neoplasms

Summary

Summary: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.

Top Publications

  1. ncbi The hallmarks of cancer
    D Hanahan
    Department of Biochemistry, Hormone Research Institute, University of California at San Francisco, 94143, USA
    Cell 100:57-70. 2000
  2. ncbi MicroRNA expression profiles classify human cancers
    Jun Lu
    Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02141, USA
    Nature 435:834-8. 2005
  3. ncbi Oncomirs - microRNAs with a role in cancer
    Aurora Esquela-Kerscher
    Yale University, Department of Molecular, Cellular and Developmental Biology, 266 Whitney Avenue, New Haven, Connecticut 06520, USA
    Nat Rev Cancer 6:259-69. 2006
  4. ncbi MicroRNA signatures in human cancers
    George A Calin
    Department of Molecular Virology, Immunology and Medical Genetics and Comprehensive Cancer Center, Ohio State University, Columbus, Ohio 43210, USA
    Nat Rev Cancer 6:857-66. 2006
  5. pmc Inflammation and cancer
    Lisa M Coussens
    Cancer Research Institute, Department of Pathology, University of California, San Francisco, California 94143, USA
    Nature 420:860-7. 2002
  6. ncbi Stem cells, cancer, and cancer stem cells
    T Reya
    Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Palo Alto, California 94305, USA
    Nature 414:105-11. 2001
  7. doi Cancer-related inflammation
    Alberto Mantovani
    Istituto Clinico Humanitas IRCCS, Via Manzoni 56, Rozzano, 20089 Milan, Italy
    Nature 454:436-44. 2008
  8. pmc Understanding the Warburg effect: the metabolic requirements of cell proliferation
    Matthew G Vander Heiden
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Science 324:1029-33. 2009
  9. pmc A microRNA expression signature of human solid tumors defines cancer gene targets
    Stefano Volinia
    Department of Molecular Virology, Immunology, and Medical Genetics and Cancer Comprehensive Center, Ohio State University, Columbus, OH 43210, USA
    Proc Natl Acad Sci U S A 103:2257-61. 2006
  10. ncbi New guidelines to evaluate the response to treatment in solid tumors. European Organization for Research and Treatment of Cancer, National Cancer Institute of the United States, National Cancer Institute of Canada
    P Therasse
    European Organization for Research and Treatment of Cancer, Brussels, Belgium
    J Natl Cancer Inst 92:205-16. 2000

Detail Information

Publications247 found, 100 shown here

  1. ncbi The hallmarks of cancer
    D Hanahan
    Department of Biochemistry, Hormone Research Institute, University of California at San Francisco, 94143, USA
    Cell 100:57-70. 2000
  2. ncbi MicroRNA expression profiles classify human cancers
    Jun Lu
    Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02141, USA
    Nature 435:834-8. 2005
    ..These findings highlight the potential of miRNA profiling in cancer diagnosis...
  3. ncbi Oncomirs - microRNAs with a role in cancer
    Aurora Esquela-Kerscher
    Yale University, Department of Molecular, Cellular and Developmental Biology, 266 Whitney Avenue, New Haven, Connecticut 06520, USA
    Nat Rev Cancer 6:259-69. 2006
    ..miRNAs have been shown to repress the expression of important cancer-related genes and might prove useful in the diagnosis and treatment of cancer...
  4. ncbi MicroRNA signatures in human cancers
    George A Calin
    Department of Molecular Virology, Immunology and Medical Genetics and Comprehensive Cancer Center, Ohio State University, Columbus, Ohio 43210, USA
    Nat Rev Cancer 6:857-66. 2006
    ..In addition, profiling has been exploited to identify miRNA genes that might represent downstream targets of activated oncogenic pathways, or that target protein-coding genes involved in cancer...
  5. pmc Inflammation and cancer
    Lisa M Coussens
    Cancer Research Institute, Department of Pathology, University of California, San Francisco, California 94143, USA
    Nature 420:860-7. 2002
    ..These insights are fostering new anti-inflammatory therapeutic approaches to cancer development...
  6. ncbi Stem cells, cancer, and cancer stem cells
    T Reya
    Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Palo Alto, California 94305, USA
    Nature 414:105-11. 2001
    ....
  7. doi Cancer-related inflammation
    Alberto Mantovani
    Istituto Clinico Humanitas IRCCS, Via Manzoni 56, Rozzano, 20089 Milan, Italy
    Nature 454:436-44. 2008
    ..The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment...
  8. pmc Understanding the Warburg effect: the metabolic requirements of cell proliferation
    Matthew G Vander Heiden
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Science 324:1029-33. 2009
    ..A better understanding of the mechanistic links between cellular metabolism and growth control may ultimately lead to better treatments for human cancer...
  9. pmc A microRNA expression signature of human solid tumors defines cancer gene targets
    Stefano Volinia
    Department of Molecular Virology, Immunology, and Medical Genetics and Cancer Comprehensive Center, Ohio State University, Columbus, OH 43210, USA
    Proc Natl Acad Sci U S A 103:2257-61. 2006
    ..Our results indicate that miRNAs are extensively involved in cancer pathogenesis of solid tumors and support their function as either dominant or recessive cancer genes...
  10. ncbi New guidelines to evaluate the response to treatment in solid tumors. European Organization for Research and Treatment of Cancer, National Cancer Institute of the United States, National Cancer Institute of Canada
    P Therasse
    European Organization for Research and Treatment of Cancer, Brussels, Belgium
    J Natl Cancer Inst 92:205-16. 2000
    ..Methods of assessing tumor lesions are better codified, briefly within the guidelines and in more detail in Appendix I. All other aspects of response evaluation have been discussed, reviewed, and amended whenever appropriate...
  11. pmc Human microRNA genes are frequently located at fragile sites and genomic regions involved in cancers
    George Adrian Calin
    Department of Microbiology and Immunology, Division of Clinical Pharmacology, Biostatistics Section, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Proc Natl Acad Sci U S A 101:2999-3004. 2004
    ..These data provide a catalog of miR genes that may have roles in cancer and argue that the full complement of miRs in a genome may be extensively involved in cancers...
  12. ncbi Mutations of the BRAF gene in human cancer
    Helen Davies
    Cancer Genome Project, The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, CB10 1SA, UK
    Nature 417:949-54. 2002
    ..As BRAF is a serine/threonine kinase that is commonly activated by somatic point mutation in human cancer, it may provide new therapeutic opportunities in malignant melanoma...
  13. ncbi Epithelial-mesenchymal transitions in tumour progression
    Jean Paul Thiery
    Centre National Recherche Scientifique Unité Mixte Recherche, 144 Institut Curie, 26 Rue d Ulm, 75248 Paris Cedex 05, France
    Nat Rev Cancer 2:442-54. 2002
  14. pmc COSMIC: mining complete cancer genomes in the Catalogue of Somatic Mutations in Cancer
    Simon A Forbes
    Cancer Genome Project, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, CB10 1SA Cambridge, UK
    Nucleic Acids Res 39:D945-50. 2011
    ..With all genomic information recently updated to GRCh37, COSMIC integrates many diverse types of mutation information and is making much closer links with Ensembl and other data resources...
  15. doi Cancer stem cells in solid tumours: accumulating evidence and unresolved questions
    Jane E Visvader
    VBCRC Laboratory, The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia
    Nat Rev Cancer 8:755-68. 2008
    ..The clinical relevance of CSCs remains a fundamental issue but preliminary findings indicate that specific targeting may be possible...
  16. doi Epigenetics in cancer
    Manel Esteller
    Cancer Epigenetics Laboratory, Spanish National Cancer Research Center, Madrid, Spain
    N Engl J Med 358:1148-59. 2008
  17. pmc The epigenomics of cancer
    Peter A Jones
    Department of Urology, Biochemistry, and Molecular Biology, USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA 90089, USA
    Cell 128:683-92. 2007
    ....
  18. ncbi Global cancer statistics, 2002
    D Max Parkin
    Unit of Descriptive Epidemiology, International Agency for Research on Cancer, Lyon, France
    CA Cancer J Clin 55:74-108. 2005
    ..Most of the international variation is due to exposure to known or suspected risk factors related to lifestyle or environment, and provides a clear challenge to prevention...
  19. ncbi Normalization of tumor vasculature: an emerging concept in antiangiogenic therapy
    Rakesh K Jain
    E L Steele Lab for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, and Harvard Medical School, COX 7, 100 Blossom Street, Boston, MA 02114, USA
    Science 307:58-62. 2005
    ....
  20. doi Cancer immunoediting: integrating immunity's roles in cancer suppression and promotion
    Robert D Schreiber
    Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO 63110, USA
    Science 331:1565-70. 2011
    ..Here, we discuss a unifying conceptual framework called "cancer immunoediting," which integrates the immune system's dual host-protective and tumor-promoting roles...
  21. pmc An embryonic stem cell-like gene expression signature in poorly differentiated aggressive human tumors
    Ittai Ben-Porath
    Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA
    Nat Genet 40:499-507. 2008
    ....
  22. pmc The landscape of somatic copy-number alteration across human cancers
    Rameen Beroukhim
    Cancer Program and Medical and Population Genetics Group, The Broad Institute of M I T and Harvard, 7 Cambridge Center
    Nature 463:899-905. 2010
    ..Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types...
  23. pmc Frequent deletions and down-regulation of micro- RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia
    George Adrian Calin
    Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Proc Natl Acad Sci U S A 99:15524-9. 2002
    ..Detailed deletion and expression analysis shows that miR15 and miR16 are located within a 30-kb region of loss in CLL, and that both genes are deleted or down-regulated in the majority ( approximately 68%) of CLL cases...
  24. pmc TGFbeta in Cancer
    Joan Massague
    Cancer Biology and Genetics Program, and Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cell 134:215-30. 2008
    ..The mechanistic basis and clinical relevance of TGFbeta's role in cancer is becoming increasingly clear, paving the way for a better understanding of the complexity and therapeutic potential of this pathway...
  25. ncbi The phosphoinositide 3-kinase pathway
    Lewis C Cantley
    Department of Cell Biology, Harvard Medical School and Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA 02115 5713, USA
    Science 296:1655-7. 2002
    ..The PI3K pathway is implicated in human diseases including diabetes and cancer, and understanding the intricacies of this pathway may provide new avenues for therapuetic intervention...
  26. ncbi The phosphatidylinositol 3-Kinase AKT pathway in human cancer
    Igor Vivanco
    Department of Medicine and Molecular Biology Institute, UCLA School of Medicine, 11 935 Factor Building, 10833 LeConte Avenue, Los Angeles, California 90095, USA
    Nat Rev Cancer 2:489-501. 2002
  27. pmc Matrix metalloproteinases: regulators of the tumor microenvironment
    Kai Kessenbrock
    Department of Anatomy and Biomedical Sciences Program, University of California, San Francisco, CA 94143 0452, USA
    Cell 141:52-67. 2010
    ..These aspects of MMP function are reorienting our approaches to cancer therapy...
  28. pmc Myeloid-derived suppressor cells as regulators of the immune system
    Dmitry I Gabrilovich
    Department of Oncologic Sciences, H Lee Moffitt Cancer Center and Research Institute, University of South Florida, Tampa, Florida 33612, USA
    Nat Rev Immunol 9:162-74. 2009
    ..In this Review, we discuss the origin, mechanisms of expansion and suppressive functions of MDSCs, as well as the potential to target these cells for therapeutic benefit...
  29. pmc A census of human cancer genes
    P Andrew Futreal
    Cancer Genome Project, Human Genome Analysis Group and Pfam Group, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton Cambs, CB10 1SA, UK
    Nat Rev Cancer 4:177-83. 2004
  30. ncbi Angiogenesis in cancer and other diseases
    P Carmeliet
    The Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology, KU Leuven, Belgium
    Nature 407:249-57. 2000
    ..This integrated understanding is leading to the development of a number of exciting and bold approaches to treat cancer and other diseases. But owing to several unanswered questions, caution is needed...
  31. pmc A comprehensive catalogue of somatic mutations from a human cancer genome
    Erin D Pleasance
    Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK
    Nature 463:191-6. 2010
    ..The results illustrate the power of a cancer genome sequence to reveal traces of the DNA damage, repair, mutation and selection processes that were operative years before the cancer became symptomatic...
  32. doi Regulation of cancer cell metabolism
    Rob A Cairns
    The Campbell Family Cancer Research Institute, Toronto, ON M56 2M9, Canada
    Nat Rev Cancer 11:85-95. 2011
    ....
  33. ncbi Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes
    Alberto Mantovani
    Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, I 20157 Milan, Italy
    Trends Immunol 23:549-55. 2002
    ..These functionally polarized cells, and similarly oriented or immature dendritic cells present in tumors, have a key role in subversion of adaptive immunity and in inflammatory circuits that promote tumor growth and progression...
  34. ncbi Cancer metastasis: building a framework
    Gaorav P Gupta
    Cancer Biology and Genetics Program, Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cell 127:679-95. 2006
    ..Recent conceptual and technological advances promote our understanding of the origins and nature of cancer metastasis...
  35. pmc The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2
    Sun Mi Park
    The Ben May Department for Cancer Research, The University of Chicago, Chicago, Illinois 60637, USA
    Genes Dev 22:894-907. 2008
    ..Conversely, inhibition of miR-200 reduced E-cadherin expression, increased expression of Vimentin, and induced EMT. Our data identify miR-200 as a powerful marker and determining factor of the epithelial phenotype of cancer cells...
  36. ncbi Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults
    Eugenia E Calle
    Department of Epidemiology and Surveillance Research, American Cancer Society, Atlanta 30329, USA
    N Engl J Med 348:1625-38. 2003
    ..The influence of excess body weight on the risk of death from cancer has not been fully characterized...
  37. pmc The cancer genome
    Michael R Stratton
    Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK
    Nature 458:719-24. 2009
    ..These studies will provide us with a detailed and comprehensive perspective on how individual cancers have developed...
  38. ncbi Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype?
    Hector Peinado
    Departamento de Bioquimica, Facultad de Medicina, Universidad Autonoma de Madrid UAM, Instituto de Investigaciones Biomedicas Alberto Sols CSIC UAM, Arturo Duperier 4, 28029 Madrid, Spain
    Nat Rev Cancer 7:415-28. 2007
    ....
  39. ncbi Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy
    Hannah Farmer
    Cancer Research UK Gene Function and Regulation Group, London, UK
    Nature 434:917-21. 2005
    ..These results illustrate how different pathways cooperate to repair damage, and suggest that the targeted inhibition of particular DNA repair pathways may allow the design of specific and less toxic therapies for cancer...
  40. ncbi Complex networks orchestrate epithelial-mesenchymal transitions
    Jean Paul Thiery
    Centre National de la Recherche Scientifique CNRS Unité Mixte Recherche UMR 144 and Institut Curie, 26 Rue d Ulm, 75248 Paris Cedex 05, France
    Nat Rev Mol Cell Biol 7:131-42. 2006
    ..Understanding how mesenchymal cells arise from an epithelial default status will also have a strong impact in unravelling the mechanisms that control fibrosis and cancer progression...
  41. pmc Patterns of somatic mutation in human cancer genomes
    Christopher Greenman
    Cancer Genome Project, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK
    Nature 446:153-8. 2007
    ..Systematic sequencing of cancer genomes therefore reveals the evolutionary diversity of cancers and implicates a larger repertoire of cancer genes than previously anticipated...
  42. ncbi Vascular endothelial growth factor: basic science and clinical progress
    Napoleone Ferrara
    Department of Molecular Oncology, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Endocr Rev 25:581-611. 2004
    ..Furthermore, VEGF is implicated in intraocular neovascularization associated with diabetic retinopathy and age-related macular degeneration...
  43. doi Diverse somatic mutation patterns and pathway alterations in human cancers
    Zhengyan Kan
    Department of Molecular Biology, Genentech Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 466:869-73. 2010
    ..Our study provides an overview of the mutational spectra across major human cancers and identifies several potential therapeutic targets...
  44. pmc Defining the role of hypoxia-inducible factor 1 in cancer biology and therapeutics
    G L Semenza
    Vascular Program, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Oncogene 29:625-34. 2010
    ....
  45. ncbi Accelerated metastasis after short-term treatment with a potent inhibitor of tumor angiogenesis
    John M L Ebos
    Molecular and Cellular Biology Research, Sunnybrook Health Sciences Centre, Toronto, ON M4N 3M5, Canada
    Cancer Cell 15:232-9. 2009
    ....
  46. ncbi High frequency of mutations of the PIK3CA gene in human cancers
    Yardena Samuels
    Sidney Kimmel Comprehensive Cancer Center, Howard Hughes Medical Institute, The Johns Hopkins University Medical Institutions, Baltimore, MD 21231, USA
    Science 304:554. 2004
  47. pmc Microenvironmental regulation of metastasis
    Johanna A Joyce
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, USA
    Nat Rev Cancer 9:239-52. 2009
    ..This Review describes experimental data demonstrating the role of the microenvironment in metastasis, identifies areas for future research and suggests possible new therapeutic avenues...
  48. ncbi Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase
    Helen E Bryant
    The Institute for Cancer Studies, University of Sheffield, Medical School, Beech Hill Road, Sheffield S10 2RX, UK
    Nature 434:913-7. 2005
    ..The use of an inhibitor of a DNA repair enzyme alone to selectively kill a tumour, in the absence of an exogenous DNA-damaging agent, represents a new concept in cancer treatment...
  49. ncbi Cell cycle, CDKs and cancer: a changing paradigm
    Marcos Malumbres
    Cell Division and Cancer Group, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncologicas CNIO, 28029 Madrid, Spain
    Nat Rev Cancer 9:153-66. 2009
    ..Emerging evidence suggests that tumour cells may also require specific interphase CDKs for proliferation. Thus, selective CDK inhibition may provide therapeutic benefit against certain human neoplasias...
  50. doi Tumor angiogenesis
    Robert S Kerbel
    Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, and the Department of Medical Biophysics, University of Toronto, Toronto
    N Engl J Med 358:2039-49. 2008
  51. doi Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers
    Peter C Fong
    Drug Development Unit, Royal Marsden National Health Service Foundation Trust and the Institute of Cancer Research, Sutton, Surrey, United Kingdom
    N Engl J Med 361:123-34. 2009
    ..We conducted a clinical evaluation in humans of olaparib (AZD2281), a novel, potent, orally active PARP inhibitor...
  52. ncbi The global health burden of infection-associated cancers in the year 2002
    Donald Maxwell Parkin
    Clinical Trials Service Unit and Epidemiological Studies Unit, University of Oxford, Headington, UK
    Int J Cancer 118:3030-44. 2006
    ..The attributable fraction at the specific sites varies from 100% of cervix cancers attributable to the papilloma viruses to a tiny proportion (0.4%) of liver cancers (worldwide) caused by liver flukes...
  53. pmc Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR inhibitors: rationale and importance to inhibiting these pathways in human health
    William H Chappell
    Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, USA
    Oncotarget 2:135-64. 2011
    ..Inhibitors targeting these pathways have many potential uses from suppression of cancer, proliferative diseases as well as aging...
  54. pmc PI3K pathway alterations in cancer: variations on a theme
    T L Yuan
    Department of Systems Biology, Harvard Medical School and Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA 2115, USA
    Oncogene 27:5497-510. 2008
    ..In this review, we will examine the oncogenic properties of these genetic alterations to understand whether they are redundant or distinct and propose treatment strategies tailored for these genetic lesions...
  55. doi Advances in understanding cancer genomes through second-generation sequencing
    Matthew Meyerson
    Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nat Rev Genet 11:685-96. 2010
    ..This Review focuses on the methodological considerations for characterizing somatic genome alterations in cancer and the future prospects for these approaches...
  56. ncbi Targeting PI3K signalling in cancer: opportunities, challenges and limitations
    Jeffrey A Engelman
    Massachusetts General Hospital Cancer Center, Boston, Massachusetts 02129, USA
    Nat Rev Cancer 9:550-62. 2009
    ..I focus on the advantages and drawbacks of different treatment strategies for targeting this pathway, the cancers that might respond best to these therapies and the challenges and limitations that confront their clinical development...
  57. pmc A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells
    Ulrike Burk
    Department of Visceral Surgery, University of Freiburg, Hugstetter Strasse 55, 79106 Freiburg, Germany
    EMBO Rep 9:582-9. 2008
    ..Alternatively, depending on the environmental trigger, this loop might switch and induce epithelial differentiation, and thus explain the strong intratumorous heterogeneity observed in many human cancers...
  58. ncbi The protein kinase complement of the human genome
    G Manning
    SUGEN Inc, 230 East Grand Avenue, South San Francisco, CA 94080, USA
    Science 298:1912-34. 2002
    ..We also identified 106 protein kinase pseudogenes. Chromosomal mapping revealed several small clusters of kinase genes and revealed that 244 kinases map to disease loci or cancer amplicons...
  59. ncbi Tumor vascular permeability and the EPR effect in macromolecular therapeutics: a review
    H Maeda
    Department of Microbiology, Kumamoto University School of Medicine, Honjo 2 2 1, Kumamoto, Japan
    J Control Release 65:271-84. 2000
    ..Tumor-specific vascular physiology is also described...
  60. ncbi Cancer genes and the pathways they control
    Bert Vogelstein
    Howard Hughes Medical Institute and The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University Medical Institutions, Baltimore, Maryland 21231, USA
    Nat Med 10:789-99. 2004
    ..The purposes of this review are to highlight examples of progress in these areas, indicate where knowledge is scarce and point out fertile grounds for future investigation...
  61. ncbi Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer
    P J Roberts
    Division of Pharmacotherapy and Experimental Therapeutics, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7295, USA
    Oncogene 26:3291-310. 2007
    ..In this review, we summarize the current status of the different approaches and targets that are under evaluation and development for the therapeutic intervention of this key signaling pathway in human disease...
  62. pmc Targeting microRNAs in cancer: rationale, strategies and challenges
    Ramiro Garzon
    Division of Haematology and Oncology, Department of Medicine, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43221, USA
    Nat Rev Drug Discov 9:775-89. 2010
    ..In this Review, we describe the role of miRNAs in tumorigenesis and critically discuss the rationale, the strategies and the challenges for the therapeutic targeting of miRNAs in cancer...
  63. ncbi Cancer cell metabolism: Warburg and beyond
    Peggy P Hsu
    Whitehead Institute for Biomedical Research and Massachusetts Institute of Technology Department of Biology, Cambridge, MA 02142, USA
    Cell 134:703-7. 2008
    ..In this Essay, we re-examine the Warburg effect and establish a framework for understanding its contribution to the altered metabolism of cancer cells...
  64. ncbi Angiogenesis: an organizing principle for drug discovery?
    Judah Folkman
    Childrens Hospital and Harvard Medical School Boston, Massachusetts, USA
    Nat Rev Drug Discov 6:273-86. 2007
    ....
  65. ncbi BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis
    Scott M Wilhelm
    Bayer Pharmaceuticals Corporation, West Haven, Connecticut 06516, USA
    Cancer Res 64:7099-109. 2004
    ..These data demonstrate that BAY 43-9006 is a novel dual action RAF kinase and VEGFR inhibitor that targets tumor cell proliferation and tumor angiogenesis...
  66. pmc The basics of epithelial-mesenchymal transition
    Raghu Kalluri
    Division of Matrix Biology, Beth Israel Deaconess Medical Center, and Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Clin Invest 119:1420-8. 2009
    ..The identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions...
  67. ncbi Defining the role of mTOR in cancer
    David A Guertin
    Whitehead Institute for Biomedical Research and Massachusetts Institute of Technology, Department of Biology, Cambridge, MA 02141, USA
    Cancer Cell 12:9-22. 2007
    ..We further discuss the use of rapamycin in oncology and conclude with a discussion on the future of mTOR-targeted therapy...
  68. pmc DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Aging (Albany NY) 2:924-35. 2010
    ..We conclude that induction of p53 does not activate the senescence program in quiescent cells. In cells with induced p53, re-activation of mTOR by serum stimulation causes senescence, as an equivalent of cellular growth...
  69. doi Integrins in cancer: biological implications and therapeutic opportunities
    Jay S Desgrosellier
    Department of Pathology, Moores University of California at San Diego Cancer Center, La Jolla, 92093 0803, United States
    Nat Rev Cancer 10:9-22. 2010
    ..These exciting clinical developments emphasize the need to identify how integrin antagonists influence the tumour and its microenvironment...
  70. pmc IDH1 and IDH2 mutations in gliomas
    Hai Yan
    Department of Pathology, Pediatric Brain Tumor Foundation Institute, Duke University Medical Center, Durham, NC 27710, USA
    N Engl J Med 360:765-73. 2009
    ....
  71. pmc VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche
    Rosandra N Kaplan
    Department of Pediatrics and the Children s Blood Foundation Laboratories, Weill Cornell Medical College of Cornell University, New York, New York 10021, USA
    Nature 438:820-7. 2005
    ..These findings demonstrate a requirement for VEGFR1+ haematopoietic progenitors in the regulation of metastasis, and suggest that expression patterns of fibronectin and VEGFR1+VLA-4+ clusters dictate organ-specific tumour spread...
  72. ncbi Why do cancers have high aerobic glycolysis?
    Robert A Gatenby
    Department of Radiology, University of Arizona, Tucson, Arizona 85721, USA
    Nat Rev Cancer 4:891-9. 2004
    ..Subsequent cell populations with upregulated glycolysis and acid resistance have a powerful growth advantage, which promotes unconstrained proliferation and invasion...
  73. ncbi Taking dendritic cells into medicine
    Ralph M Steinman
    The Rockefeller University, New York 10065, USA
    Nature 449:419-26. 2007
    ..Here we present some medical implications of DC biology that account for illness and provide opportunities for prevention and therapy...
  74. pmc Antiangiogenic therapy elicits malignant progression of tumors to increased local invasion and distant metastasis
    Marta Pàez-Ribes
    Translational Research Laboratory, Catalan Institute of Oncology, IDIBELL, 08907 L Hospitalet de Llobregat, Spain
    Cancer Cell 15:220-31. 2009
    ....
  75. doi Reflecting on 25 years with MYC
    Natalie Meyer
    Amgen Canada, Inc Mississauga, Ontario, Canada
    Nat Rev Cancer 8:976-90. 2008
    ..Here we chronicle the major advances in our understanding of MYC biology, and peer into the future of MYC research...
  76. doi The influence of glucose-lowering therapies on cancer risk in type 2 diabetes
    C J Currie
    School of Medicine, Cardiff University, The Pharma Research Centre, Cardiff Medicentre, Cardiff, CF14 4UJ, UK
    Diabetologia 52:1766-77. 2009
    ..We examined the risk of development of solid tumours in relation to treatment with oral agents, human insulin and insulin analogues...
  77. doi Insulin and insulin-like growth factor signalling in neoplasia
    Michael Pollak
    Department of Oncology, McGill University, Montreal, Quebec, Canada
    Nat Rev Cancer 8:915-28. 2008
    ..Recent results are encouraging and have justified the expansion of many translational research programmes...
  78. doi The M2 splice isoform of pyruvate kinase is important for cancer metabolism and tumour growth
    Heather R Christofk
    Department of Systems Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 452:230-3. 2008
    ..These results demonstrate that M2 expression is necessary for aerobic glycolysis and that this metabolic phenotype provides a selective growth advantage for tumour cells in vivo...
  79. ncbi Multidrug resistance in cancer: role of ATP-dependent transporters
    Michael M Gottesman
    Laboratory of Cell Biology and Cancer Therapeutics Branch, The Center for Cancer Research, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Rev Cancer 2:48-58. 2002
    ..Therefore, the ability to predict and circumvent drug resistance is likely to improve chemotherapy...
  80. ncbi The fundamental role of epigenetic events in cancer
    Peter A Jones
    USC Norris Comprehensive Cancer Center, Department of Urology, Keck School of Medicine, University of Southern California, 1441 Eastlake Avenue, MS 8302L, Los Angeles, California 90089 9181, USA
    Nat Rev Genet 3:415-28. 2002
    ..In this review, we discuss these epigenetic events and the molecular alterations that might cause them and/or underlie altered gene expression in cancer...
  81. ncbi DNA methylation and human disease
    Keith D Robertson
    Department of Biochemistry and Molecular Biology, Shands Cancer Center, University of Florida, Gainesville, Florida 32610, USA
    Nat Rev Genet 6:597-610. 2005
    ..The study of these diseases has provided new and fundamental insights into the roles that DNA methylation and other epigenetic modifications have in development and normal cellular homeostasis...
  82. ncbi Macrophage diversity enhances tumor progression and metastasis
    Bin Zhi Qian
    Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Cell 141:39-51. 2010
    ..Specialized subpopulations of macrophages may represent important new therapeutic targets...
  83. doi miR-21: a small multi-faceted RNA
    Anna M Krichevsky
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Cell Mol Med 13:39-53. 2009
    ....
  84. ncbi PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer
    J Li
    Department of Pathology, College of Physicians and Surgeons, Columbia University, 630 West 168 Street, New York, NY 10032, USA
    Science 275:1943-7. 1997
    ..These homologies suggest that PTEN may suppress tumor cell growth by antagonizing protein tyrosine kinases and may regulate tumor cell invasion and metastasis through interactions at focal adhesions...
  85. pmc Modes of resistance to anti-angiogenic therapy
    Gabriele Bergers
    University of California, San Francisco, Department of Neurological Surgery, Brain Tumour Research Center, San Francisco, California 94143, USA
    Nat Rev Cancer 8:592-603. 2008
    ....
  86. pmc Accumulation of driver and passenger mutations during tumor progression
    Ivana Bozic
    Program for Evolutionary Dynamics, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 107:18545-50. 2010
    ..This selective advantage is surprisingly small--0.004 ± 0.0004--and has major implications for experimental cancer research...
  87. ncbi Restoration of p53 function leads to tumour regression in vivo
    Andrea Ventura
    Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA
    Nature 445:661-5. 2007
    ..These results support efforts to treat human cancers by way of pharmacological reactivation of p53...
  88. pmc Boveri revisited: chromosomal instability, aneuploidy and tumorigenesis
    Andrew J Holland
    Ludwig Institute for Cancer Research and Department of Cellular and Molecular Medicine, University of California, 9500 Gilman Drive, San Diego, La Jolla, California 92093 0670, USA
    Nat Rev Mol Cell Biol 10:478-87. 2009
    ..A clearer understanding of the tumour suppressive function of aneuploidy might reveal new avenues for anticancer therapy...
  89. doi Cancer statistics, 2009
    Ahmedin Jemal
    Cancer Surveillance, Surveillance and Health Policy Research, American Cancer Society, Atlanta, Georgia 30303 1002, USA
    CA Cancer J Clin 59:225-49. 2009
    ..Further progress can be accelerated by applying existing cancer control knowledge across all segments of the population and by supporting new discoveries in cancer prevention, early detection, and treatment...
  90. ncbi Cellular senescence: when bad things happen to good cells
    Judith Campisi
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, California 94720, USA
    Nat Rev Mol Cell Biol 8:729-40. 2007
    ....
  91. ncbi Cancer as an evolutionary and ecological process
    Lauren M F Merlo
    Cellular and Molecular Oncology Program, The Wistar Institute, 3601 Spruce Street, Philadelphia, Pennsylvania 19104, USA
    Nat Rev Cancer 6:924-35. 2006
    b>Neoplasms are microcosms of evolution. Within a neoplasm, a mosaic of mutant cells compete for space and resources, evade predation by the immune system and can even cooperate to disperse and colonize new organs...
  92. pmc COSMIC (the Catalogue of Somatic Mutations in Cancer): a resource to investigate acquired mutations in human cancer
    Simon A Forbes
    Cancer Genome Project, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK
    Nucleic Acids Res 38:D652-7. 2010
    ..Graphical views provide easily interpretable summaries of large quantities of data, and export functions can provide precise details of user-selected data...
  93. ncbi Cancer immunoediting: from immunosurveillance to tumor escape
    Gavin P Dunn
    Department of Pathology and Immunology, Center for Immunology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Nat Immunol 3:991-8. 2002
    ..In this review, we will summarize the historical and experimental basis of cancer immunoediting and discuss its dual roles in promoting host protection against cancer and facilitating tumor escape from immune destruction...
  94. pmc Caloric restriction delays disease onset and mortality in rhesus monkeys
    Ricki J Colman
    Wisconsin National Primate Research Center, University of Wisconsin, Madison, WI 53715, USA
    Science 325:201-4. 2009
    ..Furthermore, CR delayed the onset of age-associated pathologies. Specifically, CR reduced the incidence of diabetes, cancer, cardiovascular disease, and brain atrophy. These data demonstrate that CR slows aging in a primate species...
  95. ncbi Cancer stem cells--perspectives on current status and future directions: AACR Workshop on cancer stem cells
    Michael F Clarke
    Stanford University School of Medicine, Stanford, California, USA
    Cancer Res 66:9339-44. 2006
  96. ncbi The Wnt signaling pathway in development and disease
    Catriona Y Logan
    Department of Developmental Biology, Beckman Center, Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA
    Annu Rev Cell Dev Biol 20:781-810. 2004
    ..The next few years are likely to see novel therapeutic reagents aimed at controlling Wnt signaling in order to alleviate these conditions...
  97. pmc Signatures of mutation and selection in the cancer genome
    Graham R Bignell
    Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK
    Nature 463:893-8. 2010
    ..The extensive copy number, genotyping, sequence and expression data available for this large series of publicly available cancer cell lines renders them informative reagents for future studies of cancer biology and drug discovery...
  98. ncbi Targeting HIF-1 for cancer therapy
    Gregg L Semenza
    McKusick Nathans Institute of Genetic Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287 3914, USA
    Nat Rev Cancer 3:721-32. 2003
    ..In preclinical studies, inhibition of HIF-1 activity has marked effects on tumour growth. Efforts are underway to identify inhibitors of HIF-1 and to test their efficacy as anticancer therapeutics...
  99. doi Heterogeneity in cancer: cancer stem cells versus clonal evolution
    Mark Shackleton
    Howard Hughes Medical Institute, Life Sciences Institute, Center for Stem Cell Biology, University of Michigan, Ann Arbor, MI 48109, USA
    Cell 138:822-9. 2009
    ....
  100. ncbi A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth
    Sebastien Bonnet
    Pulmonary Hypertension Program and Vascular Biology Group, Department of Physiology, University of Alberta, Edmonton, AB T6G 2B7, Canada
    Cancer Cell 11:37-51. 2007
    ..Molecular inhibition of PDK2 by siRNA mimics DCA. The mitochondria-NFAT-Kv axis and PDK are important therapeutic targets in cancer; the orally available DCA is a promising selective anticancer agent...
  101. ncbi Anthracyclines: molecular advances and pharmacologic developments in antitumor activity and cardiotoxicity
    Giorgio Minotti
    G d Annunzio University School of Medicine, Centro Studi Sull Invecchiamento, Room 412, Via dei Vestini, 66013 Chieti, Italy
    Pharmacol Rev 56:185-229. 2004
    ..An overview of these issues confirms that anthracyclines remain "evergreen" drugs with broad clinical indications but have still an improvable therapeutic index...

Research Grants72

  1. GENES CONTROLLING NEOPLASIA OF THE INTESTINAL EPITHELIUM
    William Dove; Fiscal Year: 2007
    ..Over the coming years, we aim to deepen our studies of early and late intestinal neoplasms by seeking molecular markers expressed within tumors and in the serum of tumor-bearing animals...
  2. Targeting EWS/FLI1-driven pathways to improve therapeutic gains in Ewing's Sarcom
    Vicente Notario; Fiscal Year: 2010
    ..DESCRIPTION (provided by applicant): Tumors of the Ewing's sarcoma family (ESFT) are solid, highly malignant neoplasms of the bone and soft tissues that most often affect children and adolescents, being the second most common bone ..
  3. Targeting EWS/FLI1-driven pathways to improve therapeutic gains in Ewing's Sarcom
    Vicente Notario; Fiscal Year: 2009
    ..DESCRIPTION (provided by applicant): Tumors of the Ewing's sarcoma family (ESFT) are solid, highly malignant neoplasms of the bone and soft tissues that most often affect children and adolescents, being the second most common bone ..
  4. Glial Dysfunction in Ataxia Telangiectasia
    Margot Mayer Proschel; Fiscal Year: 2009
    ..neuropathy, infertility, translocations of chromosomes 7 and 14, underdeveloped thymus, and increased risk of neoplasms leading to poor quality of life...
  5. HISTOMETRIC ANALYSIS OF PREMALIGNANT ENDOMETRIAL LESIONS
    Francisco Garcia; Fiscal Year: 2001
    ..It accounts for about 36,000 cases of invasive cancer each year and is among the top five neoplasms affecting women...
  6. HISTOMETRIC ANALYSIS OF PREMALIGNANT ENDOMETRIAL LESIONS
    Francisco Garcia; Fiscal Year: 2000
    ..It accounts for about 36,000 cases of invasive cancer each year and is among the top five neoplasms affecting women...
  7. HISTOMETRIC ANALYSIS OF PREMALIGNANT ENDOMETRIAL LESIONS
    Francisco Garcia; Fiscal Year: 2002
    ..It accounts for about 36,000 cases of invasive cancer each year and is among the top five neoplasms affecting women...
  8. HISTOMETRIC ANALYSIS OF PREMALIGNANT ENDOMETRIAL LESIONS
    Francisco Garcia; Fiscal Year: 1999
    ..It accounts for about 36,000 cases of invasive cancer each year and is among the top five neoplasms affecting women...
  9. HISTOMETRIC ANALYSIS OF PREMALIGNANT ENDOMETRIAL LESIONS
    Francisco Garcia; Fiscal Year: 2003
    ..It accounts for about 36,000 cases of invasive cancer each year and is among the top five neoplasms affecting women...
  10. ENDOGENOUS MODULATION OF COCHLEA INJURY
    Leonard Rybak; Fiscal Year: 2006
    Cisplatin is a potent chemotherapeutic agent widely used to treat patients with a variety of malignant neoplasms. Severe side effects including nephrotoxicity, neurotoxicity and ototoxicity limit doses that can be used...
  11. ENDOGENOUS MODULATION OF COCHLEA INJURY
    Leonard Rybak; Fiscal Year: 2004
    Cisplatin is a potent chemotherapeutic agent widely used to treat patients with a variety of malignant neoplasms. Severe side effects including nephrotoxicity, neurotoxicity and ototoxicity limit doses that can be used...
  12. ENDOGENOUS MODULATION OF COCHLEA INJURY
    Leonard Rybak; Fiscal Year: 2005
    Cisplatin is a potent chemotherapeutic agent widely used to treat patients with a variety of malignant neoplasms. Severe side effects including nephrotoxicity, neurotoxicity and ototoxicity limit doses that can be used...
  13. Effect of chronic low-dose phthalate exposure on the immature primate testis
    Ina Dobrinski; Fiscal Year: 2009
    ..to human health and has been implicated in both the apparent decline of male fertility and a rise in testicular neoplasms. Phthalate esters are widely used as plasticizers in consumer products and can leach into the environment, ..
  14. NON-GASTRIN ACID SECRETAGOGUE IN ISLET CELL TUMORS
    William Chey; Fiscal Year: 1990
    In a group of patients with pancreatic islet cell neoplasms, marked gastric acid hypersecretion and peptic ulceration and/or diarrhea, normal plasma concentrations of gastrin were found...
  15. Pax8-PPARgamma regulation of transcription and metabolism in thyroid cancer
    RONALD JAY KOENIG; Fiscal Year: 2010
    ..Gene expression profiling of PPFP thyroid cancers (compared to all other benign and malignant thyroid neoplasms) resulted in the identification of a PPFP cancer gene signature...
  16. ACTIVE SPECIFIC IMMUNOTHERAPY IN MAN: A MURINE MODEL
    Barry Kahan; Fiscal Year: 1990
    ..6 mm) or 14 (10 mm) day established MCA-F subcutaneous neoplasms, and almost vitiated spontaneous pulmonary metastases following amputation of a limb bearing the MCA-F-4 (lung ..
  17. MOLECULAR MARKERS OF PROGNOSIS IN MEDULLOBLASTOMA
    SANDRA BIGNER; Fiscal Year: 1999
    ..hindered by technical inabilities to discriminate prospectively between patients with aggressive and indolent neoplasms. Recent advances in molecular biology, cytogenetics, and immunohistochemistry now convincingly demonstrate the ..
  18. MOLECULAR MARKERS OF PROGNOSIS IN MEDULLOBLASTOMA
    SANDRA BIGNER; Fiscal Year: 2000
    ..hindered by technical inabilities to discriminate prospectively between patients with aggressive and indolent neoplasms. Recent advances in molecular biology, cytogenetics, and immunohistochemistry now convincingly demonstrate the ..
  19. MOLECULAR MARKERS OF PROGNOSIS IN MEDULLOBLASTOMA
    SANDRA BIGNER; Fiscal Year: 1999
    ..hindered by technical inabilities to discriminate prospectively between patients with aggressive and indolent neoplasms. Recent advances in molecular biology, cytogenetics, and immunohistochemistry now convincingly demonstrate the ..
  20. MOLECULAR MARKERS OF PROGNOSIS IN MEDULLOBLASTOMA
    SANDRA BIGNER; Fiscal Year: 2000
    ..hindered by technical inabilities to discriminate prospectively between patients with aggressive and indolent neoplasms. Recent advances in molecular biology, cytogenetics, and immunohistochemistry now convincingly demonstrate the ..
  21. MOLECULAR MARKERS OF PROGNOSIS IN MEDULLOBLASTOMA
    SANDRA BIGNER; Fiscal Year: 1999
    ..hindered by technical inabilities to discriminate prospectively between patients with aggressive and indolent neoplasms. Recent advances in molecular biology, cytogenetics, and immunohistochemistry now convincingly demonstrate the ..
  22. CARCINOGENICITY OF 2-NITROPROPANE--A PROBABLE MECHANISM
    Emerich Fiala; Fiscal Year: 2000
    ..of 2-NP, thereby obtaining information for predicting whether or not the compound could also cause neoplasms in man...
  23. DIET, GENETIC SUSCEPTIBILITY AND COLORECTAL ADENOMAS
    Loic Le Marchand; Fiscal Year: 1999
    ..these foods, is determined by several polymorphic genes; thus, these genes may increase the risk of colorectal neoplasms. The susceptible phenotypes for most of these genes are several times more common in Japanese than Caucasians, ..
  24. DIET, GENETIC SUSCEPTIBILITY AND COLORECTAL ADENOMAS
    Loic Le Marchand; Fiscal Year: 2000
    ..these foods, is determined by several polymorphic genes; thus, these genes may increase the risk of colorectal neoplasms. The susceptible phenotypes for most of these genes are several times more common in Japanese than Caucasians, ..
  25. CARCINOGENICITY OF 2-NITROPROPANE--A PROBABLE MECHANISM
    Emerich Fiala; Fiscal Year: 1999
    ..of 2-NP, thereby obtaining information for predicting whether or not the compound could also cause neoplasms in man...
  26. Microarray analysis of thyroid neoplasm
    Martha Zeiger; Fiscal Year: 2004
    ..Because the surgical management for benign and malignant thyroid neoplasms differ, patients with suspicious FNAs may be treated in a less than ideal fashion surgically...
  27. Microarray analysis of thyroid neoplasm
    Martha Zeiger; Fiscal Year: 2003
    ..Because the surgical management for benign and malignant thyroid neoplasms differ, patients with suspicious FNAs may be treated in a less than ideal fashion surgically...
  28. NAC for melanoma chemoprevention
    Douglas Grossman; Fiscal Year: 2010
    ..cancer that, under the influence of ultraviolet (UV) radiation, arises from isolated melanocytes or melanocytic neoplasms (moles or nevi)...
  29. Modeling Neoplastic Progression in Barrett's Esophagus
    John W Pepper; Fiscal Year: 2010
    ..b>Neoplasms progress to malignancy through a process of clonal evolution...
  30. IMMORTALIZATION OF B-LYMPHOCYTES BY EPSTEIN-BARR VIRUS
    John Howe; Fiscal Year: 1991
    ..EBV is an important human pathogen and its association with these various neoplasms makes it one of the few human cancer viruses...
  31. NAC for melanoma chemoprevention
    Douglas Grossman; Fiscal Year: 2009
    ..cancer that, under the influence of ultraviolet (UV) radiation, arises from isolated melanocytes or melanocytic neoplasms (moles or nevi)...
  32. Modeling Neoplastic Progression in Barrett's Esophagus
    Carlo Maley; Fiscal Year: 2009
    ..b>Neoplasms progress to malignancy through a process of clonal evolution...
  33. IMMORTALIZATION OF B-LYMPHOCYTES BY EPSTEIN-BARR VIRUS
    John Howe; Fiscal Year: 1990
    ..EBV is an important human pathogen and its association with these various neoplasms makes it one of the few human cancer viruses...
  34. Modeling Neoplastic Progression in Barrett's Esophagus
    Carlo C Maley; Fiscal Year: 2011
    ..b>Neoplasms progress to malignancy through a process of clonal evolution...
  35. Influence of acid reflux on stromal epithelial interaction in Barrett?s esophagus
    GANAPATHY PRASAD; Fiscal Year: 2009
    ..Myofibroblast derived growth factors are known to promote proliferation of epithelial neoplasms 5-7...
  36. IDENTITY OF THE LATENT NEOPLASTIC EPIDERMAL CELL
    Rebecca Morris; Fiscal Year: 1992
    ..hyperplasia of sufficient magnitude (promotion) can induce on the backs of mice benign and malignant cutaneous neoplasms. There are three striking characteristics of this process: i) initiation occurs quickly and is essentially ..
  37. THE IDENTITY OF THE LATENT NEOPLASTIC EPIDERMAL CELL
    Rebecca Morris; Fiscal Year: 1993
    ..hyperplasia of sufficient magnitude (promotion) can induce on the backs of mice benign and malignant cutaneous neoplasms. There are three striking characteristics of this process: i) initiation occurs quickly and is essentially ..
  38. PHEOCHROMOCYTOMAS FROM NEUROFIBROMATOSIS KNOCKOUT MICE
    Arthur Tischler; Fiscal Year: 2003
    ..Pheochromocytomas are developmentally related to neuroblastomas, which are common adrenal medullary neoplasms, and pheochromocytoma cells can undergo neuronal differentiation...
  39. PHEOCHROMOCYTOMAS FROM NEUROFIBROMATOSIS KNOCKOUT MICE
    Arthur Tischler; Fiscal Year: 2002
    ..Pheochromocytomas are developmentally related to neuroblastomas, which are common adrenal medullary neoplasms, and pheochromocytoma cells can undergo neuronal differentiation...
  40. PHEOCHROMOCYTOMAS FROM NEUROFIBROMATOSIS KNOCKOUT MICE
    Arthur Tischler; Fiscal Year: 1999
    ..Pheochromocytomas are developmentally related to neuroblastomas, which are common adrenal medullary neoplasms, and pheochromocytoma cells can undergo neuronal differentiation...
  41. PHEOCHROMOCYTOMAS FROM NEUROFIBROMATOSIS KNOCKOUT MICE
    Arthur Tischler; Fiscal Year: 2001
    ..Pheochromocytomas are developmentally related to neuroblastomas, which are common adrenal medullary neoplasms, and pheochromocytoma cells can undergo neuronal differentiation...
  42. PHEOCHROMOCYTOMAS FROM NEUROFIBROMATOSIS KNOCKOUT MICE
    Arthur Tischler; Fiscal Year: 2000
    ..Pheochromocytomas are developmentally related to neuroblastomas, which are common adrenal medullary neoplasms, and pheochromocytoma cells can undergo neuronal differentiation...
  43. Multi-Modal Lysosomotropic Death Therapy for Malignant Peripheral Nerve Sheath Tu
    KEVIN AARON ROTH; Fiscal Year: 2010
    Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive, rapidly fatal neoplasms for which new therapeutic approaches are desperately needed...
  44. Multi-Modal Lysosomotropic Death Therapy for Malignant Peripheral Nerve Sheath Tu
    Kevin Roth; Fiscal Year: 2009
    Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive, rapidly fatal neoplasms for which new therapeutic approaches are desperately needed...
  45. IRS-1 - JC T-antigen Interaction in Cerebellar Tumors
    Krzysztof Reiss; Fiscal Year: 2006
    Medulloblastomas represent about 25 percent of all pediatric intracranial neoplasms. These highly malignant tumors arise from the cerebellum and affect mainly children between ages five and fifteen...
  46. IRS-1 - JC T-antigen Interaction in Cerebellar Tumors
    Krzysztof Reiss; Fiscal Year: 2002
    Medulloblastomas represent about 25 percent of all pediatric intracranial neoplasms. These highly malignant tumors arise from the cerebellum and affect mainly children between ages five and fifteen...
  47. IRS-1 - JC T-antigen Interaction in Cerebellar Tumors
    Krzysztof Reiss; Fiscal Year: 2003
    Medulloblastomas represent about 25 percent of all pediatric intracranial neoplasms. These highly malignant tumors arise from the cerebellum and affect mainly children between ages five and fifteen...
  48. Role of Periostin in Polycystic Kidney Disease
    DARREN WALLACE; Fiscal Year: 2009
    ..Although cysts are benign neoplasms, they ultimately cause renal insufficiency through extensive nephron loss and replacement of adjacent parenchyma ..
  49. IRS-1 - JC T-antigen Interaction in Cerebellar Tumors
    Krzysztof Reiss; Fiscal Year: 2005
    Medulloblastomas represent about 25 percent of all pediatric intracranial neoplasms. These highly malignant tumors arise from the cerebellum and affect mainly children between ages five and fifteen...
  50. Role of Periostin in Polycystic Kidney Disease
    Darren P Wallace; Fiscal Year: 2010
    ..Although cysts are benign neoplasms, they ultimately cause renal insufficiency through extensive nephron loss and replacement of adjacent parenchyma ..
  51. IRS-1 - JC T-antigen Interaction in Cerebellar Tumors
    Krzysztof Reiss; Fiscal Year: 2004
    Medulloblastomas represent about 25 percent of all pediatric intracranial neoplasms. These highly malignant tumors arise from the cerebellum and affect mainly children between ages five and fifteen...
  52. Functional analysis of the CYLD tumor suppressor
    JULIDE CELEBI; Fiscal Year: 2007
    ..have been demonstrated in families with FC, and loss of heterozygosity at the CYLD locus has been found in these neoplasms, suggesting that CYLD functions as a tumor suppressor...
  53. Functional analysis of the CYLD tumor suppressor
    JULIDE CELEBI; Fiscal Year: 2005
    ..have been demonstrated in families with FC, and loss of heterozygosity at the CYLD locus has been found in these neoplasms, suggesting that CYLD functions as a tumor suppressor...
  54. Functional analysis of the CYLD tumor suppressor
    JULIDE CELEBI; Fiscal Year: 2006
    ..have been demonstrated in families with FC, and loss of heterozygosity at the CYLD locus has been found in these neoplasms, suggesting that CYLD functions as a tumor suppressor...
  55. Functional analysis of the CYLD tumor suppressor
    JULIDE CELEBI; Fiscal Year: 2009
    ..have been demonstrated in families with FC, and loss of heterozygosity at the CYLD locus has been found in these neoplasms, suggesting that CYLD functions as a tumor suppressor...
  56. GENE EXPRESSION IN BRAIN CELLS IN AIDS
    Sue Griffin; Fiscal Year: 1990
    ..The occurrence of opportunistic infections, neoplasms, and HIV infection of cells in the brain are well documented...
  57. GENE EXPRESSION IN BRAIN CELLS IN AIDS
    Sue Griffin; Fiscal Year: 1993
    ..The occurrence of opportunistic infections, neoplasms, and HIV infection of cells in the brain are well documented...
  58. Gene Targeted Therapy of Brain Tumors
    John Sampson; Fiscal Year: 2009
    Primary malignant brain tumors, like glioblastoma (GBM), remain universally fatal. Like most neoplasms, they develop through the acquisition of multiple genetic alterations that lead to a heterogeneous deregulation of cell signaling ..
  59. In Vivo Detection of Flat Colorectal Neoplasms with CT Colonography
    JANNE JOHANNES NAPPI; Fiscal Year: 2010
    ..Most colorectal cancers develop from sessile or pedunculated polypoid neoplasms. Early removal of such neoplasms has been observed to reduce the occurrence of colorectal carcinoma...
  60. MOLECULAR PATHOLOGY OF ORAL NEOPLASMS WITH HPV INFECTION
    THOMAS BROKER; Fiscal Year: 2000
    ..We propose that the E6 and E7 genes are actively transcribed in and contribute to the development of H&N neoplasms that harbor HPVs...
  61. In Vivo Detection of Flat Colorectal Neoplasms with CT Colonography
    Janne Nappi; Fiscal Year: 2009
    ..Most colorectal cancers develop from sessile or pedunculated polypoid neoplasms. Early removal of such neoplasms has been observed to reduce the occurrence of colorectal carcinoma...
  62. Leukemia Stem Cells: Essential Targets for GVL and Mediators of GVL-Resistance
    Warren D Shlomchik; Fiscal Year: 2010
    ..Unfortunately, most other neoplasms are relatively GVL-resistant...
  63. Leukemia Stem Cells: Essential Targets for GVL and Mediators of GVL-Resistance
    Warren Shlomchik; Fiscal Year: 2009
    ..Unfortunately, most other neoplasms are relatively GVL-resistant...
  64. Virologic success & immunologic failure after antiretrov
    Hernan Valdez; Fiscal Year: 2000
    ..by a progressive loss of immune function that puts patients at risk for opportunistic infections and neoplasms. This loss of immune function is characterized by decreases in the numbers of circulating total, naive and ..
  65. Virologic success & immunologic failure after antiretrov
    Hernan Valdez; Fiscal Year: 2001
    ..by a progressive loss of immune function that puts patients at risk for opportunistic infections and neoplasms. This loss of immune function is characterized by decreases in the numbers of circulating total, naive and ..
  66. Virologic success & immunologic failure after antiretrov
    Hernan Valdez; Fiscal Year: 2002
    ..by a progressive loss of immune function that puts patients at risk for opportunistic infections and neoplasms. This loss of immune function is characterized by decreases in the numbers of circulating total, naive and ..