E C Holland

Summary

Affiliation: Memorial Sloan-Kettering Cancer Center
Country: USA

Publications

  1. ncbi Dose-dependent effects of platelet-derived growth factor-B on glial tumorigenesis
    Alan H Shih
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Cancer Res 64:4783-9. 2004
  2. pmc The characteristics of astrocytomas and oligodendrogliomas are caused by two distinct and interchangeable signaling formats
    Chengkai Dai
    Department of Surgery Neurosurgery, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Neoplasia 7:397-406. 2005
  3. ncbi Applications of mouse glioma models in preclinical trials
    Xiaoyi Hu
    Department of Cell Biology and Genetics, New York, NY 10021, USA
    Mutat Res 576:54-65. 2005
  4. ncbi Genetically engineered models have advantages over xenografts for preclinical studies
    Oren J Becher
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Cancer Res 66:3355-8, discussion 3358-9. 2006
  5. ncbi Modeling and preclinical trials for gliomas
    Maria Salpietro
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Clin Neurosurg 52:104-11. 2005
  6. pmc Genetically engineered mouse models of brain cancer and the promise of preclinical testing
    Jason T Huse
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Brain Pathol 19:132-43. 2009
  7. pmc PDGF in gliomas: more than just a growth factor?
    Nanna Lindberg
    Department of Neurosurgery, Department of Cancer Biology and Genetics, and Brain Tumor Center, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, NY 10021, USA
    Ups J Med Sci 117:92-8. 2012
  8. pmc Recruited cells can become transformed and overtake PDGF-induced murine gliomas in vivo during tumor progression
    Elena I Fomchenko
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 6:e20605. 2011
  9. pmc Perifosine and CCI 779 co-operate to induce cell death and decrease proliferation in PTEN-intact and PTEN-deficient PDGF-driven murine glioblastoma
    Kenneth L Pitter
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 6:e14545. 2011
  10. pmc Astrocyte-specific expression patterns associated with the PDGF-induced glioma microenvironment
    Amanda M Katz
    Biochemistry, Cell, and Molecular Biology Program, Weill Medical College of Cornell University, New York, New York, United States of America
    PLoS ONE 7:e32453. 2012

Detail Information

Publications91

  1. ncbi Dose-dependent effects of platelet-derived growth factor-B on glial tumorigenesis
    Alan H Shih
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Cancer Res 64:4783-9. 2004
    ..Our data show that PDGFR signaling quantitatively regulates tumor grade and is required to sustain high-grade oligodendrogliomas...
  2. pmc The characteristics of astrocytomas and oligodendrogliomas are caused by two distinct and interchangeable signaling formats
    Chengkai Dai
    Department of Surgery Neurosurgery, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Neoplasia 7:397-406. 2005
    ..The ability of signaling activity to convert tumor cells from one lineage to another presents a mechanism for the development of tumors apparently comprised of cells from multiple lineages...
  3. ncbi Applications of mouse glioma models in preclinical trials
    Xiaoyi Hu
    Department of Cell Biology and Genetics, New York, NY 10021, USA
    Mutat Res 576:54-65. 2005
    ....
  4. ncbi Genetically engineered models have advantages over xenografts for preclinical studies
    Oren J Becher
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Cancer Res 66:3355-8, discussion 3358-9. 2006
    ..These new technologies will hopefully support the use of GEMs in preclinical trials and help determine if trials in GEMs are more predicative than xenografts of human responses...
  5. ncbi Modeling and preclinical trials for gliomas
    Maria Salpietro
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Clin Neurosurg 52:104-11. 2005
  6. pmc Genetically engineered mouse models of brain cancer and the promise of preclinical testing
    Jason T Huse
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Brain Pathol 19:132-43. 2009
    ..Examples showcasing the use of GEMMs in the testing of molecularly targeted therapeutics are given, and relevant topics, such as stem cell biology, in vivo imaging technology and radiotherapy, are also addressed...
  7. pmc PDGF in gliomas: more than just a growth factor?
    Nanna Lindberg
    Department of Neurosurgery, Department of Cancer Biology and Genetics, and Brain Tumor Center, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, NY 10021, USA
    Ups J Med Sci 117:92-8. 2012
    ..These fundamental questions concerning PDGF-B as a potential oncogene have not been resolved...
  8. pmc Recruited cells can become transformed and overtake PDGF-induced murine gliomas in vivo during tumor progression
    Elena I Fomchenko
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 6:e20605. 2011
    ..Glioma progression is associated with elevated growth factor signaling and loss of function of tumor suppressors Ink4a, Arf and Pten. Yet, gliomas are cellularly heterogeneous; they recruit and trap normal cells during infiltration...
  9. pmc Perifosine and CCI 779 co-operate to induce cell death and decrease proliferation in PTEN-intact and PTEN-deficient PDGF-driven murine glioblastoma
    Kenneth L Pitter
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 6:e14545. 2011
    ..It would be valuable to understand how PDGFR driven GBMs respond to Akt and mTOR inhibition...
  10. pmc Astrocyte-specific expression patterns associated with the PDGF-induced glioma microenvironment
    Amanda M Katz
    Biochemistry, Cell, and Molecular Biology Program, Weill Medical College of Cornell University, New York, New York, United States of America
    PLoS ONE 7:e32453. 2012
    ..We therefore sought to identify genes and pathways that are increased in TAAs relative to normal astrocytes and also to determine whether expression of these genes correlates with glioma behavior...
  11. pmc Identification of global alteration of translational regulation in glioma in vivo
    Karim Helmy
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 7:e46965. 2012
    ....
  12. pmc Glioblastoma subclasses can be defined by activity among signal transduction pathways and associated genomic alterations
    Cameron Brennan
    Department of Neurosurgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    PLoS ONE 4:e7752. 2009
    ..From a practical and therapeutic standpoint, classifying GBMs by signal transduction pathway activation and by mutation in pathway member genes may be particularly valuable for the development of targeted therapies...
  13. pmc 53BP1 is a haploinsufficient tumor suppressor and protects cells from radiation response in glioma
    Massimo Squatrito
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Cancer Res 72:5250-60. 2012
    ..Our data suggest that either 53BP1 or other NHEJ components may be critical molecules to be pharmacologically targeted in GBM in combination with standard therapies...
  14. ncbi Gliomagenesis: genetic alterations and mouse models
    E C Holland
    Departments of Neurosurgery, Neurology and Cell Biology, Memorial Sloan Kettering Cancer Center, 1, 275 York Avenue, New York, New York 10021, USA
    Nat Rev Genet 2:120-9. 2001
    ..Recent modelling experiments in mice are helping to delineate the molecular aetiology of this disease and are providing systems to identify and test novel and rational therapeutic strategies...
  15. ncbi Brain tumor animal models: importance and progress
    E C Holland
    Department of Cell Biology, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Curr Opin Oncol 13:143-7. 2001
    ..In addition, these mouse-modeling experiments may identify essential targets for therapy and provide test animals for preclinical trials of mechanistically designed therapeutics...
  16. ncbi Regulation of translation and cancer
    Eric C Holland
    Memorial Sloan Kettering Cancer Center, Department of Surgery Neurosurgery, New York, New York 10021, USA
    Cell Cycle 3:452-5. 2004
    ..It is not known whether this effect is sufficient to induce cancer from cells with an initial non-neoplastic gene expression profile...
  17. ncbi Signaling control of mRNA translation in cancer pathogenesis
    Eric C Holland
    Department of Surgery, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Oncogene 23:3138-44. 2004
    ..Although many studies have correlated deregulation of protein biosynthesis with cancer, it remains to be established whether this process is necessary and/or sufficient for neoplastic transformation and metastasis...
  18. ncbi Progenitor cells and glioma formation
    E C Holland
    Department of Cell Biology, Memorial Sloan Kettering Cancer Center, RRL, Rm 917B, 1275 York Ave, New York, NY 10021, USA
    Curr Opin Neurol 14:683-8. 2001
    ..These data imply that small molecules that promote differentiation may be a rational component of glioma therapy in combination with other drugs aimed at specific molecular signaling targets...
  19. ncbi Animal models of cell cycle dysregulation and the pathogenesis of gliomas
    E C Holland
    Department of Neurosurgery, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    J Neurooncol 51:265-76. 2001
    ..The results of these mouse model experiments imply a potentially complex role for cell cycle arrest disruption in human gliomagenesis...
  20. ncbi Mouse models of human cancer as tools in drug development
    Eric C Holland
    Memorial Sloan Kettering Cancer Center, Departments of Surgery Neurosurgery, Neurology, and Cell Biology and Genetics, 1275 York Avenue, New York, NY 10021, USA
    Cancer Cell 6:197-8. 2004
    ..They demonstrate that targeting signaling components downstream of tumor initiating mutations can be an effective therapeutic strategy for solid tumors...
  21. pmc Astrocytes give rise to oligodendrogliomas and astrocytomas after gene transfer of polyoma virus middle T antigen in vivo
    E C Holland
    Department of Neurosurgery, Graduate Program in Genes and Development, M D Anderson Cancer Center, Houston, Texas 77030, USA
    Am J Pathol 157:1031-7. 2000
    ..We conclude that GFAP- expressing astrocytes, with appropriate signaling abnormalities, can serve as the cell of origin for oligodendrogliomas, astrocytomas, or mixed gliomas...
  22. pmc PDGF autocrine stimulation dedifferentiates cultured astrocytes and induces oligodendrogliomas and oligoastrocytomas from neural progenitors and astrocytes in vivo
    C Dai
    Department of Neurosurgery, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA
    Genes Dev 15:1913-25. 2001
    ..Loss of Ink4a-Arf is not required for PDGF-induced glioma formation but promotes tumor progression toward a more malignant phenotype...
  23. pmc mTOR promotes survival and astrocytic characteristics induced by Pten/AKT signaling in glioblastoma
    Xiaoyi Hu
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Neoplasia 7:356-68. 2005
    ....
  24. ncbi Oncogenic Ras and Akt signaling contribute to glioblastoma formation by differential recruitment of existing mRNAs to polysomes
    Vinagolu K Rajasekhar
    Department of Surgery Neurosurgery, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Mol Cell 12:889-901. 2003
    ..These data support a model whereby Ras and Akt signaling primarily lead to cellular transformation by altering the transcriptome and producing a radical shift in the composition of mRNAs associated with actively translating polysomes...
  25. ncbi Ink4a-Arf loss cooperates with KRas activation in astrocytes and neural progenitors to generate glioblastomas of various morphologies depending on activated Akt
    Lene Uhrbom
    Department of Cell Biology, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 62:5551-8. 2002
    ..Our data strongly supports the view that one role of loss of Ink4a-Arf in gliomagenesis could be to sensitize astrocytes to transformation through dedifferentiation in response to the appropriate oncogenic stimuli...
  26. ncbi A mouse model for glioma: biology, pathology, and therapeutic opportunities
    E C Holland
    M D Anderson Cancer Center, Department of Neurosurgery, Houston, Texas 77030, USA
    Toxicol Pathol 28:171-7. 2000
    ..These genetically defined animal models for gliomas will allow for the testing of therapies that are targeted specifically at the gene products involved in the pathogenesis of gliomas...
  27. doi Akt phosphorylation of La regulates specific mRNA translation in glial progenitors
    F Brenet
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Oncogene 28:128-39. 2009
    ..Therefore, La appears to be an important contributor to Akt-mediated translational regulation of these transcripts in murine glial cells...
  28. ncbi Glioma models
    C Dai
    Departments of Cell Biology, Neurology, and Neurosurgery, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA
    Biochim Biophys Acta 1551:M19-27. 2001
    ....
  29. doi c-Myc and beta-catenin cooperate with loss of p53 to generate multiple members of the primitive neuroectodermal tumor family in mice
    H Momota
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Oncogene 27:4392-401. 2008
    ..These data provide insights into the biology and classification of human PNETs and suggest that multiple tumor types or variants can be generated from a fixed set of genetic abnormalities...
  30. ncbi Mouse models of brain tumors and their applications in preclinical trials
    Elena I Fomchenko
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Clin Cancer Res 12:5288-97. 2006
    ..These mouse models, in turn, increase our understanding of brain tumor initiation, formation, progression, and metastasis, providing an experimental system to discover novel therapeutic targets and test various therapeutic agents...
  31. ncbi Perifosine inhibits multiple signaling pathways in glial progenitors and cooperates with temozolomide to arrest cell proliferation in gliomas in vivo
    Hiroyuki Momota
    Department of Cancer Biology and Genetics and Surgery Neurosurgery and Neurology, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 65:7429-35. 2005
    ..01). These results indicate that perifosine is an effective drug in gliomas in which Akt and Ras-Erk 1/2 pathways are frequently activated, and may be a new candidate for glioma treatment in the clinic...
  32. ncbi Modeling gliomagenesis with somatic cell gene transfer using retroviral vectors
    L Uhrbom
    Department of Cell Biology, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    J Neurooncol 53:297-305. 2001
    ..The current models provide tumors, which are genetically and histologically similar to their human counterparts, making them attractive to use in drug discovery for treatment of gliomas...
  33. ncbi Gene expression microarray analysis reveals YKL-40 to be a potential serum marker for malignant character in human glioma
    Meena K Tanwar
    Department of Surgery Neurosurgery, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 62:4364-8. 2002
    ..YKL-40 serum levels were substantially elevated in many of the GBM patients. Statistical analysis of these data indicates that in patients with glioma, serum YKL-40 levels correlate with tumor grade and potentially tumor burden in GBM...
  34. ncbi Combined activation of Ras and Akt in neural progenitors induces glioblastoma formation in mice
    E C Holland
    Department of Neurosurgery, MD Anderson Cancer Center, Houston, Texas, USA
    Nat Genet 25:55-7. 2000
    ..11), and we show here that Akt activity is increased in most of these tumours, implying that combined activation of these two pathways accurately models the biology of this disease...
  35. ncbi Molecular study of malignant gliomas treated with epidermal growth factor receptor inhibitors: tissue analysis from North American Brain Tumor Consortium Trials 01-03 and 00-01
    Andrew B Lassman
    Department of Neurology, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Clin Cancer Res 11:7841-50. 2005
    ....
  36. ncbi Allelic losses at 1p36 and 19q13 in gliomas: correlation with histologic classification, definition of a 150-kb minimal deleted region on 1p36, and evaluation of CAMTA1 as a candidate tumor suppressor gene
    Violetta Barbashina
    Department of Pathology, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Clin Cancer Res 11:1119-28. 2005
    ..To better define the histologic correlates of different patterns of 1p and 19q loss, we evaluated 1p/19q status in a large group of gliomas. This also allowed us to define a very small minimal deleted region (MDR) on 1p36...
  37. pmc Tuberous sclerosis complex suppression in cerebellar development and medulloblastoma: separate regulation of mammalian target of rapamycin activity and p27 Kip1 localization
    Bobby Bhatia
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 69:7224-34. 2009
    ....
  38. ncbi Postgenomic global analysis of translational control induced by oncogenic signaling
    Vinagolu K Rajasekhar
    Department of Surgery Neurosurgery, Neurology, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, NY 10021, USA
    Oncogene 23:3248-64. 2004
    ..To what degree this translational control is either necessary or sufficient for tumor formation or maintenance remains to be determined...
  39. ncbi Incorporating molecular tools into clinical trials and treatment for gliomas?
    Andrew B Lassman
    Department of Neurology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Curr Opin Neurol 20:708-11. 2007
    ..Knowledge of the molecular biology of gliomas may improve therapy. This review highlights several recent studies on this topic...
  40. ncbi Early detection and prognosis of ovarian cancer using serum YKL-40
    Jakob Dupont
    Developmental Chemotherapy Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, Howard 905, 1275 York Ave, New York, NY 10021, USA
    J Clin Oncol 22:3330-9. 2004
    ..YKL-40 is a secreted glycoprotein (chitinase family). We compared YKL-40 with two ovarian cancer serum markers, CA125 and CA15-3, for the detection of early-stage ovarian cancer...
  41. pmc Dynamic small-animal PET imaging of tumor proliferation with 3'-deoxy-3'-18F-fluorothymidine in a genetically engineered mouse model of high-grade gliomas
    Michelle S Bradbury
    Department of Radiology, Sloan Kettering Institute for Cancer Research, New York, New York 10021, USA
    J Nucl Med 49:422-9. 2008
    ..Our goal was to develop a robust and reproducible method of kinetic analysis for the quantitative evaluation of tumor proliferation...
  42. ncbi YKL-40 and matrix metalloproteinase-9 as potential serum biomarkers for patients with high-grade gliomas
    Adilia Hormigo
    Clinical Laboratories, Neurosurgical Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Clin Cancer Res 12:5698-704. 2006
    ..We obtained prospective longitudinal serum samples from patients with gliomas to determine whether YKL-40 or MMP-9 could be used as serum markers...
  43. ncbi Genetic modeling of glioma formation in mice
    Martin Begemann
    Department of Neurology, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Brain Pathol 12:117-32. 2002
    ....
  44. pmc PI3K pathway regulates survival of cancer stem cells residing in the perivascular niche following radiation in medulloblastoma in vivo
    Dolores Hambardzumyan
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Genes Dev 22:436-48. 2008
    ..These cellular characteristics are similar to human medulloblastomas. Finally, inhibition of Akt signaling sensitizes cells in the perivascular region to radiation-induced apoptosis...
  45. pmc MRI of mouse models for gliomas shows similarities to humans and can be used to identify mice for preclinical trials
    Jason A Koutcher
    Department of Medical Physics, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Neoplasia 4:480-5. 2002
    ..In contrast, low-grade murine oligodendrogliomas do not reveal contrast enhancement, similar to human tumors. MRI can be used to identify mice with brain neoplasms as inclusion criteria in preclinical trials...
  46. pmc Notch signaling enhances nestin expression in gliomas
    Alan H Shih
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Neoplasia 8:1072-82. 2006
    ..However, activation of Notch alone is unable to induce this cellular expansion. These data suggest that Notch may have a contributing role in the stem-like character of glioma cells...
  47. doi Gli activity correlates with tumor grade in platelet-derived growth factor-induced gliomas
    Oren J Becher
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Cancer Res 68:2241-9. 2008
    ..Lastly, we observe that SHH is similarly expressed in human gliomas and note that an intact tumor microenvironment or neurosphere conditions in vitro are required for Gli activity...
  48. ncbi In vivo multiple-mouse imaging at 1.5 T
    S Xu
    Department of Medical Physics, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Magn Reson Med 49:551-7. 2003
    ..The multiple mouse coil is simple in construction and may be implemented without any significant modification to the hardware or software on a clinical scanner...
  49. pmc Constitutive activation of Raf-1 induces glioma formation in mice
    Yelena Lyustikman
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Neoplasia 10:501-10. 2008
    ..Our study suggests that the oncogenic effect of KRas in glioma formation may be transduced at least in part through Raf signaling and that therapeutic targeting of this pathway may be beneficial in glioma treatment...
  50. pmc p190RhoGAP can act to inhibit PDGF-induced gliomas in mice: a putative tumor suppressor encoded on human chromosome 19q13.3
    Rebecca M Wolf
    Department of Cell Biology, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Genes Dev 17:476-87. 2003
    ..This evidence strongly suggests that p190 regulates critical components of PDGF oncogenesis and can act as a tumor suppressor in PDGF-induced gliomas by down-regulating Rho activity...
  51. pmc c-Myc enhances sonic hedgehog-induced medulloblastoma formation from nestin-expressing neural progenitors in mice
    Ganesh Rao
    Department of Neurosurgery, University of Utah School of Medicine and Huntsman Cancer Institute, Salt Lake City, UT 84132, USA
    Neoplasia 5:198-204. 2003
    ..We conclude that nestin-expressing neural progenitors, present in the cerebellum at birth, can act as the cells-of-origin for medulloblastoma, and that c-Myc cooperates with Shh to enhance tumorigenicity...
  52. pmc PDGFRA gene rearrangements are frequent genetic events in PDGFRA-amplified glioblastomas
    Tatsuya Ozawa
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Genes Dev 24:2205-18. 2010
    ..These results suggest the possibility that these PDGFRA mutants behave as oncogenes in this subset of gliomas, and that the prevalence of such rearrangements may have been considerably underestimated...
  53. ncbi Sonic hedgehog and insulin-like growth factor signaling synergize to induce medulloblastoma formation from nestin-expressing neural progenitors in mice
    Ganesh Rao
    Department of Neurosurgery, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132 2303, USA
    Oncogene 23:6156-62. 2004
    ..These results indicate that combined activation of the Shh/Ptc and IGF signaling pathways is an important mechanism in MB pathogenesis...
  54. ncbi EGFR signaling is differentially activated in patient-derived glioblastoma stem cells
    Brian M Howard
    Laboratory for Translational Stem Cell Research, Weill Cornell Brain Tumor Center, Department of Neurological Surgery, Weill Cornell Medical College, New York, New York, 10065, USA
    J Exp Ther Oncol 8:247-60. 2010
    ..Sphere formation by EGFR-/ PTEN- GSCs was independent of EGF stimulation, but dependant on B27 growth supplement. Our data suggest that EGFR+/PTEN+ GSCs are susceptible to anti-EGFR therapy in vitro...
  55. pmc Somatic mutations of the Parkinson's disease-associated gene PARK2 in glioblastoma and other human malignancies
    Selvaraju Veeriah
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Nat Genet 42:77-82. 2010
    ..These data strongly point to PARK2 as a tumor suppressor on 6q25.2-q27. Thus, PARK2, a gene that causes neuronal dysfunction when mutated in the germline, may instead contribute to oncogenesis when altered in non-neuronal somatic cells...
  56. pmc PTEN/PI3K/Akt pathway regulates the side population phenotype and ABCG2 activity in glioma tumor stem-like cells
    Anne Marie Bleau
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cell Stem Cell 4:226-35. 2009
    ..This Akt-induced ABCG2 activation results from its transport to the plasma membrane. Temozolomide, the standard treatment of gliomas, although not an ABCG2 substrate, increases the SP in glioma cells, especially in cells missing PTEN...
  57. doi New strategy for the analysis of phenotypic marker antigens in brain tumor-derived neurospheres in mice and humans
    Anne Marie Bleau
    Department of Neurological Surgery, Memorial Sloan Kettering Cancer Center, New York, USA
    Neurosurg Focus 24:E28. 2008
    ..Therefore, the purpose of this study was to develop a new method to better understand the proteomic profile of the entire population of cells within a sphere...
  58. pmc TRIM3, a tumor suppressor linked to regulation of p21(Waf1/Cip1.)
    Y Liu
    Programs in Molecular Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Oncogene 33:308-15. 2014
    ..Thus, we conclude that TRIM3 is a tumor suppressor mapping to chromosome 11p15.5 and that it might block tumor growth by sequestering p21 and preventing it from facilitating the accumulation of cyclin D1-cdk4. ..
  59. doi Activated EGFR signaling increases proliferation, survival, and migration and blocks neuronal differentiation in post-natal neural stem cells
    Angel Ayuso-Sacido
    Department of Neurosurgery, Neurosurgical Laboratory for Translational Stem Cell Research, Weill Cornell Brain Tumor Center, Weill Cornell Medical College of Cornell University, New York, NY, USA
    J Neurooncol 97:323-37. 2010
    ..Understanding the regulatory mechanisms of NSCs may lend insight into deregulated mechanisms of GBM TSC invasion, proliferation, survival and resistance to current treatment modalities...
  60. doi Glioma formation, cancer stem cells, and akt signaling
    Dolores Hambardzumyan
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Stem Cell Rev 4:203-10. 2008
    ..In human gliomas, these two theories are not mutually exclusive. In this review we will summarize both theories, and highlight outstanding issues that remain to be resolved...
  61. ncbi Cancer stem cells and survival pathways
    Dolores Hambardzumyan
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Cell Cycle 7:1371-8. 2008
    ..1) It remains to be determined whether this mechanism of tumor resistance applies to the more complex stem-cell niche and tumor bulk of gliomas...
  62. doi Targeting brain cancer: advances in the molecular pathology of malignant glioma and medulloblastoma
    Jason T Huse
    Departments of Pathology, 408 East 69th Street Z1304, New York, NY 10065, USA
    Nat Rev Cancer 10:319-31. 2010
    ..This Review summarizes these developments in the context of the evolving notion of molecular pathology and discusses the implications that this work has on the design of new treatment regimens...
  63. ncbi Serum peptide profiling by magnetic particle-assisted, automated sample processing and MALDI-TOF mass spectrometry
    Josep Villanueva
    Protein Center, Molecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Anal Chem 76:1560-70. 2004
    ..This, in turn, served to create a learning algorithm that correctly predicted 96.4% of the samples as either normal or diseased...
  64. pmc Trapping the mouse genome to hunt human alterations
    Anne Marie Bleau
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 104:7737-8. 2007
  65. pmc The PTEN-regulating microRNA miR-26a is amplified in high-grade glioma and facilitates gliomagenesis in vivo
    Jason T Huse
    Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Genes Dev 23:1327-37. 2009
    ..Our results document a new epigenetic mechanism for PTEN regulation in glioma and further highlight dysregulation of Akt signaling as crucial to the development of these tumors...
  66. ncbi Platelet-derived growth factor-mediated gliomagenesis and brain tumor recruitment
    Elena I Fomchenko
    Department of Cancer Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Neurosurg Clin N Am 18:39-58, viii. 2007
    ..In this view, glioma formation involves recruitment of cells from the adjacent brain and possibly other sites...
  67. pmc Oncogenic YAP promotes radioresistance and genomic instability in medulloblastoma through IGF2-mediated Akt activation
    A Fernandez-L
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Oncogene 31:1923-37. 2012
    ..Our results establish a central role for YAP in counteracting radiation-based therapies and driving genomic instability, and indicate the YAP/IGF2/Akt axis as a therapeutic target in medulloblastoma...
  68. ncbi Surgical resection of intrinsic insular tumors: complication avoidance
    F F Lang
    Department of Neurosurgery, The University of Texas M D Anderson Cancer Center, Houston, USA
    J Neurosurg 95:638-50. 2001
    ....
  69. pmc The perivascular niche microenvironment in brain tumor progression
    Nikki Charles
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Cell Cycle 9:3012-21. 2010
    ..Characterization of the signaling pathways and intercellular communication between resident cell types in the microvascular niche of brain tumors is critical to the identification of potential BTSC-specific targets for therapy...
  70. pmc Preclinical evaluation of radiation and perifosine in a genetically and histologically accurate model of brainstem glioma
    Oren J Becher
    Departments of Cancer Biology and Genetics, Brain Tumor Center, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 70:2548-57. 2010
    ..92). Perifosine + 10 Gy did not result in a significantly increased survival relative to 10 Gy alone (P = 0.23). This PDGF-induced BSG model can serve as a preclinical tool for the testing of novel agents...
  71. ncbi Organ donors with malignant gliomas: an update
    Federic P Collignon
    Department of Surgery, Division of Neurosurgery, Memorial Sloane Kettering Cancer Center, 1275 York Avenue, New York, NY, USA
    Am J Transplant 4:15-21. 2004
    ..We will then present recent knowledge regarding basic glioma biology that speaks to their metastatic potential and suggest rational strategies for the post-transplant management of recipients of organs from donors with glioma...
  72. pmc MYC expression promotes the proliferation of neural progenitor cells in culture and in vivo
    Dan Fults
    Department of Neurosurgery, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City 84132 2303, USA
    Neoplasia 4:32-9. 2002
    ..Although overexpression of MYC is not sufficient to cause intraparenchymal tumors, it may facilitate PNET formation by sustaining the growth of undifferentiated progenitor cells...
  73. ncbi The ABCG2 resistance network of glioblastoma
    Anne Marie Bleau
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Cell Cycle 8:2936-44. 2009
    ....
  74. ncbi Radiation resistance and stem-like cells in brain tumors
    Dolores Hambardzumyan
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Cell 10:454-6. 2006
    ..The data raise many questions about the details of radiobiology of stem-like cells in their native environment within tumors in vivo. These answers may lead to better optimization of radiation treatments and schedules for these patients...
  75. ncbi Bioluminescence technology for imaging cell proliferation
    Hiroyuki Momota
    Department of Cancer Biology, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Curr Opin Biotechnol 16:681-6. 2005
    ..These technologies support more detailed preclinical trials and could enable other biological pathways to be monitored in living cells...
  76. ncbi Developmental neurobiology and the origin of brain tumors
    Alan H Shih
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    J Neurooncol 70:125-36. 2004
    ..By appreciating the inter-relationship between tumor formation and development, we maybe able to design new therapeutics targeting tumors for new modes of treatment...
  77. ncbi Astrocyte differentiation states and glioma formation
    Chengkai Dai
    Department of Cell Biology, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer J 9:72-81. 2003
    ..In this review, we discuss new insights into the parallels between glial differentiation and glioma formation as well as the potential application of differentiation-inducing therapy...
  78. ncbi Origins of brain tumors--a disease of stem cells?
    Elena I Fomchenko
    Department of Cancer Biology and Genetics, Weill Cornell Graduate School of Medical Sciences, New York, NY, USA
    Nat Clin Pract Neurol 2:288-9. 2006
  79. ncbi Platelet-derived growth factor (PDGF) and glial tumorigenesis
    Alan H Shih
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cancer Lett 232:139-47. 2006
    ..The development of small molecules that inhibit the PDGF receptor and various subsequent signaling components promises to introduce new approaches to the treatment of gliomas...
  80. ncbi Stem cells and brain cancer
    Elena I Fomchenko
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Exp Cell Res 306:323-9. 2005
    ..It is likely that a complete description of the role of stem cells in brain tumors will be more complex than our current models...
  81. pmc Perivascular nitric oxide activates notch signaling and promotes stem-like character in PDGF-induced glioma cells
    Nikki Charles
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cell Stem Cell 6:141-52. 2010
    ..This mechanism is conserved in human PDGFR amplified gliomas. The NO/cGMP/PKG pathway's promotion of stem cell-like character in the tumor PVN may identify therapeutic targets for this subset of gliomas...
  82. ncbi Magnetic resonance imaging determination of tumor grade and early response to temozolomide in a genetically engineered mouse model of glioma
    Patrick McConville
    MIR Preclinical Services, Inc, Ann Arbor, Michigan, USA
    Clin Cancer Res 13:2897-904. 2007
    ..The nestin tv-a (Ntv-a) genetically engineered mouse spontaneously develops glioma when infected with ALV-A expressing platelet-derived growth factor, resulting in autocrine platelet-derived growth factor signaling...
  83. pmc Insulin-like growth factor binding protein 2 promotes glioma development and progression
    Sarah M Dunlap
    Department of Pathology, University of Texas M D Anderson Cancer Center, Houston, TX 77030, USA
    Proc Natl Acad Sci U S A 104:11736-41. 2007
    ..Thus, this study provides definitive evidence that IGFBP2 plays a key role in activation of the Akt pathway and collaborates with K-Ras or PDGFB in the development and progression of two major types of glioma...
  84. pmc Dissection of the c-Kit signaling pathway in mouse primordial germ cells by retroviral-mediated gene transfer
    Maria P De Miguel
    Kimmel Cancer Center, Thomas Jefferson University, Bluemle Life Sciences Building, Room 706, 233 South 10th Street, Philadelphia, PA 19107, USA
    Proc Natl Acad Sci U S A 99:10458-63. 2002
    ..Such technology for manipulating gene expression in PGCs will allow many of the molecular mechanisms regulating germ cell growth, behavior, and differentiation to be comprehensively analyzed...
  85. ncbi Cell type-specific tumor suppression by Ink4a and Arf in Kras-induced mouse gliomagenesis
    Lene Uhrbom
    Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala, Sweden
    Cancer Res 65:2065-9. 2005
    ..Thus, Ink4a and Arf have independent and differential tumor suppressor functions in vivo in the glial cell compartment...
  86. ncbi Huntingtin interacting protein 1 is a novel brain tumor marker that associates with epidermal growth factor receptor
    Sarah V Bradley
    Department of Internal Medicine, University of Michigan Medical School, 1500 East Medical Center Drive, Ann Arbor, MI 48109, USA
    Cancer Res 67:3609-15. 2007
    ..Further investigation of HIP1 function in brain cancer biology and validation of its use as a prognostic or predictive brain tumor marker are now warranted...
  87. ncbi Using mice to decipher the molecular genetics of brain tumors
    Göran Hesselager
    Departments of Neurosciences Division of Neurosurgery and Genetics and Pathology, University Hospital, Uppsala, Sweden
    Neurosurgery 53:685-94; discussion 695. 2003
    ..We present here a review of current models, with a focus on gliomas and medulloblastomas...
  88. ncbi Cooperative translational control of gene expression by Ras and Akt in cancer
    Andrew T Parsa
    Department of Neurological Surgery, University of California San Francisco, CA 94143, USA
    Trends Mol Med 10:607-13. 2004
    ..The downstream components of these pathways have provided therapeutic targets that are currently being tested in clinical trials...
  89. ncbi Dissecting tumor maintenance requirements using bioluminescence imaging of cell proliferation in a mouse glioma model
    Lene Uhrbom
    Uppsala University, Department of Genetics and Pathology, Rudbeck Laboratory, SE 75185 Uppsala, Sweden
    Nat Med 10:1257-60. 2004
    ..In these platelet-derived growth factor (PDGF)-driven oligodendrogliomas, G1 cell-cycle arrest is generated by blockade of either the PDGF receptor or mTOR using small-molecule inhibitors...
  90. pmc Differential exoprotease activities confer tumor-specific serum peptidome patterns
    Josep Villanueva
    Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    J Clin Invest 116:271-84. 2006
    ..Our findings also have important implications for future peptide biomarker discovery efforts...
  91. ncbi Molecular imaging of Akt kinase activity
    Limin Zhang
    Department of Radiation Oncology, University of Michigan, Ann Arbor, Michigan 48109, USA
    Nat Med 13:1114-9. 2007
    ..The results provide unique insights into the pharmacokinetics and pharmacodynamics of agents that modulate Akt activity, revealing the usefulness of this reporter for rapid dose and schedule optimization in the drug development process...

Research Grants16

  1. Pre-Clinical Trials of GEM Models for Gliomas
    Eric Holland; Fiscal Year: 2007
    ..abstract_text> ..
  2. Modeling the effects of INK4 alpha ARF loss on gliomas
    Eric Holland; Fiscal Year: 2001
    ....
  3. The Role of Signaling Pathways in Brain Tumors in Mice
    Eric Holland; Fiscal Year: 2009
    ..This grant proposes to use mouse models medulloblastomas and gliomas to understand the biology of stem cells in these tumors and their response to therapy. ..
  4. Requirements for generation and maintenance of gliomas
    Eric Holland; Fiscal Year: 2007
    ..In this grant we will address these questions using the RCAS/tv-a mouse modeling system for Ras + Akt-induced gliomas. ..
  5. Requirements for generation and maintenance of gliomas
    Eric Holland; Fiscal Year: 2006
    ..In this grant we will address these questions using the RCAS/tv-a mouse modeling system for Ras + Akt-induced gliomas. ..
  6. Pre-Clinical Trials of GEM Models for Gliomas
    Eric Holland; Fiscal Year: 2006
    ..abstract_text> ..
  7. Requirements for generation and maintenance of gliomas
    Eric Holland; Fiscal Year: 2005
    ..In this grant we will address these questions using the RCAS/tv-a mouse modeling system for Ras + Akt-induced gliomas. ..
  8. Pre-Clinical Trials of GEM Models for Gliomas
    Eric Holland; Fiscal Year: 2005
    ..abstract_text> ..
  9. Requirements for generation and maintenance of gliomas
    Eric Holland; Fiscal Year: 2004
    ..In this grant we will address these questions using the RCAS/tv-a mouse modeling system for Ras + Akt-induced gliomas. ..
  10. Pre-Clinical Trials of GEM Models for Gliomas
    Eric Holland; Fiscal Year: 2004
    ..abstract_text> ..
  11. Modeling the effects of INK4 alpha ARF loss on gliomas
    Eric Holland; Fiscal Year: 2003
    ....
  12. Requirements for generation and maintenance of gliomas
    Eric Holland; Fiscal Year: 2003
    ..In this grant we will address these questions using the RCAS/tv-a mouse modeling system for Ras + Akt-induced gliomas. ..
  13. Pre-Clinical Trials of GEM Models for Gliomas
    Eric Holland; Fiscal Year: 2003
    ..abstract_text> ..
  14. Modeling the effects of INK4 alpha ARF loss on gliomas
    Eric Holland; Fiscal Year: 2002
    ....
  15. The Role of Signaling Pathways in Brain Tumors in Mice
    Eric C Holland; Fiscal Year: 2010
    ..This grant proposes to use mouse models medulloblastomas and gliomas to understand the biology of stem cells in these tumors and their response to therapy. ..