William Sellers

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi The EZH2 polycomb transcriptional repressor--a marker or mover of metastatic prostate cancer?
    William R Sellers
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 2:349-50. 2002
  2. ncbi Growth factor requirements and basal phenotype of an immortalized mammary epithelial cell line
    James DiRenzo
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 62:89-98. 2002
  3. ncbi Signal transducer and activator of transcription 3 is required for the oncogenic effects of non-small-cell lung cancer-associated mutations of the epidermal growth factor receptor
    James V Alvarez
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 66:3162-8. 2006
  4. ncbi From integrated genomics to tumor lineage dependency
    Levi A Garraway
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 66:2506-8. 2006
  5. pmc Allele-specific amplification in cancer revealed by SNP array analysis
    Thomas LaFramboise
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
    PLoS Comput Biol 1:e65. 2005
  6. ncbi Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors
    Ingo K Mellinghoff
    Department of Molecular and Medical Pharmacology and Medicine, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles 90095 1732, USA
    N Engl J Med 353:2012-24. 2005
  7. ncbi Epidermal growth factor-independent transformation of Ba/F3 cells with cancer-derived epidermal growth factor receptor mutants induces gefitinib-sensitive cell cycle progression
    Jingrui Jiang
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 65:8968-74. 2005
  8. pmc Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutants
    Heidi Greulich
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
    PLoS Med 2:e313. 2005
  9. ncbi Amplification and overexpression of prosaposin in prostate cancer
    Shahriar Koochekpour
    Department of Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA
    Genes Chromosomes Cancer 44:351-64. 2005
  10. ncbi Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma
    Levi A Garraway
    Department of Medical Oncology, and Melanoma Program in Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA
    Nature 436:117-22. 2005

Collaborators

Detail Information

Publications63

  1. ncbi The EZH2 polycomb transcriptional repressor--a marker or mover of metastatic prostate cancer?
    William R Sellers
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 2:349-50. 2002
    ....
  2. ncbi Growth factor requirements and basal phenotype of an immortalized mammary epithelial cell line
    James DiRenzo
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 62:89-98. 2002
    ..Our studies suggest that the immortalization of basal epithelial cells of the mammary gland may be an early step in the initiation of a subset of breast cancers with a basal epithelial phenotype...
  3. ncbi Signal transducer and activator of transcription 3 is required for the oncogenic effects of non-small-cell lung cancer-associated mutations of the epidermal growth factor receptor
    James V Alvarez
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 66:3162-8. 2006
    ..Thus, STAT3 is a critical mediator of the oncogenic effects of somatic EGFR mutations and targeting STAT3 may be an effective strategy for treating tumors characterized by these mutations...
  4. ncbi From integrated genomics to tumor lineage dependency
    Levi A Garraway
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 66:2506-8. 2006
    ..Similar combined genomic approaches may be useful in other cancer types to learn how critical regulators of tumor lineage are linked to genomic alterations in cancer cells...
  5. pmc Allele-specific amplification in cancer revealed by SNP array analysis
    Thomas LaFramboise
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
    PLoS Comput Biol 1:e65. 2005
    ..An R software package containing the methods described in this paper is freely available at http://genome.dfci.harvard.edu/~tlaframb/PLASQ...
  6. ncbi Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors
    Ingo K Mellinghoff
    Department of Molecular and Medical Pharmacology and Medicine, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles 90095 1732, USA
    N Engl J Med 353:2012-24. 2005
    ..The mechanism of responsiveness of glioblastomas to these inhibitors is unknown...
  7. ncbi Epidermal growth factor-independent transformation of Ba/F3 cells with cancer-derived epidermal growth factor receptor mutants induces gefitinib-sensitive cell cycle progression
    Jingrui Jiang
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 65:8968-74. 2005
    ..Our results provide a model system to study the function of mutated EGFR and the differential effects of pharmacologic EGFR inhibition on the distinct mutant forms of this tyrosine kinase...
  8. pmc Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutants
    Heidi Greulich
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
    PLoS Med 2:e313. 2005
    ..The presence of mutations correlates with tumor sensitivity to the EGFR inhibitors erlotinib and gefitinib, but the transforming potential of specific mutations and their relationship to drug sensitivity have not been described...
  9. ncbi Amplification and overexpression of prosaposin in prostate cancer
    Shahriar Koochekpour
    Department of Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA
    Genes Chromosomes Cancer 44:351-64. 2005
    ....
  10. ncbi Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma
    Levi A Garraway
    Department of Medical Oncology, and Melanoma Program in Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA
    Nature 436:117-22. 2005
    ..Together, these data suggest that MITF represents a distinct class of 'lineage survival' or 'lineage addiction' oncogenes required for both tissue-specific cancer development and tumour progression...
  11. ncbi Homozygous deletions and chromosome amplifications in human lung carcinomas revealed by single nucleotide polymorphism array analysis
    Xiaojun Zhao
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 65:5561-70. 2005
    ..EGFR amplification was shown to be independent of kinase domain mutational status...
  12. ncbi Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis
    Ross L Levine
    Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Cell 7:387-97. 2005
    ..In vitro analysis demonstrated that JAK2V617F is a constitutively active tyrosine kinase...
  13. ncbi Selective ablation of retinoblastoma protein function by the RET finger protein
    Maja Kr├╝tzfeldt
    Centre for Cell and Molecular Biology, Chester Beatty Laboratories, 237 Fulham Road, SW3 6JB London, United Kingdom
    Mol Cell 18:213-24. 2005
    ..These findings provide precedent for a regulatory pathway that uncouples different Rb-dependent activities and thus silences specific cellular responses to Rb in a selective way...
  14. pmc Inferring loss-of-heterozygosity from unpaired tumors using high-density oligonucleotide SNP arrays
    Rameen Beroukhim
    Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    PLoS Comput Biol 2:e41. 2006
    ..We have developed a method for analyzing high-density oligonucleotide SNP array data to accurately identify of regions of LOH and retention in tumors without the need for paired normal samples...
  15. ncbi Development of an integrated prostate cancer research information system
    William K Oh
    Lank Center for Genitourinary Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Clin Genitourin Cancer 5:61-6. 2006
    ..In this article, we describe the design and implementation of a comprehensive prostate cancer database developed to collect, store, and access clinical, treatment, and outcomes data for research and clinical care...
  16. pmc Major copy proportion analysis of tumor samples using SNP arrays
    Cheng Li
    Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute and Harvard School of Public Health, 3 Blackfan Circle, Boston, MA 02115, USA
    BMC Bioinformatics 9:204. 2008
    ..We have previously used Hidden Markov Models (HMM) to analyze SNP array data for inferring copy numbers and loss-of-heterozygosity (LOH) from paired normal and tumor samples and unpaired tumor samples...
  17. pmc PTEN nuclear localization is regulated by oxidative stress and mediates p53-dependent tumor suppression
    Chun Ju Chang
    Molecular and Medical Pharmacology, UCLA School of Medicine, Los Angeles, CA 90095, USA
    Mol Cell Biol 28:3281-9. 2008
    ..Since tumor cells are constantly exposed to oxidative stress, our study elucidates the cooperative roles of nuclear PTEN with p53 in tumor suppression...
  18. pmc SNP panel identification assay (SPIA): a genetic-based assay for the identification of cell lines
    Francesca Demichelis
    Department of Pathology, Brigham and Women s Hospital, Boston, MA, USA
    Nucleic Acids Res 36:2446-56. 2008
    ....
  19. doi Modeling genomic diversity and tumor dependency in malignant melanoma
    William M Lin
    Department of Medical Oncology, Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 68:664-73. 2008
    ..Genetically defined cell culture collections therefore offer a rich framework for systematic functional studies in melanoma and other tumors...
  20. ncbi HER-2/neu expression is associated with high tumor cell proliferation and aggressive phenotype in a population based patient series of endometrial carcinomas
    Ingeborg B Engelsen
    Department of Obstetrics and Gynecology, Haukeland University Hospital, Bergen, Norway
    Int J Oncol 32:307-16. 2008
    ..These results motivate further clinical trials with trastuzumab based on HER-2/neu status in endometrial carcinomas...
  21. pmc Focal gains of VEGFA and molecular classification of hepatocellular carcinoma
    Derek Y Chiang
    Department of Medical Oncology and Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 68:6779-88. 2008
    ..Furthermore, the prevalence of VEGFA high-level gains in multiple tumor types suggests indications for clinical trials of antiangiogenic therapies...
  22. pmc Identification of prostate cancer modifier pathways using parental strain expression mapping
    Qing Xu
    Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115
    Proc Natl Acad Sci U S A 104:17771-6. 2007
    ..Together, these data suggest that parental strain expression mapping can directly identify germ-line modifier pathways of relevance to human disease...
  23. ncbi High-throughput oncogene mutation profiling in human cancer
    Roman K Thomas
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
    Nat Genet 39:347-51. 2007
    ..These results offer a new dimension in tumor genetics, where mutations involving multiple cancer genes may be interrogated simultaneously and in 'real time' to guide cancer classification and rational therapeutic intervention...
  24. pmc Epidermal growth factor receptor activation in glioblastoma through novel missense mutations in the extracellular domain
    Jeffrey C Lee
    Department of Medical Oncology and Center for Cancer Genome Discovery, Dana Farber Cancer Institute Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS Med 3:e485. 2006
    ..Missense mutations in the EGFR kinase domain, for example, have recently been identified in patients who showed clinical responses to EGFR kinase inhibitor therapy...
  25. ncbi TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer
    Sven Perner
    Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, EBRC 442A, 221 Longwood Avenue, Boston, MA 02115 6110, USA
    Cancer Res 66:8337-41. 2006
    ..The deletion as cause of TMPRSS2:ERG fusion is associated with clinical features for prostate cancer progression compared with tumors that lack the TMPRSS2:ERG rearrangement...
  26. ncbi Lineage dependency and lineage-survival oncogenes in human cancer
    Levi A Garraway
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nat Rev Cancer 6:593-602. 2006
    ..MITF and other lineage-survival genes therefore implicate lineage dependency (or lineage addiction) as a newly recognized mechanism that is affected by tumour genetic alterations...
  27. ncbi EGFR gene mutations: a call for global x global views of cancer
    William R Sellers
    J Natl Cancer Inst 97:326-8. 2005
  28. ncbi Androgen-induced differentiation and tumorigenicity of human prostate epithelial cells
    Raanan Berger
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Cancer Res 64:8867-75. 2004
    ..These observations indicate that androgen receptor expression is oncogenic and addictive for the human prostate epithelium...
  29. ncbi Activating mutations of the noonan syndrome-associated SHP2/PTPN11 gene in human solid tumors and adult acute myelogenous leukemia
    Mohamed Bentires-Alj
    Cancer Biology Program, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
    Cancer Res 64:8816-20. 2004
    ..Our data demonstrate that mutations in PTPN11 occur at low frequency in several human cancers, especially neuroblastoma and AML, and suggest that Shp2 may be a novel target for antineoplastic therapy...
  30. ncbi mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia through regulation of apoptotic and HIF-1-dependent pathways
    Pradip K Majumder
    Department of Medical Oncology, Dana Farber Cancer Institute, and Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Med 10:594-601. 2004
    ....
  31. ncbi Genome-wide loss of heterozygosity analysis from laser capture microdissected prostate cancer using single nucleotide polymorphic allele (SNP) arrays and a novel bioinformatics platform dChipSNP
    Marshall E Lieberfarb
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 63:4781-5. 2003
    ..This organizational strategy revealed apparently distinct genetic subsets of prostate cancer...
  32. pmc Genome coverage and sequence fidelity of phi29 polymerase-based multiple strand displacement whole genome amplification
    J Guillermo Paez
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Nucleic Acids Res 32:e71. 2004
    ..These results suggest that phi29MDA yields high fidelity, near-complete genome representation suitable for high resolution genetic analysis...
  33. ncbi 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...
  34. ncbi EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy
    J Guillermo Paez
    Departments of Medical Oncology and Cancer Biology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Science 304:1497-500. 2004
    ..These results suggest that EGFR mutations may predict sensitivity to gefitinib...
  35. ncbi TSC2 regulates VEGF through mTOR-dependent and -independent pathways
    James B Brugarolas
    Dana Farber Cancer Institute and Brigham and Women s Hospital, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
    Cancer Cell 4:147-58. 2003
    ..This pathway may involve chromatin remodeling since the HDAC inhibitor Trichostatin A downregulates VEGF in TSC2(-/-) cells...
  36. ncbi dChipSNP: significance curve and clustering of SNP-array-based loss-of-heterozygosity data
    Ming Lin
    Department of Biostatistics, Harvard School of Public Health, Boston, MA 02115, USA
    Bioinformatics 20:1233-40. 2004
    ..Recently, this technology has been applied to loss-of-heterozygosity (LOH) analysis of paired normal and tumor samples. However, methods and software for analyzing such data are not fully developed...
  37. ncbi A chemical genetic screen identifies inhibitors of regulated nuclear export of a Forkhead transcription factor in PTEN-deficient tumor cells
    Tweeny R Kau
    Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 4:463-76. 2003
    ..Novel general export inhibitors were found that react with CRM1 as well as a number of compounds that inhibit PI3K/Akt signaling, among which are included multiple antagonists of calmodulin signaling...
  38. ncbi Use of expression analysis to predict outcome after radical prostatectomy
    Phillip G Febbo
    Department of Medical Oncology, Dana Farber Cancer Institute, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02118, USA
    J Urol 170:S11-9; discussion S19-20. 2003
    ..We summarize and discuss our recent work exploring the use of gene expression analysis for the prediction of histopathological features of prostate cancer and patient outcome following radical prostatectomy...
  39. ncbi Overexpression, amplification, and androgen regulation of TPD52 in prostate cancer
    Mark A Rubin
    Department of Pathology, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Cancer Res 64:3814-22. 2004
    ..In summary, these findings suggest that dysregulation of TPD52 by genomic amplification and androgen induction may play a role in prostate cancer progression...
  40. ncbi Multiple genes in human 20q13 chromosomal region are involved in an advanced prostate cancer xenograft
    Anat Bar-Shira
    Genetic Institute, Tel Aviv Sourasky Medical Center, Tel Aviv 64239, Israel
    Cancer Res 62:6803-7. 2002
    ..Our data suggest these genes to be involved in advanced stages of prostate tumorigenesis and as such, they may serve as markers for tumor progression...
  41. ncbi The biology and clinical relevance of the PTEN tumor suppressor pathway
    Isabelle Sansal
    Department of Medical Oncology, Dana Farber Cancer Institute, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
    J Clin Oncol 22:2954-63. 2004
    ..Akt kinase inhibitors are still in development; however, as a first test of this hypothesis, phase I and phase II trials of inhibitors of mTOR, namely, rapamycin and rapamycin analogs are underway...
  42. ncbi Molecular characterization of the tumor microenvironment in breast cancer
    Minna Allinen
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Cell 6:17-32. 2004
    ..Thus, chemokines may play a role in breast tumorigenesis by acting as paracrine factors...
  43. ncbi A novel mechanism of gene regulation and tumor suppression by the transcription factor FKHR
    Shivapriya Ramaswamy
    Department of Adult Oncology and Department of Internal Medicine, Dana Farber Cancer Institute and Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Cell 2:81-91. 2002
    ..These data suggest that a novel mechanism of FKHR-mediated gene regulation is linked to its activity as a suppressor of tumor growth...
  44. ncbi Analysis of androgen regulated homeobox gene NKX3.1 during prostate carcinogenesis
    Ceren G Korkmaz
    Department of Molecular Biosciences, and Biotechnology Centre of Oslo, University of Oslo, Oslo, Norway
    J Urol 172:1134-9. 2004
    ..1 might have a direct role in prostate carcinogenesis, possibly functioning as a tumor suppressor protein. Previous studies of the levels of NKX3.1 mRNA or protein in prostate cancer specimens have resulted in conflicting findings...
  45. ncbi Frequent HIN-1 promoter methylation and lack of expression in multiple human tumor types
    Ian Krop
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, D740C, Boston, MA 02115, USA
    Mol Cancer Res 2:489-94. 2004
    ..Thus, silencing of HIN-1 expression and methylation of its promoter occurs in multiple human cancer types, suggesting that elimination of HIN-1 function may contribute to several forms of epithelial tumorigenesis...
  46. ncbi PI3K/PTEN/AKT pathway. A critical mediator of oncogenic signaling
    Juan Paez
    Department of Adult Oncology, Dana Farber Cancer Institute, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Cancer Treat Res 115:145-67. 2003
  47. pmc Drug-sensitive FGFR2 mutations in endometrial carcinoma
    Amit Dutt
    Department of Medical Oncology and Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 105:8713-7. 2008
    ..Inhibition of FGFR2 kinase activity in endometrial carcinoma cell lines bearing such FGFR2 mutations inhibits transformation and survival, implicating FGFR2 as a novel therapeutic target in endometrial carcinoma...
  48. ncbi A 2-Mb critical region implicated in the microcephaly associated with terminal 1q deletion syndrome
    Anthony D Hill
    Howard Hughes Medical Institute, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    Am J Med Genet A 143:1692-8. 2007
    ..0-Mb microcephaly critical region including the 1q43-1q44 boundary and no more than 11 genes...
  49. ncbi Gene expression correlates of clinical prostate cancer behavior
    Dinesh Singh
    Department of Adult Oncology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 1:203-9. 2002
    ..These results support the notion that the clinical behavior of prostate cancer is linked to underlying gene expression differences that are detectable at the time of diagnosis...
  50. pmc Assessing the significance of chromosomal aberrations in cancer: methodology and application to glioma
    Rameen Beroukhim
    Broad Institute, Massachusetts Institute of Technology and Harvard University, 7 Cambridge Center, Cambridge, MA 02142, USA
    Proc Natl Acad Sci U S A 104:20007-12. 2007
    ..Our results support the feasibility and utility of systematic characterization of the cancer genome...
  51. pmc Prostate intraepithelial neoplasia induced by prostate restricted Akt activation: the MPAKT model
    Pradip K Majumder
    Department of Medical Oncology, Dana Farber Cancer Institute, and Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 100:7841-6. 2003
    ..Thus, the MPAKT model may be useful in studying the role of Akt in prostate epithelial cell transformation and in the discovery of molecular markers relevant to human disease...
  52. ncbi Third international conference on innovations and challenges in prostate cancer: prevention, detection and treatment
    Peter R Carroll
    Department of Urology, University of California School of Medicine, San Francisco 94115 1711, USA
    J Urol 170:S3-5. 2003
  53. pmc A library of siRNA duplexes targeting the phosphoinositide 3-kinase pathway: determinants of gene silencing for use in cell-based screens
    Andrew C Hsieh
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Nucleic Acids Res 32:893-901. 2004
    ..These data help to lay the foundation for genome-wide siRNA screens in mammalian cells...
  54. ncbi Fourth International Conference on Innovations and Challenges in Prostate Cancer: Prevention, Detection and Treatment
    Peter R Carroll
    Department of Urology, University of California School of Medicine, San Francisco 94115 1711, USA
    J Urol 172:S3-5. 2004
  55. ncbi High tumor incidence and activation of the PI3K/AKT pathway in transgenic mice define AIB1 as an oncogene
    Maria I Torres-Arzayus
    Division of Molecular and Cellular Oncology, Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
    Cancer Cell 6:263-74. 2004
    ..Knockdown of AIB1 expression in cultured AIB1-tg mammary tumor cells leads to reduced IGF-I mRNA levels and increased apoptosis, suggesting that an autocrine IGF-I loop underlies the mechanism of AIB1-induced oncogenesis...
  56. pmc p63 regulates commitment to the prostate cell lineage
    Sabina Signoretti
    Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:11355-60. 2005
    ..Finally, in contrast with the prostate findings, analysis of the urothelium from rescued p63-/- chimeras shows that umbrella (superficial) cells can develop and be maintained independently from p63-positive basal and intermediate cells...
  57. ncbi Identifying and characterizing a novel activating mutation of the FLT3 tyrosine kinase in AML
    Jingrui Jiang
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney St, D720C, Boston, MA 02115, USA
    Blood 104:1855-8. 2004
    ..These results suggest that mutations at N841 represent a significant new activating mutation in patients with AML and that patients with such mutations may respond to small-molecule FLT3 inhibitors such as PKC412...
  58. pmc BRAF mutation predicts sensitivity to MEK inhibition
    David B Solit
    Department of Medicine, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
    Nature 439:358-62. 2006
    ..These data suggest an exquisite dependency on MEK activity in BRAF mutant tumours, and offer a rational therapeutic strategy for this genetically defined tumour subtype...
  59. ncbi Akt-regulated pathways in prostate cancer
    Pradip K Majumder
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Oncogene 24:7465-74. 2005
    ....
  60. ncbi Seventeenth Annual Pezcoller Symposium: molecular understanding of solid tumors
    Enrico Mihich
    Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Cancer Res 65:11251-4. 2005
  61. ncbi Validating cancer drug targets
    John D Benson
    Novartis Institutes for BioMedical Research, 250 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA
    Nature 441:451-6. 2006
    ..Although the outcome of validation studies can guide cancer research programmes, strictly defined universal validation criteria have not been established...
  62. ncbi Sensitive mutation detection in heterogeneous cancer specimens by massively parallel picoliter reactor sequencing
    Roman K Thomas
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
    Nat Med 12:852-5. 2006
    ..This technology can thereby facilitate accurate molecular diagnosis of heterogeneous cancer specimens and enable patient selection for targeted cancer therapies...
  63. ncbi A Smac mimetic rescue screen reveals roles for inhibitor of apoptosis proteins in tumor necrosis factor-alpha signaling
    Alex Gaither
    Oncology Disease Area and Developmental and Molecular Pathways, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts 02139, USA
    Cancer Res 67:11493-8. 2007
    ..Mechanistic studies indicate that in this context, XIAP is a positive modulator of TNFalpha induction whereas cellular inhibitor of apoptosis protein 1 negatively regulates TNFalpha-mediated apoptosis...