62 additional SGA newborns per 1,000 births, 95% confidence interval [CI] 46-78; P〈.001), perinatal death (14 additional deaths per 1,000 births, 95% CI 8-20; P〈.001), postneonatal death (5 additional deaths per 1,000 births, 95% CI 2-9; P〈.001), and maternal death (5 additional deaths per 1,000 births, 95% CI 2-9; P〈.001). The presence of chronic maternal heart disease is associated with elevated risk for poor maternal, perinatal, and postneonatal outcomes.
    Keywords: Fetal Mortality ; Infant Mortality ; Heart Diseases -- Epidemiology
    ISSN: 00297844
    E-ISSN: 1873-233X
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  • 10
    Language: English
    In: Journal of pediatric hematology/oncology, May 2016, Vol.38(4), pp.269-73
    Description: Survival after recurrence of medulloblastoma has not been reported in an unselected cohort of patients in the contemporary era. We reviewed 55 patients diagnosed with medulloblastoma between 2000 and 2010, and treated at Seattle Children's Hospital to evaluate patterns of relapse treatment and survival. Fourteen of 47 patients (30%) over the age of 3 experienced recurrent or progressive medulloblastoma after standard therapy. The median time from diagnosis to recurrence was 18.0 months (range, 3.6 to 62.6 mo), and site of recurrence was metastatic in 86%. The median survival after relapse was 10.3 months (range, 1.3 to 80.5 mo); 3-year survival after relapse was 18%. There were trend associations between longer survival and having received additional chemotherapy (median survival 12.8 vs. 1.3 mo, P=0.16) and radiation therapy (15.4 vs. 5.9 mo, P=0.20). Isolated local relapse was significantly associated with shorter survival (1.3 vs. 12.8 mo, P=0.009). Recurrence of medulloblastoma is more likely to be metastatic than reported in previous eras. Within the limits of our small sample, our data suggest a potential survival benefit from retreatment with cytotoxic chemotherapy and radiation even in heavily pretreated patients. This report serves as a baseline against which to evaluate novel therapy combinations.
    Keywords: Medulloblastoma -- Mortality
    ISSN: 10774114
    E-ISSN: 1536-3678
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