Jonathan Pollack

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. pmc Molecular profiling of breast cancer cell lines defines relevant tumor models and provides a resource for cancer gene discovery
    Jessica Kao
    Department of Pathology, Stanford University, Stanford, CA, USA
    PLoS ONE 4:e6146. 2009
  2. pmc Genomic profiling identifies GATA6 as a candidate oncogene amplified in pancreatobiliary cancer
    Kevin A Kwei
    Department of Pathology, Stanford University, Stanford, California, United States of America
    PLoS Genet 4:e1000081. 2008
  3. pmc Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types
    Craig P Giacomini
    Department of Pathology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS Genet 9:e1003464. 2013
  4. pmc Genomic and functional analysis identifies CRKL as an oncogene amplified in lung cancer
    Y H Kim
    Department of Pathology, Stanford University, Stanford, CA 94305 5176, USA
    Oncogene 29:1421-30. 2010
  5. pmc The spectrum of SWI/SNF mutations, ubiquitous in human cancers
    A Hunter Shain
    Department of Pathology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 8:e55119. 2013
  6. pmc Integrative bioinformatics links HNF1B with clear cell carcinoma and tumor-associated thrombosis
    Justin Cuff
    Department of Pathology, Stanford University, Stanford, California, United States of America
    PLoS ONE 8:e74562. 2013
  7. pmc SMURF1 amplification promotes invasiveness in pancreatic cancer
    Kevin A Kwei
    Department of Pathology, Stanford University, Stanford, California, United States of America
    PLoS ONE 6:e23924. 2011
  8. pmc Integrative genomic and functional profiling of the pancreatic cancer genome
    A Hunter Shain
    Departments of Pathology, Stanford University School of Medicine, 269 Campus Drive, CCSR 3245A, Stanford, CA 94305 5176, USA
    BMC Genomics 14:624. 2013
  9. pmc Lineage-specific gene duplication and loss in human and great ape evolution
    Andrew Fortna
    Department of Pharmacology and Human Medical Genetics Program, University of Colorado Health Sciences Center, Denver, Colorado, USA
    PLoS Biol 2:E207. 2004
  10. pmc A DNA microarray survey of gene expression in normal human tissues
    Radha Shyamsundar
    Department of Pathology, Stanford University School of Medicine, 269 Campus Drive, CCSR 3245A, Stanford, CA 94305 5176, USA
    Genome Biol 6:R22. 2005

Research Grants

  1. Gene Amplification and Deletion in Pancreatic Cancer
    Jonathan Pollack; Fiscal Year: 2007
  2. Role of Gene Amplification in Breast Cancer
    Jonathan Pollack; Fiscal Year: 2003
  3. Gene Amplification and Deletion in Pancreatic Cancer
    Jonathan Pollack; Fiscal Year: 2009
  4. Role of Gene Amplification in Breast Cancer
    Jonathan Pollack; Fiscal Year: 2006
  5. Gene Amplification and Deletion in Pancreatic Cancer
    Jonathan Pollack; Fiscal Year: 2006
  6. Pathogenetics of a Clinically-favorable Prostate Cancer Subtype
    Jonathan R Pollack; Fiscal Year: 2010
  7. Role of Gene Amplification in Breast Cancer
    Jonathan Pollack; Fiscal Year: 2004
  8. Pathogenetics of a Clinically-favorable Prostate Cancer Subtype
    Jonathan Pollack; Fiscal Year: 2009
  9. Gene Amplification and Deletion in Pancreatic Cancer
    Jonathan R Pollack; Fiscal Year: 2010
  10. Role of Gene Amplification in Breast Cancer
    Jonathan Pollack; Fiscal Year: 2005

Detail Information

Publications57

  1. pmc Molecular profiling of breast cancer cell lines defines relevant tumor models and provides a resource for cancer gene discovery
    Jessica Kao
    Department of Pathology, Stanford University, Stanford, CA, USA
    PLoS ONE 4:e6146. 2009
    ..Here, we studied a collection of breast cancer cell lines to catalog molecular profiles and to assess their relation to breast cancer subtypes...
  2. pmc Genomic profiling identifies GATA6 as a candidate oncogene amplified in pancreatobiliary cancer
    Kevin A Kwei
    Department of Pathology, Stanford University, Stanford, California, United States of America
    PLoS Genet 4:e1000081. 2008
    ....
  3. pmc Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types
    Craig P Giacomini
    Department of Pathology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS Genet 9:e1003464. 2013
    ..Taken together, we provide a robust approach for gene fusion discovery, and our results highlight a more widespread role of fusion genes in cancer pathogenesis...
  4. pmc Genomic and functional analysis identifies CRKL as an oncogene amplified in lung cancer
    Y H Kim
    Department of Pathology, Stanford University, Stanford, CA 94305 5176, USA
    Oncogene 29:1421-30. 2010
    ....
  5. pmc The spectrum of SWI/SNF mutations, ubiquitous in human cancers
    A Hunter Shain
    Department of Pathology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 8:e55119. 2013
    ..Our findings implicate SWI/SNF as an important but under-recognized tumor suppressor in diverse human cancers, and provide a key resource to guide future investigations...
  6. pmc Integrative bioinformatics links HNF1B with clear cell carcinoma and tumor-associated thrombosis
    Justin Cuff
    Department of Pathology, Stanford University, Stanford, California, United States of America
    PLoS ONE 8:e74562. 2013
    ..Our findings also implicate a novel mechanism of tumor-associated thrombosis (a major cause of cancer mortality), based on the direct production of clotting factors by cancer cells...
  7. pmc SMURF1 amplification promotes invasiveness in pancreatic cancer
    Kevin A Kwei
    Department of Pathology, Stanford University, Stanford, California, United States of America
    PLoS ONE 6:e23924. 2011
    ..Together, these findings identify SMURF1 as an amplified oncogene driving multiple tumorigenic phenotypes in pancreatic cancer, and provide a new druggable target for molecularly directed therapy...
  8. pmc Integrative genomic and functional profiling of the pancreatic cancer genome
    A Hunter Shain
    Departments of Pathology, Stanford University School of Medicine, 269 Campus Drive, CCSR 3245A, Stanford, CA 94305 5176, USA
    BMC Genomics 14:624. 2013
    ..To address this challenge, here we have devised a highly-parallel RNA interference-based functional screen to evaluate many genomically-nominated candidate pancreatic cancer genes simultaneously...
  9. pmc Lineage-specific gene duplication and loss in human and great ape evolution
    Andrew Fortna
    Department of Pharmacology and Human Medical Genetics Program, University of Colorado Health Sciences Center, Denver, Colorado, USA
    PLoS Biol 2:E207. 2004
    ....
  10. pmc A DNA microarray survey of gene expression in normal human tissues
    Radha Shyamsundar
    Department of Pathology, Stanford University School of Medicine, 269 Campus Drive, CCSR 3245A, Stanford, CA 94305 5176, USA
    Genome Biol 6:R22. 2005
    ....
  11. pmc A transcriptional response to Wnt protein in human embryonic carcinoma cells
    Jennifer Willert
    Department of Developmental Biology, Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305 USA
    BMC Dev Biol 2:8. 2002
    ..Wnt signaling is implicated in many developmental decisions, including stem cell control, as well as in cancer. There are relatively few target genes known of the Wnt pathway...
  12. pmc A perspective on DNA microarrays in pathology research and practice
    Jonathan R Pollack
    Department of Pathology, Stanford University School of Medicine, CCSR 3245A, 269 Campus Dr, Stanford, CA 94305 5176, USA
    Am J Pathol 171:375-85. 2007
    ..This review highlights some of the key contributions of DNA microarrays to experimental pathology, focusing in the area of cancer research. Also discussed are some of the current challenges in translating utility to clinical practice...
  13. pmc Microarray analysis reveals a major direct role of DNA copy number alteration in the transcriptional program of human breast tumors
    Jonathan R Pollack
    Departments of Pathology, Genetics, Surgery, Health Research and Policy, and Biochemistry, and Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 99:12963-8. 2002
    ..These findings provide evidence that widespread DNA copy number alteration can lead directly to global deregulation of gene expression, which may contribute to the development or progression of cancer...
  14. ncbi request reprint A method for calling gains and losses in array CGH data
    Pei Wang
    Department of Statistics, Stanford University, CA, 94305, USA
    Biostatistics 6:45-58. 2005
    ..We illustrate the method using an application of CLAC on a lung cancer microarray CGH data set as well as a BAC array CGH data set of aneuploid cell strains...
  15. ncbi request reprint Genomic profiling reveals alternative genetic pathways of prostate tumorigenesis
    Jacques Lapointe
    Department of Pathology, Stanford University, Stanford, California, USA
    Cancer Res 67:8504-10. 2007
    ..The resultant molecular genetic subtypes provide a new framework for investigating prostate cancer biology and explain in part the clinical heterogeneity of the disease...
  16. doi request reprint DNA microarray technology. Introduction
    Jonathan R Pollack
    Department of Pathology, Stanford University, Stanford, CA, USA
    Methods Mol Biol 556:1-6. 2009
    ..e., chromatin and transcription factor) interactions, DNA replication, and the integration of diverse genome-scale data types. Also provided is a perspective on recent advances and future directions in characterizing the physical genome...
  17. pmc Array-based comparative genomic hybridization identifies localized DNA amplifications and homozygous deletions in pancreatic cancer
    Murali D Bashyam
    Department of Pathology, Stanford University, Stanford, CA, USA
    Neoplasia 7:556-62. 2005
    ..Our findings suggest candidate genes and pathways, which may contribute to the development or progression of pancreatic cancer...
  18. pmc Genomic instability in breast cancer: pathogenesis and clinical implications
    Kevin A Kwei
    Department of Pathology, Stanford University School of Medicine, CCSR 3245A, 269 Campus Drive, Stanford, CA 94305 5176, USA
    Mol Oncol 4:255-66. 2010
    ..Future studies should clarify the pathogenesis of breast cancers with amplifier and complex-pattern genomes, and will likely identify new therapeutic opportunities...
  19. ncbi request reprint Characterizing the physical genome
    Jonathan R Pollack
    Department of Pathology, Stanford University School of Medicine, CCSR Building, Room 3245A, 269 Campus Drive, Stanford, California 94305 5176, USA
    Nat Genet 32:515-21. 2002
    ..Methods based on microarrays are beginning to provide a detailed picture of this physical genome, and they complement the genome-wide studies of mRNA expression profiling that have previously been so successful...
  20. pmc Gene expression patterns and gene copy number changes in dermatofibrosarcoma protuberans
    Sabine C Linn
    Departments of Pathology, Genetics, and Biochemistry, and Howard Hughes Medical Institute, Stanford University Medical Center, Stanford, California 94305, USA
    Am J Pathol 163:2383-95. 2003
    ....
  21. ncbi request reprint Use of gene-expression profiling to identify prognostic subclasses in adult acute myeloid leukemia
    Lars Bullinger
    Department of Pathology, Stanford University, Stanford, Calif, USA
    N Engl J Med 350:1605-16. 2004
    ..However, the current classification system does not fully reflect the molecular heterogeneity of the disease, and treatment stratification is difficult, especially for patients with intermediate-risk AML with a normal karyotype...
  22. pmc DR-Integrator: a new analytic tool for integrating DNA copy number and gene expression data
    Keyan Salari
    Department of Pathology, Stanford University, Stanford, CA, USA
    Bioinformatics 26:414-6. 2010
    ....
  23. ncbi request reprint Genome-wide characterization of gene expression variations and DNA copy number changes in prostate cancer cell lines
    Hongjuan Zhao
    Department of Urology, Stanford University School of Medicine, Stanford, California, USA
    Prostate 63:187-97. 2005
    ..The aim of this study was to characterize gene expression and DNA copy number profiles in androgen sensitive (AS) and androgen insensitive (AI) prostate cancer cell lines on a genome-wide scale...
  24. pmc The diagnosis and management of pre-invasive breast disease: promise of new technologies in understanding pre-invasive breast lesions
    Stefanie S Jeffrey
    Stanford University School of Medicine, Stanford, California, USA
    Breast Cancer Res 5:320-8. 2003
    ..It is expected that molecular technologies will identify breast tissue at risk for the development of unfavorable subtypes of invasive breast cancer and reveal strategies for targeted chemoprevention or eradication...
  25. pmc DNA microarray and proteomic strategies for understanding alcohol action
    James M Sikela
    University of Colorado at Denver and Health Sciences Center, Aurora, Colorado, USA
    Alcohol Clin Exp Res 30:700-8. 2006
    ..Kerns; and (4) Quantitative Proteomic Analysis of AC7-Modified Mice, by Kathleen J. Grant...
  26. pmc Identification of candidate prostate cancer genes through comparative expression-profiling of seminal vesicle
    Maxwell Thompson
    Department of Pathology, Stanford University, Stanford, California 94305 5176, USA
    Prostate 68:1248-56. 2008
    ..We hypothesized that gene-expression differences between prostate and seminal vesicle might inform mechanisms underlying the higher incidence of prostate cancer...
  27. ncbi request reprint Challenges in developing a molecular characterization of cancer
    Jonathan R Pollack
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Semin Oncol 29:280-5. 2002
    ..Here, we detail some of the challenges in developing a molecular characterization of cancer and in translating these new discoveries towards clinical utility...
  28. ncbi request reprint Application of genomic technologies to human prostate cancer
    Shijun Li
    Department of Urology, Stanford University of Medicine, Stanford, California 94305 5118, USA
    OMICS 10:261-75. 2006
    ..Continued improvements in methods of tissue preparation, microarray technology and data analysis will overcome existing challenges and fuel future discoveries...
  29. pmc Target discovery and validation in pancreatic cancer
    Robert M Beaty
    Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Methods Mol Biol 360:57-89. 2007
    ....
  30. pmc Amplification of whole tumor genomes and gene-by-gene mapping of genomic aberrations from limited sources of fresh-frozen and paraffin-embedded DNA
    Markus Bredel
    Division of Oncology, Clinical Sciences Research, Stanford University School of Medicine, 269 Campus Dr, CCSR 1105, Stanford, CA 94305 5151, USA
    J Mol Diagn 7:171-82. 2005
    ..Therefore, this amplification method should lend itself to high-throughput genetic analyses of limited sources of tumor, such as fine-needle biopsies, laser-microdissected tissue, and small paraffin-embedded specimens...
  31. ncbi request reprint Parallel analysis of gene copy number and expression using cDNA microarrays
    Jonathan R Pollack
    Department of Pathology, Stanford University School of Medicine, Palo Alto, CA, USA
    Methods Mol Biol 224:89-97. 2003
  32. ncbi request reprint The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer
    Hanna Kim
    Department of Pathology, Stanford University, Stanford, California 94305 5176, USA
    Cancer Res 65:8118-24. 2005
    ..Taken together, our findings implicate ALDH1a2 as a candidate tumor suppressor gene in prostate cancer and further support a role of retinoids in the prevention or treatment of prostate cancer...
  33. ncbi request reprint Comparative genomic hybridization on mouse cDNA microarrays and its application to a murine lymphoma model
    Sandrine Sander
    Department of Pathology, Stanford University, Stanford, CA 94305 5176, USA
    Oncogene 24:6101-7. 2005
    ....
  34. pmc Development of an orthotopic model of invasive pancreatic cancer in an immunocompetent murine host
    William W Tseng
    Department of Pathology, Stanford University, Palo Alto, California, USA
    Clin Cancer Res 16:3684-95. 2010
    ..We sought to develop an immunocompetent, orthotopic mouse model of pancreatic cancer with rapid and predictable growth kinetics...
  35. doi request reprint Integration of diverse microarray data types
    Keyan Salari
    Departments of Pathology and Genetics, Stanford University, Stanford, CA, USA
    Methods Mol Biol 556:205-16. 2009
    ..This chapter will outline general approaches to microarray data integration and provide an introduction to DR-Integrator, a broadly useful analysis tool for the integration of DNA copy number and gene-expression microarray data...
  36. pmc Interlaboratory performance of a microarray-based gene expression test to determine tissue of origin in poorly differentiated and undifferentiated cancers
    Catherine I Dumur
    Department of Pathology, Virginia Commonwealth University, Richmond, Virginia, USA
    J Mol Diagn 10:67-77. 2008
    ....
  37. doi request reprint Comparative genomic hybridization on spotted oligonucleotide microarrays
    Young H Kim
    Department of Pathology, Stanford University, Stanford, CA, USA
    Methods Mol Biol 556:21-32. 2009
    ....
  38. ncbi request reprint A gene expression signature of genetic instability in colon cancer
    Craig P Giacomini
    Department of Pathology, Stanford University, Stanford, CA 94305 5176, USA
    Cancer Res 65:9200-5. 2005
    ..Further, among the MSI signature genes, our findings implicate a role of elevated metallothionein expression in the clinical behavior of MSI cancers...
  39. ncbi request reprint Gene expression profiling in prostate cancer cells with Akt activation reveals Fra-1 as an Akt-inducible gene
    Gunjan Tiwari
    Department of Molecular Pharmacology, Stanford University and Department of Pathology, Stanford University School of Medicine, Stanford, CA
    Mol Cancer Res 1:475-84. 2003
    ..Moreover, the identification of Fra-1 as an Akt-regulated gene may have implications for the ability of Akt to transform cells since Fra-1 has been implicated in cell growth and the aggressiveness of tumors...
  40. ncbi request reprint RNA interference-based functional dissection of the 17q12 amplicon in breast cancer reveals contribution of coamplified genes
    Jessica Kao
    Department of Pathology, Stanford University, Stanford, California 94305, USA
    Genes Chromosomes Cancer 45:761-9. 2006
    ..Our findings validate the utility of RNAi in the functional interrogation of tumor amplicons, and provide evidence for a contribution of coamplified genes to tumor phenotypes...
  41. ncbi request reprint High-resolution array-based comparative genomic hybridization for distinguishing paraffin-embedded Spitz nevi and melanomas
    Jeff D Harvell
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Diagn Mol Pathol 13:22-5. 2004
    ....
  42. pmc Gene expression profiling identifies clinically relevant subtypes of prostate cancer
    Jacques Lapointe
    Department of Pathology, Stanford University, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 101:811-6. 2004
    ..Our results suggest that prostate tumors can be usefully classified according to their gene expression patterns, and these tumor subtypes may provide a basis for improved prognostication and treatment stratification...
  43. pmc Gene expression patterns in renal cell carcinoma assessed by complementary DNA microarray
    John P T Higgins
    Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA
    Am J Pathol 162:925-32. 2003
    ..Characterization of renal cell carcinomas based on gene expression patterns provides a revised classification of these tumors and has the potential to supply significant biological and clinical insights...
  44. doi request reprint hCAP-D3 expression marks a prostate cancer subtype with favorable clinical behavior and androgen signaling signature
    Jacques Lapointe
    Department of Pathology, Stanford University, Stanford, CA 94305 51, USA
    Am J Surg Pathol 32:205-9. 2008
    ..019). Our findings identify hCAP-D3 as a new biomarker for subtype-1 tumors that improves prognostication, and reveal androgen signaling as an important biologic feature of this potentially clinically favorable molecular subtype...
  45. ncbi request reprint Disclosure of candidate genes in acute myeloid leukemia with complex karyotypes using microarray-based molecular characterization
    Frank G Rücker
    Department of Neural Information Processing, University Hospital of Ulm, Ulm, Germany
    J Clin Oncol 24:3887-94. 2006
    ....
  46. ncbi request reprint Genomics in myeloid leukemias: an array of possibilities
    Lars Bullinger
    Department of Internal Medicine III, University of Ulm, Germany
    Rev Clin Exp Hematol 9:E2. 2005
    ..We expect whole genome approaches will significantly contribute to a better understanding of the pathogenesis and result in a refined molecular classification of myeloid leukemias...
  47. ncbi request reprint Molecular characterisation of soft tissue tumours: a gene expression study
    Torsten O Nielsen
    Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada
    Lancet 359:1301-7. 2002
    ..We aimed to start molecular characterisation of these rare neoplasms and to do a genome-wide search for new diagnostic markers...
  48. pmc Gene copy number variation spanning 60 million years of human and primate evolution
    Laura Dumas
    Human Medical Genetics Program, University of Colorado at Denver and Health Sciences Center, Aurora, Colorado 80045, USA
    Genome Res 17:1266-77. 2007
    ....
  49. ncbi request reprint Distinct patterns of DNA copy number alteration are associated with different clinicopathological features and gene-expression subtypes of breast cancer
    Anna Bergamaschi
    Department of Genetics, Institute for Cancer Research, Rikshospitalet Radiumhospitalet Medical Center, Oslo, Norway
    Genes Chromosomes Cancer 45:1033-40. 2006
    ..This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045-2257/suppmat..
  50. pmc A genome-wide screen for promoter methylation in lung cancer identifies novel methylation markers for multiple malignancies
    David S Shames
    Hamon Center for Therapeutic Oncology Research, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, United States of America
    PLoS Med 3:e486. 2006
    ....
  51. ncbi request reprint Gene-expression profiling identifies distinct subclasses of core binding factor acute myeloid leukemia
    Lars Bullinger
    Department of Internal Medicine III, University of Ulm, Ulm, Germany
    Blood 110:1291-300. 2007
    ..While the leukemogenic relevance of these signatures remains to be validated, their existence nevertheless supports a prognostically relevant biologic basis for the heterogeneity observed in CBF leukemia...
  52. ncbi request reprint Chromosome instability leaves its mark
    Jonathan R Pollack
    Nat Genet 38:973-4. 2006
  53. ncbi request reprint An expression-based site of origin diagnostic method designed for clinical application to cancer of unknown origin
    Richard W Tothill
    Ian Potter Centre for Cancer Genomics and Predictive Medicine, Department of Haematology and Medical Oncology, Peter MacCallum Cancer Centre, St Andrew s Place, East Melbourne, Victoria, Australia
    Cancer Res 65:4031-40. 2005
    ..We show that the microarray SVM classifier was capable of making high confidence predictions in 11 of 13 cases. These predictions were supported by comprehensive review of the patients' clinical histories...
  54. ncbi request reprint Aberrant epidermal growth factor receptor signaling and enhanced sensitivity to EGFR inhibitors in lung cancer
    Joseph Amann
    Vanderbilt Ingram Cancer Center, Nashville, TN 37232, USA
    Cancer Res 65:226-35. 2005
    ..Thus, in addition to EGFR mutations, other factors in NSCLC cells, such as high expression of ErbB family members, may constitutively activate AKT and sensitize cells to EGFR inhibitors...
  55. doi request reprint An FLT3 gene-expression signature predicts clinical outcome in normal karyotype AML
    Lars Bullinger
    Department of Internal Medicine III, University of Ulm, Ulm, Germany
    Blood 111:4490-5. 2008
    ..Our findings support the potential clinical utility of a gene expression-based measure of FLT3 pathway activation in AML...
  56. ncbi request reprint Evolutionary and biomedical insights from the rhesus macaque genome
    Richard A Gibbs
    Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX 77030, USA
    Science 316:222-34. 2007
    ..The complete description of the macaque genome blueprint enhances the utility of this animal model for biomedical research and improves our understanding of the basic biology of the species...
  57. pmc Physical mapping of genes in somatic cell radiation hybrids by comparative genomic hybridization to cDNA microarrays
    Johann Y Lin
    Department of Vascular Biology, The Scripps Research Institute, 10550 N, Torrey Pines Road, La Jolla, CA 92037, USA
    Genome Biol 3:RESEARCH0026. 2002
    ..Here we report experiments that establish the validity and efficacy of the methodology...

Research Grants13

  1. Gene Amplification and Deletion in Pancreatic Cancer
    Jonathan Pollack; Fiscal Year: 2007
    ....
  2. Role of Gene Amplification in Breast Cancer
    Jonathan Pollack; Fiscal Year: 2003
    ..abstract_text> ..
  3. Gene Amplification and Deletion in Pancreatic Cancer
    Jonathan Pollack; Fiscal Year: 2009
    ..abstract_text> ..
  4. Role of Gene Amplification in Breast Cancer
    Jonathan Pollack; Fiscal Year: 2006
    ..abstract_text> ..
  5. Gene Amplification and Deletion in Pancreatic Cancer
    Jonathan Pollack; Fiscal Year: 2006
    ....
  6. Pathogenetics of a Clinically-favorable Prostate Cancer Subtype
    Jonathan R Pollack; Fiscal Year: 2010
    ..Our findings may also suggest novel gene-based markers for the diagnosis of clinically- favorable tumors, leading to improved treatment stratification and clinical management of men with prostate cancer. ..
  7. Role of Gene Amplification in Breast Cancer
    Jonathan Pollack; Fiscal Year: 2004
    ..abstract_text> ..
  8. Pathogenetics of a Clinically-favorable Prostate Cancer Subtype
    Jonathan Pollack; Fiscal Year: 2009
    ..Our findings will further our understanding of the pathogenesis of prostate cancer, and may suggest novel gene-based markers for an improved classification of prostate tumors and management of patients with prostate cancer. ..
  9. Gene Amplification and Deletion in Pancreatic Cancer
    Jonathan R Pollack; Fiscal Year: 2010
    ..abstract_text> ..
  10. Role of Gene Amplification in Breast Cancer
    Jonathan Pollack; Fiscal Year: 2005
    ..abstract_text> ..
  11. Role of Gene Amplification in Breast Cancer
    Jonathan Pollack; Fiscal Year: 2007
    ..abstract_text> ..