Tumorigenesis and Neoplastic Progression NPAS 3 Demonstrates Features of a Tumor Suppressive Role in Driving the Progression of Astrocytomas

From the Centre de Recherche de l’Hôtel-Dieu de Québec,* Québec, Québec, Canada; the Department of Pathology, and the PRP Laboratory, Laboratory Medicine Program, University Health Network, Toronto, Ontario, Canada; the Pediatric Research Unit, Centre de Recherche du CHUL, Québec, Québec, Canada; the Division of Anatomic Pathology, Department of Medical Biology, CHAUQ Hôpital de l’Enfant-Jésus, Québec, Québec, Canada; the Brain Tumor Research Center, Department of Neurological Surgery, University of California San Francisco, San Francisco, California; and the Department of Pediatrics, Laval University, Québec, Québec, Canada

[1]  D. Brat,et al.  The neuronal PAS domain protein 3 transcription factor controls FGF-mediated adult hippocampal neurogenesis in mice. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[2]  Alona Muzikansky,et al.  The prognostic significance of phosphatidylinositol 3-kinase pathway activation in human gliomas. , 2004, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[3]  Carol Dudley,et al.  Behavioral and regulatory abnormalities in mice deficient in the NPAS1 and NPAS3 transcription factors. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[4]  A. Kaye,et al.  Tumour angiogenesis: Its mechanism and therapeutic implications in malignant gliomas , 2009, Journal of Clinical Neuroscience.

[5]  K. Aldape,et al.  Formation of intracranial tumors by genetically modified human astrocytes defines four pathways critical in the development of human anaplastic astrocytoma. , 2001, Cancer research.

[6]  C. Vorhees,et al.  Abnormal neurodevelopment, neurosignaling and behaviour in Npas3‐deficient mice , 2005, The European journal of neuroscience.

[7]  G. Broggi,et al.  Bone morphogenetic proteins inhibit the tumorigenic potential of human brain tumour-initiating cells , 2006, Nature.

[8]  D. Kamnasaran,et al.  Immunohistochemical Analyses of NPAS3 Expression in the Developing Human Fetal Brain , 2011, Anatomia, histologia, embryologia.

[9]  D. Busam,et al.  An Integrated Genomic Analysis of Human Glioblastoma Multiforme , 2008, Science.

[10]  C. Chelala,et al.  Genome-wide DNA copy number analysis in pancreatic cancer using high-density single nucleotide polymorphism arrays , 2008, Oncogene.

[11]  D W Cox,et al.  Disruption of the neuronal PAS3 gene in a family affected with schizophrenia , 2003, Journal of medical genetics.

[12]  W. M. Foster,et al.  NPAS3 is a trachealess homolog critical for lung development and homeostasis , 2009, Proceedings of the National Academy of Sciences.

[13]  L. Chin,et al.  Marked genomic differences characterize primary and secondary glioblastoma subtypes and identify two distinct molecular and clinical secondary glioblastoma entities. , 2006, Cancer research.

[14]  G. Rouleau,et al.  Association of NPAS3 exonic variation with schizophrenia , 2010, Schizophrenia Research.

[15]  Mitchel S Berger,et al.  Neural stem cells and the origin of gliomas. , 2005, The New England journal of medicine.

[16]  M. Tate,et al.  Biology of angiogenesis and invasion in glioma , 2009, Neurotherapeutics.

[17]  A. Kaye,et al.  Caspase 8 is absent or low in many ex vivo gliomas , 2005, Cancer.

[18]  G. Fuller,et al.  Overexpression of c-MYC promotes an undifferentiated phenotype in cultured astrocytes and allows elevated Ras and Akt signaling to induce gliomas from GFAP-expressing cells in mice. , 2004, Neuron glia biology.

[19]  Paul Gardina,et al.  Comprehensive analysis of loss of heterozygosity events in glioblastoma using the 100K SNP mapping arrays and comparison with copy number abnormalities defined by BAC array comparative genomic hybridization , 2008, Genes, chromosomes & cancer.

[20]  J. Herman,et al.  GATA-4 and GATA-5 Transcription Factor Genes and Potential Downstream Antitumor Target Genes Are Epigenetically Silenced in Colorectal and Gastric Cancer , 2003, Molecular and Cellular Biology.

[21]  Shin Ta Liu,et al.  SAS® Survival Analysis Techniques for Medical Research , 2004, Technometrics.

[22]  K. Devriendt,et al.  Defining a holoprosencephaly locus on human chromosome 14q13 and characterization of potential candidate genes. , 2005, Genomics.

[23]  G. Turashvili,et al.  Novel markers for differentiation of lobular and ductal invasive breast carcinomas by laser microdissection and microarray analysis , 2007, BMC Cancer.

[24]  D. Witte,et al.  Characterization of Npas3, a novel basic helix-loop-helix PAS gene expressed in the developing mouse nervous system , 1999, Mechanisms of Development.

[25]  R. Strausberg,et al.  A new cancer genome anatomy project web resource for the community. , 2001, Cancer journal.

[26]  C. Fan,et al.  Remembrance of things PAS: regulation of development by bHLH-PAS proteins. , 1999, Current opinion in genetics & development.

[27]  L. Maquat Nonsense-mediated mRNA decay , 2002, Current Biology.

[28]  M. Berger,et al.  Akt pathway activation converts anaplastic astrocytoma to glioblastoma multiforme in a human astrocyte model of glioma. , 2001, Cancer research.

[29]  G. Riggins,et al.  Glioblastoma cell growth is suppressed by disruption of fibroblast growth factor pathway signaling , 2009, Journal of Neuro-Oncology.

[30]  Masha Kocherginsky,et al.  Progression of Barrett's metaplasia to adenocarcinoma is associated with the suppression of the transcriptional programs of epidermal differentiation. , 2005, Cancer research.

[31]  S. Hayashi,et al.  The role of proteolysis in tumor invasiveness in glioblastoma and metastatic brain tumors. , 2002, Anticancer research.

[32]  R. Wilson,et al.  Identification of a CpG island methylator phenotype that defines a distinct subgroup of glioma. , 2010, Cancer cell.

[33]  J. Squire,et al.  Molecular cytogenetic analysis in the study of brain tumors: findings and applications. , 2005, Neurosurgical focus.

[34]  J. Little,et al.  Human tumor cells segregate into radiosensitivity groups that associate with ATM and TP53 status , 2007, Acta oncologica.

[35]  R. Jove,et al.  Spontaneous activation and signaling by overexpressed epidermal growth factor receptors in glioblastoma cells , 2003, International journal of cancer.

[36]  M. Polymeropoulos,et al.  Association of the NPAS3 gene and five other loci with response to the antipsychotic iloperidone identified in a whole genome association study , 2009, Molecular Psychiatry.

[37]  Gerald C. Chu,et al.  Pten and p53 converge on c-Myc to control differentiation, self-renewal, and transformation of normal and neoplastic stem cells in glioblastoma. , 2008, Cold Spring Harbor symposia on quantitative biology.

[38]  Shuang-yin Han,et al.  c-Jun NH(2)-terminal kinase 2alpha2 promotes the tumorigenicity of human glioblastoma cells. , 2006, Cancer research.

[39]  N. Socci,et al.  Oncogenic Ras and Akt signaling contribute to glioblastoma formation by differential recruitment of existing mRNAs to polysomes. , 2003, Molecular cell.

[40]  Yuri Kotliarov,et al.  High-resolution global genomic survey of 178 gliomas reveals novel regions of copy number alteration and allelic imbalances. , 2006, Cancer research.

[41]  M. Nakao,et al.  Promyelocytic leukemia protein induces apoptosis due to caspase-8 activation via the repression of NFkappaB activation in glioblastoma. , 2009, Neuro-oncology.

[42]  S. Gabriel,et al.  Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1. , 2010, Cancer cell.

[43]  M Reick,et al.  Impaired cued and contextual memory in NPAS2-deficient mice. , 2000, Science.