Genomes and Genes
Rani E George
Affiliation: Harvard University
- Seek and Ye Shall Find: Subclonal Anaplastic Lymphoma Kinase MutationsRani E George
Department of Pediatric Hematology and Oncology, Dana Farber Cancer Institute and Boston Children s Hospital, Harvard Medical School, Boston, Massachusetts
Clin Cancer Res 21:4747-9. 2015..Although the significance of these subclonal aberrations is not yet understood, deep sequencing could identify patients whose tumors may respond to ALK inhibitors...
- Tumor histology during induction therapy in patients with high-risk neuroblastomaRani E George
Department of Pediatric Hematology and Oncology, Dana Farber Cancer Institute and Children s Hospital, Boston, MA 02115, USA
Pediatr Blood Cancer 59:506-10. 2012..We sought to determine whether histological changes in the primary tumor following induction therapy could be used as a marker of response...
- Expression of the neuron-specific protein CHD5 is an independent marker of outcome in neuroblastomaIdoia Garcia
Developmental Tumor Biology Laboratory, Hospital Sant Joan de Deu, Fundación Sant Joan de Déu, Barcelona, Spain
Mol Cancer 9:277. 2010..CHD5 gene and protein expression was reexamined after induction chemotherapy in a subset of high risk tumors to identify potential changes reflecting tumor response...
- Association between congenital cardiovascular malformations and neuroblastomaRani E George
Department of Pediatric Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA
J Pediatr 144:444-8. 2004..We explored the association between neuroblastoma and congenital cardiovascular malformations (CCM), previously described in case reports...
- Genome-wide analysis of neuroblastomas using high-density single nucleotide polymorphism arraysRani E George
Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
PLoS ONE 2:e255. 2007..We analyzed paired blood and primary tumor samples from 22 children with high-risk neuroblastoma for loss of heterozygosity (LOH) and DNA copy number change using the Affymetrix 10K single nucleotide polymorphism (SNP) array...
- High-risk neuroblastoma treated with tandem autologous peripheral-blood stem cell-supported transplantation: long-term survival updateRani E George
Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
J Clin Oncol 24:2891-6. 2006..To provide an update on long-term survival of patients with high-risk neuroblastoma treated with tandem cycles of myeloablative therapy and peripheral-blood stem-cell rescue (PBSCR)...
- Hyperdiploidy plus nonamplified MYCN confers a favorable prognosis in children 12 to 18 months old with disseminated neuroblastoma: a Pediatric Oncology Group studyRani E George
Department of Pediatric Hematology and Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
J Clin Oncol 23:6466-73. 2005..To determine predictive strength of tumor cell ploidy and MYCN gene amplification on survival of children older than 12 months with disseminated neuroblastoma (NB)...
- Zebrafish foxd3 is selectively required for neural crest specification, migration and survivalRodney A Stewart
Department of Pediatric Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
Dev Biol 292:174-88. 2006....
- Distinct neuroblastoma-associated alterations of PHOX2B impair sympathetic neuronal differentiation in zebrafish modelsDesheng Pei
Department of Pediatric Oncology, Dana Farber Cancer Institute, Division of Hematology Oncology, Boston Children s Hospital, Harvard Medical School, Boston, MA, USA
PLoS Genet 9:e1003533. 2013....
- Phase I study of decitabine with doxorubicin and cyclophosphamide in children with neuroblastoma and other solid tumors: a Children's Oncology Group studyRani E George
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children s Hospital, Boston, Massachusetts 02115, USA rani
Pediatr Blood Cancer 55:629-38. 2010..We conducted a phase I trial to determine the toxicity and molecular effects of the demethylating agent, decitabine, followed by doxorubicin and cyclophosphamide in children with refractory solid tumors...
- Activating mutations in ALK provide a therapeutic target in neuroblastomaRani E George
Department of Pediatric Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 455:975-8. 2008....
- Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastomaNathan F Moore
Departments of Pediatric Hematology Oncology, Dana Farber Cancer Institute, Boston, MA These authors contributed equally to this work
Oncotarget 5:8737-49. 2014..Our findings should enable a more precise selection of molecularly targeted agents for patients with ALK-mutated tumors. ..
- Activated ALK collaborates with MYCN in neuroblastoma pathogenesisShizhen Zhu
Department of Pediatric Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cancer Cell 21:362-73. 2012..Coexpression of activated ALK with MYCN provides prosurvival signals that block this apoptotic response and allow continued expansion and oncogenic transformation of hyperplastic neuroblasts, thus promoting progression to neuroblastoma...
- The kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressorSusanne Schlisio
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Genes Dev 22:884-93. 2008....
- Pharmacotherapy of neuroblastomaRani E George
Dana Faber Cancer Institute, Department of Pediatric Oncology, Boston, MA, USA
Expert Opin Pharmacother 11:1467-78. 2010..High risk disease in older children remains a therapeutic challenge, despite high-intensity therapy with correspondingly significant short- and long-term toxicities...
- Emerging importance of ALK in neuroblastomaAnna M Azarova
Department of Pediatric Hematology and Oncology, Dana Farber Cancer Institute and Children s Hospital Boston, Harvard Medical School, 450 Brookline Ave, Boston, MA 02115, USA
Semin Cancer Biol 21:267-75. 2011..This review addresses many of the current issues surrounding the role of ALK in normal development and neuroblastoma pathogenesis, and discusses the prospects for clinically effective targeted treatments based on ALK inhibition...
- Does MYCN amplification manifested as homogeneously staining regions at diagnosis predict a worse outcome in children with neuroblastoma? A Children's Oncology Group studyLisa A Moreau
The National Center for Pediatric Cancer Genetics, Children s Oncology Group, University of Florida, Gainesville, FL, USA
Clin Cancer Res 12:5693-7. 2006..The aim of this study was to determine whether children with neuroblastoma in which MYCN oncogene amplification is manifested as HSRs at diagnosis have a worse prognosis than those whose tumors exhibit dmins...
- Neuroblastoma cells isolated from bone marrow metastases contain a naturally enriched tumor-initiating cellLoen M Hansford
Cell Biology Program, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada
Cancer Res 67:11234-43. 2007..These cells may serve as a model system to identify the molecular determinants of neuroblastoma and to develop new therapeutic strategies for this tumor...
- Development of a real-time polymerase chain reaction assay for prediction of the uptake of meta-[(131)I]iodobenzylguanidine by neuroblastoma tumorsSean Carlin
Departments of Radiation Oncology and Child Health, University of Glasgow, Cancer Research UK Beatson Laboratories, Glasgow G61 1BD, United Kingdom
Clin Cancer Res 9:3338-44. 2003..EXPERMENTAL DESIGN: Tumor specimens from 54 neuroblastoma patients were analyzed using real-time PCR, and NAT expression was compared with the corresponding diagnostic scintigrams...
- Zebrafish Peripheral Sympathetic Nervous System Development and NeuroblastomaRANI GEORGE; Fiscal Year: 2008..Insight into the proteins encoded by such modifier genes may lead to the discovery of genes that could serve as novel drug targets for the treatment of older children with advanced disease. [unreadable] [unreadable]..