Joe W Gray

Summary

Affiliation: Lawrence Berkeley National Laboratory
Country: USA

Publications

  1. ncbi request reprint Evidence emerges for early metastasis and parallel evolution of primary and metastatic tumors
    Joe W Gray
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Cancer Cell 4:4-6. 2003
  2. pmc A sequence-based survey of the complex structural organization of tumor genomes
    Benjamin J Raphael
    Department of Computer Science and Center for Computational Molecular Biology, Brown University, Waterman Street, Providence, RI 02912 1910, USA
    Genome Biol 9:R59. 2008
  3. pmc Analysis of molecular inversion probe performance for allele copy number determination
    Yuker Wang
    Affymetrix Inc, Shoreline Blvd, South San Francisco, CA 94080, USA
    Genome Biol 8:R246. 2007
  4. pmc Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast cancer
    Chad J Creighton
    Dan L Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
    Breast Cancer Res 12:R40. 2010
  5. pmc Aging impacts transcriptomes but not genomes of hormone-dependent breast cancers
    Christina Yau
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Breast Cancer Res 9:R59. 2007
  6. pmc Enhanced NF kappa B and AP-1 transcriptional activity associated with antiestrogen resistant breast cancer
    Yamei Zhou
    Buck Institute for Age Research, Novato, CA 94945, USA
    BMC Cancer 7:59. 2007
  7. pmc Breast tumor copy number aberration phenotypes and genomic instability
    Jane Fridlyand
    Department of Epidemiology and Biostatistics, University of California San Francisco, CA 94143, USA
    BMC Cancer 6:96. 2006
  8. pmc Ovarian carcinomas with genetic and epigenetic BRCA1 loss have distinct molecular abnormalities
    Joshua Z Press
    Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada
    BMC Cancer 8:17. 2008
  9. pmc ATM suppresses SATB1-induced malignant progression in breast epithelial cells
    ELLEN ORDINARIO
    Life Sciences Division, Lawrence Berkeley National Laboratory, University of California, Berkeley, California, USA
    PLoS ONE 7:e51786. 2012
  10. pmc The expression level of HJURP has an independent prognostic impact and predicts the sensitivity to radiotherapy in breast cancer
    Zhi Hu
    Life Sciences Division, Lawrence Berkeley National Laboratory, One Cyclotron Road, Berkeley, CA 94720, USA
    Breast Cancer Res 12:R18. 2010

Research Grants

  1. SPORE IN BREAST CANCER
    Joe Gray; Fiscal Year: 2007

Detail Information

Publications78

  1. ncbi request reprint Evidence emerges for early metastasis and parallel evolution of primary and metastatic tumors
    Joe W Gray
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Cancer Cell 4:4-6. 2003
    ..Their model suggests that adjuvant therapies should be targeted to lesions in the disseminated cells rather than lesions found in primary tumors...
  2. pmc A sequence-based survey of the complex structural organization of tumor genomes
    Benjamin J Raphael
    Department of Computer Science and Center for Computational Molecular Biology, Brown University, Waterman Street, Providence, RI 02912 1910, USA
    Genome Biol 9:R59. 2008
    ..The genomes of many epithelial tumors exhibit extensive chromosomal rearrangements. All classes of genome rearrangements can be identified using end sequencing profiling, which relies on paired-end sequencing of cloned tumor genomes...
  3. pmc Analysis of molecular inversion probe performance for allele copy number determination
    Yuker Wang
    Affymetrix Inc, Shoreline Blvd, South San Francisco, CA 94080, USA
    Genome Biol 8:R246. 2007
    ....
  4. pmc Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast cancer
    Chad J Creighton
    Dan L Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
    Breast Cancer Res 12:R40. 2010
    ..We thus examined whether deregulated PI3K signaling in luminal ER+ breast tumors is associated with ER level and activity and intrinsic molecular subtype...
  5. pmc Aging impacts transcriptomes but not genomes of hormone-dependent breast cancers
    Christina Yau
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Breast Cancer Res 9:R59. 2007
    ..Except for inherited forms of breast cancer, however, there is little genetic or epigenetic understanding of the biological basis linking aging with sporadic breast cancer incidence and its clinical behavior...
  6. pmc Enhanced NF kappa B and AP-1 transcriptional activity associated with antiestrogen resistant breast cancer
    Yamei Zhou
    Buck Institute for Age Research, Novato, CA 94945, USA
    BMC Cancer 7:59. 2007
    ..Signaling pathways that converge on two different transcription factor complexes, NFkappaB and AP-1, have been identified in estrogen receptor (ER)-positive breast cancers resistant to the antiestrogen, tamoxifen...
  7. pmc Breast tumor copy number aberration phenotypes and genomic instability
    Jane Fridlyand
    Department of Epidemiology and Biostatistics, University of California San Francisco, CA 94143, USA
    BMC Cancer 6:96. 2006
    ..g. those involved in mitosis, replication, repair, and telomeres) are rarely mutated in chromosomally unstable sporadic tumors, even though such mutations are associated with some heritable cancer prone syndromes...
  8. pmc Ovarian carcinomas with genetic and epigenetic BRCA1 loss have distinct molecular abnormalities
    Joshua Z Press
    Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada
    BMC Cancer 8:17. 2008
    ..The mechanism of BRCA1/2 loss is a potential method of subclassifying high grade serous carcinomas...
  9. pmc ATM suppresses SATB1-induced malignant progression in breast epithelial cells
    ELLEN ORDINARIO
    Life Sciences Division, Lawrence Berkeley National Laboratory, University of California, Berkeley, California, USA
    PLoS ONE 7:e51786. 2012
    ..These data indicate a novel role for ATM as a suppressor of SATB1-induced malignancy in breast epithelial cells, but also raise a cautionary note that phenotypic drift could lead to dramatically different functional outcomes...
  10. pmc The expression level of HJURP has an independent prognostic impact and predicts the sensitivity to radiotherapy in breast cancer
    Zhi Hu
    Life Sciences Division, Lawrence Berkeley National Laboratory, One Cyclotron Road, Berkeley, CA 94720, USA
    Breast Cancer Res 12:R18. 2010
    ..However its role in tumor development remains largely unknown. The goal of this study was to investigate the clinical significance of HJURP in breast cancer and its correlation with radiotherapeutic outcome...
  11. pmc Subtype and pathway specific responses to anticancer compounds in breast cancer
    Laura M Heiser
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Proc Natl Acad Sci U S A 109:2724-9. 2012
    ..These observations suggest mechanisms of response and resistance and may inform efforts to develop molecular assays that predict clinical response...
  12. pmc Prediction of epigenetically regulated genes in breast cancer cell lines
    Leandro A Loss
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA, USA
    BMC Bioinformatics 11:305. 2010
    ..Finally, the methylation-expression associations are ranked through a logistic regression, and their significance is quantified through permutation analysis...
  13. pmc p27Kip1 mediates addiction of ovarian cancer cells to MYCC (c-MYC) and their dependence on MYC paralogs
    Tulsiram Prathapam
    Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA
    J Biol Chem 285:32529-38. 2010
    ..They also suggest that growth of ovarian cancers may be blocked by inhibition of MYCC or MYC paralogs...
  14. pmc Morphometic analysis of TCGA glioblastoma multiforme
    Hang Chang
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA
    BMC Bioinformatics 12:484. 2011
    ..Thus far, analysis is limited to Glioblastoma Multiforme (GBM) and kidney renal clear cell carcinoma tissue sections. The final results are being distributed for subtyping and linking the histology sections to the genomic data...
  15. pmc A systems analysis of the chemosensitivity of breast cancer cells to the polyamine analogue PG-11047
    Wen Lin Kuo
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA
    BMC Med 7:77. 2009
    ....
  16. pmc HER2 signaling pathway activation and response of breast cancer cells to HER2-targeting agents is dependent strongly on the 3D microenvironment
    Britta Weigelt
    Life Sciences Division, Lawrence Berkeley National Laboratory, University of California Berkeley, Mailstop 977R225A, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Breast Cancer Res Treat 122:35-43. 2010
    ....
  17. pmc Molecular predictors of 3D morphogenesis by breast cancer cell lines in 3D culture
    Ju Han
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, United States of America
    PLoS Comput Biol 6:e1000684. 2010
    ..Specifically, PPARgamma has been associated with the invasive stellate morphological phenotype, which corresponds to triple-negative pathobiology. PPARgamma has been validated through two supporting biological assays...
  18. pmc The morphologies of breast cancer cell lines in three-dimensional assays correlate with their profiles of gene expression
    Paraic A Kenny
    Life Sciences Division, Lawrence Berkeley National Laboratory, University of California, Berkeley, CA 94720, USA
    Mol Oncol 1:84-96. 2007
    ..We further demonstrate that consistent differences in genes encoding signal transduction proteins emerge when even tumor cells are cultured in 3D microenvironments...
  19. pmc Temporal dissection of tumorigenesis in primary cancers
    Steffen Durinck
    Life Sciences Division, Lawrence Berkeley National Laboratories, USA
    Cancer Discov 1:137-43. 2011
    ..These results reframe paradigms in which TP53 mutation is required later, to bypass senescence induced by driver oncogenes...
  20. pmc Subtypes of pancreatic ductal adenocarcinoma and their differing responses to therapy
    Eric A Collisson
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA
    Nat Med 17:500-3. 2011
    ..We further define gene signatures for these subtypes that may have utility in stratifying patients for treatment and present preclinical model systems that may be used to identify new subtype specific therapies...
  21. pmc Exon-level microarray analyses identify alternative splicing programs in breast cancer
    Anna Lapuk
    Life Sciences Division, Lawrence Berkeley National Laboratory, University of California at Berkeley, Berkeley, California 94720, USA
    Mol Cancer Res 8:961-74. 2010
    ..These data also suggest the possibility of reducing the toxicity of protein-targeted breast cancer treatments by targeting protein isoforms that are not present in limiting normal tissues...
  22. pmc Invariant delineation of nuclear architecture in glioblastoma multiforme for clinical and molecular association
    Hang Chang
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    IEEE Trans Med Imaging 32:670-82. 2013
    ..lbl.gov for correlation with TCGA molecular data. The website also provides an interface for panning and zooming of whole mount tissue sections with/without overlaid segmentation results for quality control...
  23. pmc Genetic differences in transcript responses to low-dose ionizing radiation identify tissue functions associated with breast cancer susceptibility
    Antoine M Snijders
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA
    PLoS ONE 7:e45394. 2012
    ....
  24. pmc Restriction of receptor movement alters cellular response: physical force sensing by EphA2
    Khalid Salaita
    Howard Hughes Medical Institute, Department of Chemistry, University of California, Berkeley, CA 94720, USA
    Science 327:1380-5. 2010
    ..These observations reveal a mechanism for spatio-mechanical regulation of EphA2 signaling pathways...
  25. pmc Genomic aberrations in normal tissue adjacent to HER2-amplified breast cancers: field cancerization or contaminating tumor cells?
    Anguraj Sadanandam
    Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Breast Cancer Res Treat 136:693-703. 2012
    ....
  26. pmc A human breast cell model of preinvasive to invasive transition
    Aylin Rizki
    Life Sciences Division, Ernest Orlando Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Cancer Res 68:1378-87. 2008
    ..This model provides a new tool for dissection of mechanisms by which preinvasive breast cells could acquire invasiveness in a metaplastic context...
  27. pmc Breast cancer genomes--form and function
    James Korkola
    Life Sciences Division, Lawrence Berkeley National Laboratory, One Cyclotron Road, MS977 250, Berkeley, CA 94127, United States
    Curr Opin Genet Dev 20:4-14. 2010
    ....
  28. pmc 'Omic approaches to preventing or managing metastatic breast cancer
    Obi L Griffith
    Lawrence Berkeley National Laboratory, Life Sciences Division, Cancer and DNA Damage Responses, One Cyclotron Road, Berkeley, CA 94720, USA
    Breast Cancer Res 13:230. 2011
    ..Knowledge of these features also will guide development of therapeutic strategies that can be applied when metastatic disease burden is low, thereby increasing the probability of a curative response...
  29. pmc Integrated analysis of breast cancer cell lines reveals unique signaling pathways
    Laura M Heiser
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Genome Biol 10:R31. 2009
    ..Deregulation in signaling along the EgfR-MAPK pathway is common in breast cancer, though the manner in which deregulation occurs varies between both individuals and cancer subtypes...
  30. pmc Sparse multitask regression for identifying common mechanism of response to therapeutic targets
    Kai Zhang
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Bioinformatics 26:i97-105. 2010
    ..As a result, the complex coordination among the genes responsible for a phenotypic profile is potentially lost. More importantly, univariate analysis can potentially hide new insights into common mechanism of response...
  31. pmc Radiosensitivity profiles from a panel of ovarian cancer cell lines exhibiting genetic alterations in p53 and disparate DNA-dependent protein kinase activities
    Gregory T Langland
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Oncol Rep 23:1021-6. 2010
    ..These data suggest that the activity of regulatory molecules such as p53 may be better indicators of radiation sensitivity than DNA repair enzymes such as DNA-PK in ovarian cancer...
  32. pmc Loss-of-function mutations in Notch receptors in cutaneous and lung squamous cell carcinoma
    Nicholas J Wang
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
    Proc Natl Acad Sci U S A 108:17761-6. 2011
    ..The bifunctional role of Notch in human cancer thus emphasizes the context dependency of signaling outcomes and suggests that targeted inhibition of the Notch pathway may induce squamous epithelial malignancies...
  33. pmc Systems biology in cancer research: genomics to cellomics
    Jackie L Stilwell
    Lawrence Berkeley National Laboratory, Berkeley, CA, USA
    Methods Mol Biol 356:353-65. 2007
    ....
  34. pmc c-Src Modulates Estrogen-Induced Stress and Apoptosis in Estrogen-Deprived Breast Cancer Cells
    Ping Fan
    Authors Affiliations Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, District of Columbia Lawrence Berkeley National Laboratory, Life Sciences Division, Cancer and DNA Damage Responses, Berkeley, California Department of Chemistry, University of Illinois at Urbana Champaign, Urbana, Illinois and Biomedical Engineering Department, Oregon Health and Science University, Portland, Oregon
    Cancer Res 73:4510-20. 2013
    ..This work offers a mechanistic rationale for a new approach in the treatment of endocrine-resistant breast cancer. Cancer Res; 73(14); 4510-20. ©2013 AACR. ..
  35. ncbi request reprint Amplification of PVT1 contributes to the pathophysiology of ovarian and breast cancer
    Yinghui Guan
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    Clin Cancer Res 13:5745-55. 2007
    ..This study was designed to elucidate the role of amplification at 8q24 in the pathophysiology of ovarian and breast cancer because increased copy number at this locus is one of the most frequent genomic abnormalities in these cancers...
  36. pmc A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes
    Richard M Neve
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94270, USA
    Cancer Cell 10:515-27. 2006
    ..We show, using Trastuzumab (Herceptin) monotherapy as an example, that the system can be used to identify molecular features that predict or indicate response to targeted therapies or other physiological perturbations...
  37. pmc Loss of cell-surface laminin anchoring promotes tumor growth and is associated with poor clinical outcomes
    Armin Akhavan
    California Pacific Medical Center Research Institute, San Francisco, CA, USA
    Cancer Res 72:2578-88. 2012
    ..Together, our findings suggest that defects in laminin anchoring occur commonly in cancer cells, are characteristic of aggressive cancer subtypes, and are important drivers of disease progression...
  38. pmc Cellular effect of high doses of silica-coated quantum dot profiled with high throughput gene expression analysis and high content cellomics measurements
    Tingting Zhang
    Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    Nano Lett 6:800-8. 2006
    ..This study indicates that PEG-coated silanized Qdots pose minimal impact to cells and are a very promising alternative to uncoated Qdots...
  39. pmc Molecular characterization of the cytotoxic mechanism of multiwall carbon nanotubes and nano-onions on human skin fibroblast
    Lianghao Ding
    Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
    Nano Lett 5:2448-64. 2005
    ....
  40. pmc ESR1 gene amplification in breast cancer: a common phenomenon?
    Lindsay A Brown
    Nat Genet 40:806-7; author reply 810-2. 2008
  41. pmc Decoding the fine-scale structure of a breast cancer genome and transcriptome
    Stanislav Volik
    Department of Urology, and Cancer Research Institute, University of California San Francisco Comprehensive Cancer Center, San Francisco, California 94115, USA
    Genome Res 16:394-404. 2006
    ..Given these properties, ESP could play an important role in a tumor genome project...
  42. pmc Integrating data on DNA copy number with gene expression levels and drug sensitivities in the NCI-60 cell line panel
    Kimberly J Bussey
    Laboratory of Molecular Pharmacology, National Cancer Institute, Building 37, Room 5056, NIH, MSC 4255, 9000 Rockville Pike, Bethesda, MD 20892 4255, USA
    Mol Cancer Ther 5:853-67. 2006
    ..The DNA copy number database presented here will enable other investigators to explore DNA transcript-drug relationships in their own domains of research focus...
  43. ncbi request reprint Genomic and transcriptional aberrations linked to breast cancer pathophysiologies
    Koei Chin
    Comprehensive Cancer Center, 2340 Sutter Street, University of California, San Francisco, San Francisco, California 94143
    Cancer Cell 10:529-41. 2006
    ..Nine of these (FGFR1, IKBKB, ERBB2, PROCC, ADAM9, FNTA, ACACA, PNMT, and NR1D1) are considered druggable. Low-level CNAs appear to contribute to cancer progression by altering RNA and cellular metabolism...
  44. ncbi request reprint An integrated view of copy number and allelic alterations in the cancer genome using single nucleotide polymorphism arrays
    Xiaojun Zhao
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 64:3060-71. 2004
    ..The simultaneous measurement of DNA copy number changes and loss of heterozygosity events by SNP arrays should strengthen our ability to discover cancer-causing genes and to refine cancer diagnosis...
  45. ncbi request reprint Frequent silencing of low density lipoprotein receptor-related protein 1B (LRP1B) expression by genetic and epigenetic mechanisms in esophageal squamous cell carcinoma
    Itaru Sonoda
    Department of Molecular Cytogenetics, Medical Research Institute, and Maxillofacial Surgery, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan
    Cancer Res 64:3741-7. 2004
    ..These results suggest that loss of LRP1B function in esophageal carcinogenesis most often occurs either by homozygous deletion or by transcriptional silencing through hypermethylation of its CpG island...
  46. ncbi request reprint Amplification of MDS1/EVI1 and EVI1, located in the 3q26.2 amplicon, is associated with favorable patient prognosis in ovarian cancer
    Meera Nanjundan
    Department of Molecular Therapeutics, M D Anderson Cancer Center, University of Texas, Houston, Texas, USA
    Cancer Res 67:3074-84. 2007
    ..Collectively, these studies suggest that MDS1/EVI1 and EVI1, previously implicated in acute myelogenous leukemia, contribute to the pathophysiology of epithelial ovarian cancer...
  47. ncbi request reprint In situ analyses of genome instability in breast cancer
    Koei Chin
    Department of Laboratory Medicine and Comprehensive Cancer Center, University of California San Francisco, California, USA
    Nat Genet 36:984-8. 2004
    ..Taken together, the data suggest that transition through telomere crisis and immortalization in breast cancer occurs during progression from usual ductal hyperplasia to ductal carcinoma in situ...
  48. ncbi request reprint The RAB25 small GTPase determines aggressiveness of ovarian and breast cancers
    Kwai Wa Cheng
    Department of Molecular Therapeutics, University of Texas MD Anderson Cancer Center, Houston, Texas 77054, USA
    Nat Med 10:1251-6. 2004
    ..Overall, these studies implicate RAB25, and thus the RAB family of small G proteins, in aggressiveness of epithelial cancers...
  49. pmc A screen for genes that suppress loss of contact inhibition: identification of ING4 as a candidate tumor suppressor gene in human cancer
    Suwon Kim
    The G W Hooper Research Foundation and Department of Microbiology and Immunology, Department of Laboratory Medicine and Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA
    Proc Natl Acad Sci U S A 101:16251-6. 2004
    ..Ectopic expression of ING4 attenuated the growth of T47D human breast cancer cells in soft agar. We conclude that ING4 is a strong candidate as a tumor suppressor gene...
  50. ncbi request reprint Oncogene expression and genetic background influence the frequency of DNA copy number abnormalities in mouse pancreatic islet cell carcinomas
    Jeffrey H Hager
    Department of Biochemistry, University of California at San Francisco Diabetes and Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California 94143, USA
    Cancer Res 64:2406-10. 2004
    ..These studies illustrate the utility of transgenic animal models for investigation of factors influencing genomic heterogeneity despite the commonalty of target cell type and initiating oncogene...
  51. ncbi request reprint The role of p53 in suppression of KSHV cyclin-induced lymphomagenesis
    Emmy W Verschuren
    Comprehensive Cancer Center and Department of Cellular and Molecular Pharmacology, University of California San Francisco, San Francisco, California, USA
    Cancer Res 64:581-9. 2004
    ..Together, our data support a model in which K cyclin-induced genome instability arises early in the pre-tumorigenic lymphocyte population and that loss of p53 licenses subsequent expansion of tumorigenic clones...
  52. ncbi request reprint Computational BAC clone contig assembly for comprehensive genome analysis
    Anna Lapuk
    Department of Laboratory Medicine and UCSF Comprehensive Cancer Center, University of California San Francisco, USA
    Genes Chromosomes Cancer 40:66-71. 2004
    ..We also show illustrative analyses of regions of amplification in these regions in breast and ovarian tumor cell lines by use of array CGH with arrays comprising contiguous BACs...
  53. ncbi request reprint Genome-wide array CGH analysis of murine neuroblastoma reveals distinct genomic aberrations which parallel those in human tumors
    Christopher S Hackett
    Department of Neurology, University of California, San Francisco, California 94143 0114, USA
    Cancer Res 63:5266-73. 2003
    ..These data demonstrate conservation of many genetic changes in murine and human neuroblastoma and suggest that further delineation of genetic abnormalities in murine tumors may identify genes important in human disease...
  54. ncbi request reprint Chromosome aberrations in solid tumors
    Donna G Albertson
    Cancer Research Institute, University of California San Francisco, San Francisco, California 94143 0808, USA
    Nat Genet 34:369-76. 2003
    ....
  55. pmc End-sequence profiling: sequence-based analysis of aberrant genomes
    Stanislav Volik
    Cancer Research Institute and Department of Laboratory Medicine, University of California Comprehensive Cancer Center, 2340 Sutter Street, San Francisco, CA 94115, USA
    Proc Natl Acad Sci U S A 100:7696-701. 2003
    ....
  56. ncbi request reprint Genome amplification of chromosome 20 in breast cancer
    J Graeme Hodgson
    Department of Laboratory Medicine, University of California at San Francisco, San Francisco, CA, USA
    Breast Cancer Res Treat 78:337-45. 2003
    ....
  57. ncbi request reprint Induction of tumors in mice by genomic hypomethylation
    François Gaudet
    Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA
    Science 300:489-92. 2003
    ..These results indicate that DNA hypomethylation plays a causal role in tumor formation, possibly by promoting chromosomal instability...
  58. ncbi request reprint Specific keynote: genome copy number abnormalities in ovarian cancer
    Joe W Gray
    University of California, Los Angeles, USA
    Gynecol Oncol 88:S16-21; discussion S22-4. 2003
  59. ncbi request reprint Biallelic inactivation of the thyroid hormone receptor beta1 gene in early stage breast cancer
    Zheng Li
    Geraldine Brush Cancer Research Institute, California Pacific Medical Center, San Francisco, California 94115, USA
    Cancer Res 62:1939-43. 2002
    ..The observation of early, frequent, and multiple mechanisms of TRbeta1 inactivation suggests a potential role for this gene in the suppression of breast tumorigenesis...
  60. ncbi request reprint Identification of a novel homozygous deletion region at 6q23.1 in medulloblastomas using high-resolution array comparative genomic hybridization analysis
    Angela B Y Hui
    Department of Anatomical and Cellular Pathology, Chinese University of Hong Kong, Hong Kong SAR, PR China
    Clin Cancer Res 11:4707-16. 2005
    ..The aim of this study is to comprehensively characterize genome copy number aberrations in medulloblastomas using high-resolution array comparative genomic hybridization...
  61. ncbi request reprint A conditional feedback loop regulates Ras activity through EphA2
    Madhu Macrae
    Cancer Research Institute and Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California 94143, USA
    Cancer Cell 8:111-8. 2005
    ..Our results suggest that an escape from the negative effects of this interaction may be important in the development of cancer...
  62. pmc The melanocyte differentiation program predisposes to metastasis after neoplastic transformation
    Piyush B Gupta
    Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA
    Nat Genet 37:1047-54. 2005
    ..Moreover, Slug is required for the metastasis of the transformed melanoma cells. These findings indicate that melanocyte-specific factors present before neoplastic transformation can have a pivotal role in governing melanoma progression...
  63. pmc Crosstalk between Aurora-A and p53: frequent deletion or downregulation of Aurora-A in tumors from p53 null mice
    Jian Hua Mao
    Cancer Research Institute, University of California, San Francisco, San Francisco, CA 94143, USA
    Cancer Cell 11:161-73. 2007
    ..These data have implications for the design of approaches to targeted cancer therapy involving the crosstalk between Aurora-A kinase and p53 pathways...
  64. ncbi request reprint Multiple roles of the candidate oncogene ZNF217 in ovarian epithelial neoplastic progression
    Peixiang Li
    Department of Obstetrics and Gynecology, University of British Columbia, Vancouver, BC, Canada
    Int J Cancer 120:1863-73. 2007
    ..The resemblance of the genomic changes in the ZNF217-overexpressing lines to ovarian carcinomas provides a unique model to investigate interrelationships between these changes and ovarian neoplastic phenotypes...
  65. ncbi request reprint Deletion of chromosome 11q predicts response to anthracycline-based chemotherapy in early breast cancer
    Joan Climent
    Division of Oncology, Center for Applied Medical Research, University of Navarra, Pamplona, and Department of Hematology and Medical Oncology, Hospital Clinico, University of Valencia, Spain
    Cancer Res 67:818-26. 2007
    ..However, these initial findings should be evaluated in randomized clinical trials...
  66. pmc Translating insights from the cancer genome into clinical practice
    Lynda Chin
    Dana Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
    Nature 452:553-63. 2008
    ....
  67. pmc Ovarian cancer: linking genomics to new target discovery and molecular markers--the way ahead
    Bryan T Hennessy
    Department of Molecular Therapeutics, MD Anderson Cancer Center, Houston, TX, USA
    Adv Exp Med Biol 617:23-40. 2008
  68. pmc Prognostic value of PAI1 in invasive breast cancer: evidence that tumor-specific factors are more important than genetic variation in regulating PAI1 expression
    Mark D Sternlicht
    Department of Anatomy, University of California San Francisco, 513 Parnassus Avenue, HSW 1301 San Francisco, CA 94143 0452, USA
    Cancer Epidemiol Biomarkers Prev 15:2107-14. 2006
    ..Thus, local factors, such as CTGF and genomic amplification, seem to be more important than germ line genetic variation in influencing PAI1 expression and its untoward effects in breast cancer...
  69. ncbi request reprint EGFR Intron 1 polymorphism in Asian Populations and its correlation with EGFR gene expression and amplification in breast tumor tissues
    Qingyu Zhou
    Laboratory of Clinical Pharmacology, National Cancer Centre, Singapore
    Cancer Biol Ther 5:1445-9. 2006
    ....
  70. pmc The eukaryotic translation elongation factor eEF1A2 induces neoplastic properties and mediates tumorigenic effects of ZNF217 in precursor cells of human ovarian carcinomas
    Yu Sun
    Department of Obstetrics and Gynecology, University of British Columbia, Vancouver, British Columbia, Canada
    Int J Cancer 123:1761-9. 2008
    ..Our data define neoplastic properties that are caused by eEF1A2 in nontumorigenic ovarian cancer precursor cells, and suggest that eEF1A2 plays a role in mediating ZNF217-induced neoplastic progression...
  71. pmc An integrative genomic and proteomic analysis of PIK3CA, PTEN, and AKT mutations in breast cancer
    Katherine Stemke-Hale
    Department of Systems Biology, The University of Texas MD Anderson Cancer, Houston, Texas 77030, USA
    Cancer Res 68:6084-91. 2008
    ..The specific aberration present may have implications for the selection of PI3K-targeted therapies in hormone receptor-positive breast cancer...
  72. pmc Translational Research Working Group developmental pathway for biospecimen-based assessment modalities
    Sudhir Srivastava
    Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland, USA
    Clin Cancer Res 14:5672-7. 2008
    ..This paper introduces the pathway in the context of prior work and discusses key challenges associated with the biomarker development process in light of the pathway...
  73. ncbi request reprint Asparagine synthetase as a causal, predictive biomarker for L-asparaginase activity in ovarian cancer cells
    Philip L Lorenzi
    Genomics and Bioinformatics Group, Room 5056B, 37 Convent Drive, Bethesda, MD 20892, USA
    Mol Cancer Ther 5:2613-23. 2006
    ..Overall, this pharmacogenomic/pharmacoproteomic study suggests the use of l-ASP for treatment of a subset of ovarian cancers (and perhaps other tumor types), with ASNS as a biomarker for patient selection...
  74. pmc Beta1 integrin inhibitory antibody induces apoptosis of breast cancer cells, inhibits growth, and distinguishes malignant from normal phenotype in three dimensional cultures and in vivo
    Catherine C Park
    Departments of Radiation Oncology and Pathology, University of California San Francisco Mt Zion Cancer Center, 1600 Divisadero Street, San Francisco, CA 94143 1708, USA
    Cancer Res 66:1526-35. 2006
    ..Our findings indicate that beta(1) integrin is a promising therapeutic target, and that the three-dimensional lrECM culture assay can be used to effectively distinguish malignant and normal tissue response to therapy...
  75. pmc Mapping and characterization of the amplicon near APOA2 in 1q23 in human sarcomas by FISH and array CGH
    Stine H Kresse
    Department of Tumour Biology, The Norwegian Radium Hospital, Oslo, Norway
    Mol Cancer 4:39. 2005
    ..In this study we have mapped and characterized the amplicon in 1q23 in more detail...
  76. ncbi request reprint Array-based comparative genomic hybridization analysis identified cyclin D1 as a target oncogene at 11q13.3 in nasopharyngeal carcinoma
    Angela Bik Yu Hui
    Departments of Anatomical and Cellular Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong SAR
    Cancer Res 65:8125-33. 2005
    ..The findings suggest that cyclin D1 is a target oncogene at 11q13 in nasopharyngeal carcinoma and its activation plays a significant role in nasopharyngeal carcinoma tumorigenesis...
  77. ncbi request reprint Increased risk of local recurrence is associated with allelic loss in normal lobules of breast cancer patients
    Zheng Li
    Geraldine Brush Cancer Research Institute, California Pacific Medical Center, San Francisco, California 94115, USA
    Cancer Res 62:1000-3. 2002
    ..These data provide a strong rationale to assess histologically normal breast tissue at the margins of surgically excised cancers for molecular predictors of local recurrence after breast-conserving treatment...

Research Grants5

  1. SPORE IN BREAST CANCER
    Joe Gray; Fiscal Year: 2007
    ..The SPORE is located organizationally in the Cancer Center Breast Oncology Program and takes full advantage of 13 Cancer Center Cores. ..