S E Kern

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. pmc Improved DNA electrophoresis in conditions favoring polyborates and lewis acid complexation
    Hari Singhal
    Department of Biomedical Engineering, The Johns Hopkins University and the Sidney Kimmel Comprehensive Center at Johns Hopkins, Baltimore, Maryland, United States of America
    PLoS ONE 5:e11318. 2010
  2. pmc A thymidylate synthase ternary complex-specific antibody, FTS, permits functional monitoring of fluoropyrimidines dosing
    Kalpesh Patel
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA
    Oncotarget 3:678-85. 2012
  3. pmc DNA-intercalators causing rapid re-expression of methylated and silenced genes in cancer cells
    M Zulfiquer Hossain
    Sidney Kimmel Comprehensive Cancer Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Oncotarget 4:298-309. 2013
  4. pmc Analysis of polymorphisms and haplotype structure of the human thymidylate synthase genetic region: a tool for pharmacogenetic studies
    Soma Ghosh
    Department of Oncology, Johns Hopkins School of Medicine, Johns Hopkins University, Baltimore, Maryland, United States of America
    PLoS ONE 7:e34426. 2012
  5. pmc Why your new cancer biomarker may never work: recurrent patterns and remarkable diversity in biomarker failures
    Scott E Kern
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Department of Oncology, 1650 Orleans Avenue, Baltimore, MD 21287, USA
    Cancer Res 72:6097-101. 2012
  6. pmc Analytic model for academic research productivity having factors, interactions and implications
    Scott Kern
    Department of Oncology, Johns Hopkins University, Baltimore, MD, USA
    Cancer Biol Ther 12:949-56. 2011
  7. pmc Does tumorigenesis select for or against mutations of the DNA repair-associated genes BRCA2 and MRE11?: considerations from somatic mutations in microsatellite unstable (MSI) gastrointestinal cancers
    Michiel S Van Der Heijden
    From the department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
    BMC Genet 7:3. 2006
  8. ncbi request reprint Quantitative selection constants
    Scott E Kern
    Department of Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 1:189-94. 2002
  9. ncbi request reprint Fellowship goals for PhDs and MDs: a primer on the molecular biology postdoctoral experience
    Scott E Kern
    Department of Oncology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 1:74-5. 2002
  10. pmc Where's the passion?
    Scott E Kern
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA
    Cancer Biol Ther 10:655-7. 2010

Detail Information

Publications105 found, 100 shown here

  1. pmc Improved DNA electrophoresis in conditions favoring polyborates and lewis acid complexation
    Hari Singhal
    Department of Biomedical Engineering, The Johns Hopkins University and the Sidney Kimmel Comprehensive Center at Johns Hopkins, Baltimore, Maryland, United States of America
    PLoS ONE 5:e11318. 2010
    ..5) favoring the formation of borate polyanions and having lower conductance and Joule heating, delayed electrolyte exhaustion, faster electrophoretic run-speed, and sharper separation of DNA bands from 100 bp to 12 kb in a single run...
  2. pmc A thymidylate synthase ternary complex-specific antibody, FTS, permits functional monitoring of fluoropyrimidines dosing
    Kalpesh Patel
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA
    Oncotarget 3:678-85. 2012
    ..Such a development might aid preclinical analytic studies or make practical the individual tailoring of dosing...
  3. pmc DNA-intercalators causing rapid re-expression of methylated and silenced genes in cancer cells
    M Zulfiquer Hossain
    Sidney Kimmel Comprehensive Cancer Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Oncotarget 4:298-309. 2013
    ..Rapid mechanisms for chemical desilencing of methylated genes therefore exist...
  4. pmc Analysis of polymorphisms and haplotype structure of the human thymidylate synthase genetic region: a tool for pharmacogenetic studies
    Soma Ghosh
    Department of Oncology, Johns Hopkins School of Medicine, Johns Hopkins University, Baltimore, Maryland, United States of America
    PLoS ONE 7:e34426. 2012
    ..The presence of multiple long (up to 26 nt), polymorphic monothymidine repeats in the promoter region of the sole human thymidylate synthetic enzyme is intriguing...
  5. pmc Why your new cancer biomarker may never work: recurrent patterns and remarkable diversity in biomarker failures
    Scott E Kern
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Department of Oncology, 1650 Orleans Avenue, Baltimore, MD 21287, USA
    Cancer Res 72:6097-101. 2012
    ....
  6. pmc Analytic model for academic research productivity having factors, interactions and implications
    Scott Kern
    Department of Oncology, Johns Hopkins University, Baltimore, MD, USA
    Cancer Biol Ther 12:949-56. 2011
    ..Their interactions produce output and patterned influences between factors. Strategies for optimizing output are enabled...
  7. pmc Does tumorigenesis select for or against mutations of the DNA repair-associated genes BRCA2 and MRE11?: considerations from somatic mutations in microsatellite unstable (MSI) gastrointestinal cancers
    Michiel S Van Der Heijden
    From the department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
    BMC Genet 7:3. 2006
    ..Somatic mutations of BRCA2 are rare in typical sporadic cancers. In tumors having microsatellite instability (MSI), somatic truncating mutations in a poly [A] tract of BRCA2 are reported on occasion...
  8. ncbi request reprint Quantitative selection constants
    Scott E Kern
    Department of Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 1:189-94. 2002
    ..Some intuitive mathematical models can be used to organize and formalize our interpretation of the mutation rates of tumor-suppressor genes...
  9. ncbi request reprint Fellowship goals for PhDs and MDs: a primer on the molecular biology postdoctoral experience
    Scott E Kern
    Department of Oncology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 1:74-5. 2002
  10. pmc Where's the passion?
    Scott E Kern
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA
    Cancer Biol Ther 10:655-7. 2010
    ..In his article, Dr. Kern asks whether research is evolving into a predictable career rather than a creative frontier and what that might portend...
  11. pmc The complexity of pancreatic ductal cancers and multidimensional strategies for therapeutic targeting
    Scott E Kern
    Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21231, USA
    J Pathol 223:295-306. 2011
    ..Simplistic expectations, often falsely optimistic, for individualized care may fail to 'pan out' in the real world. The development of individualized care will be efficient only when the full complexity of the disease is embraced...
  12. ncbi request reprint Whose hypothesis? Ciphering, sectorials, D lesions, freckles and the operation of Stigler's Law
    Scott E Kern
    The Johns Hopkins University School of Medicine, 451 Cancer Research Building, 1650 Orleans Street, Baltimore, MD 21231, USA
    Cancer Biol Ther 1:571-81. 2002
    ..The current work is intended to raise the appreciation for this rich history and to address some of the more common errors...
  13. ncbi request reprint An introduction to pancreatic adenocarcinoma genetics, pathology and therapy
    Scott E Kern
    Department of Oncology, Surgery, and Pathology, The Sidney Kimmel Comphrehensive Cancer Center, John s Hopkins, Baltimore, MD, USA
    Cancer Biol Ther 1:607-13. 2002
    ..The accumulating discoveries regarding the genetic basis of pancreatic cancer and developments in the clinical management of the disease provide hope for meaningful improvements in the understanding and control of this disease...
  14. ncbi request reprint Ultra-fast high-resolution agarose electrophoresis of DNA and RNA using low-molarity conductive media
    Jonathan R Brody
    The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Biotechniques 37:598, 600, 602. 2004
    ..These novel media reduce the Joule heating of the electrophoretic system and allow for easy-to-use, ultra-fast separation of DNA fragments...
  15. ncbi request reprint The fuzzy math of solid tumor stem cells: a perspective
    Scott E Kern
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, Maryland 21231, USA
    Cancer Res 67:8985-8. 2007
    ..Mathematical arguments should be used more consistently, because they can serve as a guide for interpreting studies into cancer stem cells of solid tumors...
  16. ncbi request reprint Elegance, silence and nonsense in the mutations literature for solid tumors
    Scott E Kern
    Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 5:349-59. 2006
    ..These patterns provide support for a systematic approach to the critical analysis of the somatic mutation literature offered in the accompanying paper...
  17. ncbi request reprint Molecular genetic alterations in ductal pancreatic adenocarcinomas
    S E Kern
    Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Med Clin North Am 84:691-5, xi. 2000
    ....
  18. ncbi request reprint Homozygous deletion map at 18q21.1 in pancreatic cancer
    S A Hahn
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Cancer Res 56:490-4. 1996
    ....
  19. pmc Targeted deletion of Smad4 shows it is required for transforming growth factor beta and activin signaling in colorectal cancer cells
    S Zhou
    The Howard Hughes Medical Institute at Johns Hopkins University, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 95:2412-6. 1998
    ..These results provide unequivocal evidence that mutational inactivation of Smad4 causes TGF-beta unresponsiveness and provide a basis for understanding the physiologic role of this gene in tumorigenesis...
  20. ncbi request reprint Discovery of new markers of cancer through serial analysis of gene expression: prostate stem cell antigen is overexpressed in pancreatic adenocarcinoma
    P Argani
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA
    Cancer Res 61:4320-4. 2001
    ..PSCA is a novel tumor marker for pancreatic carcinoma that has potential diagnostic and therapeutic implications. These results establish the validity of analyses of SAGE databases to identify novel tumor markers...
  21. ncbi request reprint Differing rates of loss of DPC4 expression and of p53 overexpression among carcinomas of the proximal and distal bile ducts
    P Argani
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Cancer 91:1332-41. 2001
    ..Biliary tract carcinomas are clinically heterogeneous. It is not known if molecular heterogeneity underlies the clinical differences...
  22. ncbi request reprint Homozygous deletions inactivate DCC, but not MADH4/DPC4/SMAD4, in a subset of pancreatic and biliary cancers
    W Hilgers
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    Genes Chromosomes Cancer 27:353-7. 2000
    ..These data are the strongest mutational evidence presented yet in support of the hypothesis that DCC or another gene in the region distal to MADH4 is inactivated, playing a causal role in cancer development...
  23. pmc Germline and somatic mutations of the STK11/LKB1 Peutz-Jeghers gene in pancreatic and biliary cancers
    G H Su
    Departments of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Am J Pathol 154:1835-40. 1999
    ..Our results demonstrate that germline and somatic genetic alterations of the STK11/LKB1 gene may play a causal role in carcinogenesis and that the same gene contributes to the development of both sporadic and familial forms of cancer...
  24. ncbi request reprint Frequent germline deletion polymorphism of chromosomal region 8p12-p21 identified as a recurrent homozygous deletion in human tumors
    B Ryu
    Department of Oncology, The Johns Hopkins Medical Institutes, Baltimore, Maryland 21231, USA
    Genomics 72:108-12. 2001
    ..This problem would be accentuated in studies of cell lines where a paired sample of constitutional DNA is often unavailable...
  25. ncbi request reprint Mad-related genes in the human
    G J Riggins
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Nat Genet 13:347-9. 1996
    ..These data suggest that this gene family may prove to be important in the suppression of neoplasia, imparting the growth inhibitory effects of TGF-beta-like ligands...
  26. ncbi request reprint DPC4 gene in various tumor types
    M Schutte
    Gepartment of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 2196, USA
    Cancer Res 56:2527-30. 1996
    ..The tissue restriction of alterations in DPC4, as in many other tumor-suppressor genes, emphasizes the complexity of rate-limiting checkpoints in human tumorigenesis...
  27. ncbi request reprint Detection of mitochondrial DNA mutations in pancreatic cancer offers a "mass"-ive advantage over detection of nuclear DNA mutations
    J B Jones
    Predoctoral Program in Human Genetics Johns Hopkins University, Baltimore, Maryland 21231, USA
    Cancer Res 61:1299-304. 2001
    ..Nevertheless, the nearly ubiquitous prevalence and high copy number of mtDNA mutations suggest that they be considered of promising clinical utility in diagnostic applications...
  28. ncbi request reprint Novel germline p16(INK4) allele (Asp145Cys) in a family with multiple pancreatic carcinomas. Mutations in brief no. 148. Online
    C A Moskaluk
    The Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Hum Mutat 12:70. 1998
    ..This coding change is not a known polymorphism, and occurs at a codon position in which another missese/splicing change has been shown to be linked to familial melanoma/pancreas cancer...
  29. ncbi request reprint Identification of a chromosome 18q gene that is altered in colorectal cancers
    E R Fearon
    Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231
    Science 247:49-56. 1990
    ..17-kb fragment immediately downstream of one of the exons. The DCC gene may play a role in the pathogenesis of human colorectal neoplasia, perhaps through alteration of the normal cell-cell interactions controlling growth...
  30. ncbi request reprint Mesothelin is overexpressed in the vast majority of ductal adenocarcinomas of the pancreas: identification of a new pancreatic cancer marker by serial analysis of gene expression (SAGE)
    P Argani
    Department of Pathology, The Johns Hopkins Medical Institutions, 2242 Weinberg, 410 North Broadway, Baltimore, MD 21231 2410, USA
    Clin Cancer Res 7:3862-8. 2001
    ..In this study, we evaluate the potential utility of mesothelin as a tumor marker for pancreatic adenocarcinoma...
  31. ncbi request reprint DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1
    S A Hahn
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Science 271:350-3. 1996
    ..1. These results identify DPC4 as a candidate tumor suppressor gene whose inactivation may play a role in pancreatic and possibly other human cancers...
  32. pmc High-throughput drug screening of the DPC4 tumor-suppressor pathway in human pancreatic cancer cells
    T A Sohn
    Departments of Surgery, Pathology, and Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Ann Surg 233:696-703. 2001
    ..In addition, random drug screening provides an unbiased method for identifying drugs or lead compounds for potential therapeutic use...
  33. pmc ACVR1B (ALK4, activin receptor type 1B) gene mutations in pancreatic carcinoma
    G H Su
    Department of Oncology, Pathology, and Surgery, The Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 98:3254-7. 2001
    ..Here we describe the gene structure and novel somatic mutations of the activin type I receptor, ACVR1B, in pancreatic cancer. ACVR1B has not been described previously as a mutated tumor-suppressor gene...
  34. ncbi request reprint Abrogation of the Rb/p16 tumor-suppressive pathway in virtually all pancreatic carcinomas
    M Schutte
    Department of Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA
    Cancer Res 57:3126-30. 1997
    ..Similar results were obtained in an independently analyzed series of 19 pancreatic carcinomas. These data demonstrate the central role of the Rb/p16 pathway in the development of pancreatic carcinoma...
  35. ncbi request reprint Genetic alterations of the transforming growth factor beta receptor genes in pancreatic and biliary adenocarcinomas
    M Goggins
    Department of Oncology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA
    Cancer Res 58:5329-32. 1998
    ..Our results indicate that the TGF-beta type I and type II receptor genes are selective targets of genetic inactivation in pancreatic and biliary cancers...
  36. ncbi request reprint Genomic sequencing of DPC4 in the analysis of familial pancreatic carcinoma
    C A Moskaluk
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    Diagn Mol Pathol 6:85-90. 1997
    ..No mutations in the coding sequences of the DPC4 gene were found; hence, it appears that germline mutations in DPC4 cannot account for many of the familial aggregations of pancreatic carcinoma...
  37. ncbi request reprint Alterations in pancreatic, biliary, and breast carcinomas support MKK4 as a genetically targeted tumor suppressor gene
    G H Su
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 2196, USA
    Cancer Res 58:2339-42. 1998
    ..Coexistent mutations of other tumor suppressor genes in MKK4-deficient tumors suggest that MKK4 may participate in a tumor suppressive signaling pathway distinct from DPC4, p16, p53, and BRCA2...
  38. ncbi request reprint Pancreatic intraepithelial neoplasia and infiltrating adenocarcinoma: analysis of progression and recurrence by DPC4 immunohistochemical labeling
    D M McCarthy
    Departments of Pathology, Surgery, and Oncology, The Johns Hopkins Medical Institutions, Baltimore, MD, USA
    Hum Pathol 32:638-42. 2001
    ..Additionally, Dpc4 expression can be used to differentiate recurrent or persistent adenocarcinoma from a second primary adenocarcinoma...
  39. pmc Functional mapping of the MH1 DNA-binding domain of DPC4/SMAD4
    J B Jones
    Predoctoral Program in Human Genetics, Johns Hopkins University, Baltimore, MD, USA
    Nucleic Acids Res 28:2363-8. 2000
    ..Our results demonstrate that the MH1 domain as a whole is very sensitive to changes in overall structure, and that tumorigenic mutations within the region of L43-R135 indeed would target DNA-binding...
  40. ncbi request reprint Human Smad3 and Smad4 are sequence-specific transcription activators
    L Zawel
    Molecular Genetics Laboratory, Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Mol Cell 1:611-7. 1998
    ..These results define a novel biochemical property of Smad proteins that is likely to play a direct role in the biologic responses to TGF beta and related ligands...
  41. ncbi request reprint Oncogenic levels of mitogen-activated protein kinase (MAPK) signaling of the dinucleotide KRAS2 mutations G12F and GG12-13VC
    D M Feldser
    Predoctoral Program in Human Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Hum Mutat 18:357. 2001
    ..Therefore, it is advisable to consider dinucleotide KRAS2 mutants in the strategic design of mutational screens used to assay clinical tumor samples. Hum Mutat 18:357, 2001...
  42. ncbi request reprint Differentially expressed genes in pancreatic ductal adenocarcinomas identified through serial analysis of gene expression
    Steven R Hustinx
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 3:1254-61. 2004
    ..TAGmapper should prove to be a powerful tool for the discovery of novel tumor markers through assignment of uncharacterized SAGE tags...
  43. ncbi request reprint Molecular pathology of pancreatic cancer
    R H Hruban
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Cancer J 7:251-8. 2001
    ..In this article, we review the genetic alterations identified in pancreatic cancer and provide examples of how this information can be applied to patient care...
  44. ncbi request reprint The SMAD4 protein and prognosis of pancreatic ductal adenocarcinoma
    M Tascilar
    Department of Pathology, The Johns Hopkins University School of Medicine, 632 Ross Building, Baltimore, MD 21205, USA
    Clin Cancer Res 7:4115-21. 2001
    ..36 (95% confidence interval, 1.01-1.83; P = 0.04). CONCLUSION: Patients undergoing Whipple resection for pancreatic adenocarcinoma survive longer if their cancers express SMAD4...
  45. pmc Exploration of global gene expression patterns in pancreatic adenocarcinoma using cDNA microarrays
    Christine A Iacobuzio-Donahue
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA
    Am J Pathol 162:1151-62. 2003
    ..The genes and expressed sequence tags presented in this study provide clues to the pathobiology of pancreatic cancer and implicate a large number of potentially new molecular markers for the detection and treatment of pancreatic cancer...
  46. pmc Core signaling pathways in human pancreatic cancers revealed by global genomic analyses
    Sian Jones
    Sol Goldman Pancreatic Cancer Research Center, Ludwig Center and Howard Hughes Medical Institute at the Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA
    Science 321:1801-6. 2008
    ..Dysregulation of these core pathways and processes through mutation can explain the major features of pancreatic tumorigenesis...
  47. ncbi request reprint Identification of novel highly expressed genes in pancreatic ductal adenocarcinomas through a bioinformatics analysis of expressed sequence tags
    Dengfeng Cao
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 3:1081-9; discussion 1090-1. 2004
    ....
  48. ncbi request reprint Invasion-specific genes in malignancy: serial analysis of gene expression comparisons of primary and passaged cancers
    B Ryu
    Department of Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Res 61:1833-8. 2001
    ..This cluster contains genes that derive from distinct components of the host reaction, including some that may be useful as diagnostic markers and therapeutic targets...
  49. ncbi request reprint Missense mutations of MADH4: characterization of the mutational hot spot and functional consequences in human tumors
    Christine A Iacobuzio-Donahue
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Clin Cancer Res 10:1597-604. 2004
    ..We present the MADH4 genetic status determined on a new set of pancreatic, biliary, and duodenal cancers with comparison to the mutational data reported for various tumor types...
  50. ncbi request reprint Fanconi anemia gene mutations in young-onset pancreatic cancer
    Michiel S Van Der Heijden
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231, USA
    Cancer Res 63:2585-8. 2003
    ..S. Sasaki, Nature (Lond.), 257: 501-503, 1975] suggests a therapeutic utility for a more complete characterization of the DNA repair defects and their causative genetic mutations in pancreatic cancer...
  51. ncbi request reprint Immunohistochemical validation of a novel epithelial and a novel stromal marker of pancreatic ductal adenocarcinoma identified by global expression microarrays: sea urchin fascin homolog and heat shock protein 47
    Anirban Maitra
    Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
    Am J Clin Pathol 118:52-9. 2002
    ..Fascin and HSP47 are novel tumor markers with potential diagnostic and therapeutic implications for pancreatic carcinoma. These results establish the usefulness of global expression platforms to identify novel tumor markers...
  52. pmc Discovery of novel tumor markers of pancreatic cancer using global gene expression technology
    Christine A Iacobuzio-Donahue
    Department of Pathology, The Johns Hopkins MedicalInstitutions, Baltimore, Maryland 21231 2410, USA
    Am J Pathol 160:1239-49. 2002
    ..The remaining 69 genes have not been implicated in pancreatic cancer before, and have immediate potential as novel therapeutic targets and tumor markers of pancreatic cancer...
  53. ncbi request reprint Pancreatic cancer
    Theresa Pluth Yeo
    Departments of Surgery, Oncology, Pathology and Medicine Johns Hopkins Medical Institutions Baltimore, Maryland, USA
    Curr Probl Cancer 26:176-275. 2002
  54. ncbi request reprint Pancreatic intraepithelial neoplasia: a new nomenclature and classification system for pancreatic duct lesions
    R H Hruban
    Departments of Pathology, The Johns Hopkins Hospital, Baltimore, Maryland 21231, USA
    Am J Surg Pathol 25:579-86. 2001
    ..The acceptance of a standard classification system will facilitate the study of pancreatic duct lesions, and will lead ultimately to a better understanding of their biologic importance...
  55. ncbi request reprint Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma
    C Caldas
    Department of Oncology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205
    Nat Genet 8:27-32. 1994
    ..Coexistent inactivations of both MTS1 and p53 was common and suggests that abnormal regulation of cyclin-dependent kinases may play an important role in the biology of pancreatic carcinoma...
  56. ncbi request reprint Increased prevalence of the BRCA2 polymorphic stop codon K3326X among individuals with familial pancreatic cancer
    Sean T Martin
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21205 2196, USA
    Oncogene 24:3652-6. 2005
    ..37, 95% CI: 0.61-9.27). The increased prevalence of the BRCA2 K3326X polymorphism in patients with familial pancreatic cancer suggests that this polymorphism is deleterious and contributes to pancreatic cancer risk...
  57. ncbi request reprint Molecular pathogenesis of pancreatic cancer
    Anirban Maitra
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Best Pract Res Clin Gastroenterol 20:211-26. 2006
    ..This chapter will provide an overview of the molecular pathogenesis of pancreatic cancer with emphasis on clinical applications...
  58. ncbi request reprint Theoretical proposal: allele dosage of MAP2K4/MKK4 could rationalize frequent 17p loss in diverse human cancers
    Steven C Cunningham
    Department of Oncology, The Sidney Kimmel Cancer Research Center at Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Cell Cycle 5:1090-3. 2006
    ..Consideration of gene dosage changes specifically affecting members of positive feedback loops may permit integration of the aneuploidy process into a conventional model of clonal selection in tumorigenesis...
  59. ncbi request reprint Identifying allelic loss and homozygous deletions in pancreatic cancer without matched normals using high-density single-nucleotide polymorphism arrays
    Eric S Calhoun
    Department of Oncology, The Sol Goldman Pancreatic Cancer Research Center at the Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins Medical Institutes, Baltimore, MD 21231, USA
    Cancer Res 66:7920-8. 2006
    ..This study provides previously unavailable high-resolution allelotype and deletion breakpoint maps in widely shared pancreatic cancer cell lines and effectively eliminates the need for matched normal tissue to define informative loci...
  60. ncbi request reprint Somatic mutations of GUCY2F, EPHA3, and NTRK3 in human cancers
    Laura D Wood
    The Ludwig Center for Cancer Genetics and Therapeutics, The Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, Maryland 21231, USA
    Hum Mutat 27:1060-1. 2006
    ..Our results implicate these tyrosine kinase genes in the pathogenesis of other tumor types and suggest that they may be useful targets for diagnostic and therapeutic intervention in selected patients...
  61. ncbi request reprint Genomic copy number changes affecting the thymidylate synthase (TYMS) gene in cancer: a model for patient classification to aid fluoropyrimidine therapy
    Jonathan R Brody
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Cancer Res 66:9369-73. 2006
    ..The data suggest that TS copy number in a patient's tumor may be a dominating variable affecting 5FU responsiveness...
  62. ncbi request reprint High cancer-specific expression of mesothelin (MSLN) is attributable to an upstream enhancer containing a transcription enhancer factor dependent MCAT motif
    Tomas Hucl
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD 21231, USA
    Cancer Res 67:9055-65. 2007
    ..The CanScript sequence represents a modular element for cancer-specific targeting, potentially suitable for nearly a third of human malignancies...
  63. pmc Precursors to pancreatic cancer
    Ralph H Hruban
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Gastroenterol Clin North Am 36:831-49, vi. 2007
    ..Pancreatic intraepithelial neoplasia is a microscopic lesion. This article focuses on the clinical significance of these three important precursor lesions, with emphasis on their clinical manifestations, detection, and treatment...
  64. ncbi request reprint Multiple-criterion evaluation of reported mutations: a proposed scoring system for the intragenic somatic mutation literature
    Jordan M Winter
    Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 5:360-70. 2006
    ..Scores in the range of 10 to 15 are suggestive of well-presented reports of disease-inducing somatic mutations. Reports with scores less than 10 should be viewed with skepticism...
  65. ncbi request reprint Molecular pathogenesis of pancreatic cancer
    Donna E Hansel
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Annu Rev Genomics Hum Genet 4:237-56. 2003
    ..Ultimately, understanding the genetic events underlying the development of pancreatic cancer may serve as a useful adjunct in the screening and treatment of patients suffering from, or at risk for, pancreatic cancer...
  66. ncbi request reprint The essential similarity of TGFbeta and activin receptor transcriptional responses in cancer cells
    Byungwoo Ryu
    Department of Oncology, The Johns Hopkins Medical Institutions Baltimore, Maryland 21231, USA
    Cancer Biol Ther 2:164-70. 2003
    ..This similarity helps relate the mutations seen in both receptor systems and their Smad mediators in human cancers...
  67. ncbi request reprint Polymorphisms of SPINK1 N34S and CFTR in patients with sporadic and familial pancreatic cancer
    Hiroyuki Matsubayashi
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 2196, USA
    Cancer Biol Ther 2:652-5. 2003
    ..Furthermore, the N34S polymorphism is rarely found in patients with severe idiopathic chronic pancreatitis...
  68. ncbi request reprint Highly expressed genes in pancreatic ductal adenocarcinomas: a comprehensive characterization and comparison of the transcription profiles obtained from three major technologies
    Christine A Iacobuzio-Donahue
    Departments of Pathology, Surgery, Oncology, and Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA
    Cancer Res 63:8614-22. 2003
    ....
  69. ncbi request reprint Focus on pancreas cancer
    Elizabeth M Jaffee
    The Sidney Kimmel Cancer Center, Johns Hopkins University, Baltimore, Maryland 21231, USA
    Cancer Cell 2:25-8. 2002
  70. ncbi request reprint Relationships and differentially expressed genes among pancreatic cancers examined by large-scale serial analysis of gene expression
    Byungwoo Ryu
    Department of Oncology, 451 Cancer Research Building, The Johns Hopkins Medical Institutions, 1650 Orleans Street, Baltimore, MD 21231, USA
    Cancer Res 62:819-26. 2002
    ..Others suggest potential novel therapeutic targets...
  71. ncbi request reprint Evidence of selection for clones having genetic inactivation of the activin A type II receptor (ACVR2) gene in gastrointestinal cancers
    Paula M Hempen
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231, USA
    Cancer Res 63:994-9. 2003
    ..This evidence is compatible with a high degree of selection for inactivation of the ACVR2 gene in tumorigenesis, supporting ACVR2 as a candidate tumor suppressor gene in gastrointestinal cancers...
  72. ncbi request reprint Identification of p53 as a sequence-specific DNA-binding protein
    S E Kern
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231
    Science 252:1708-11. 1991
    ..These data suggest that a function of p53 may be mediated by its ability to bind to specific DNA sequences in the human genome, and that this activity is altered by mutations that occur in human tumors...
  73. ncbi request reprint Pancreaticobiliary cancers with deficient methylenetetrahydrofolate reductase genotypes
    Hiroyuki Matsubayashi
    Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 2196, USA
    Clin Gastroenterol Hepatol 3:752-60. 2005
    ..Methyl group deficiency might promote carcinogenesis by inducing DNA breaks and DNA hypomethylation. We hypothesized that deficient methylenetetrahydrofolate reductase (MTHFR) genotypes could promote pancreatic cancer development...
  74. ncbi request reprint Clinical importance of precursor lesions in the pancreas
    Ralph H Hruban
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Weinberg Room 2242, 401 North Broadway, Baltimore, MD, USA
    J Hepatobiliary Pancreat Surg 14:255-63. 2007
    ..The early detection and treatment of these lesions can interrupt the progression of a curable noninvasive precursor to an almost uniformly deadly invasive cancer...
  75. pmc Multifocal neoplastic precursor lesions associated with lobular atrophy of the pancreas in patients having a strong family history of pancreatic cancer
    Kieran Brune
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Am J Surg Pathol 30:1067-76. 2006
    ..The multifocal nature of familial pancreatic neoplasia suggests that surveillance of these patients is warranted after partial pancreatectomy...
  76. ncbi request reprint The desmoplastic response to infiltrating breast carcinoma: gene expression at the site of primary invasion and implications for comparisons between tumor types
    Christine A Iacobuzio-Donahue
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Cancer Res 62:5351-7. 2002
    ..Some of the genes presented are novel markers of the invasive process, imply communication at the host/tumor interface, and suggest potential therapeutic targets...
  77. ncbi request reprint Targeted disruption of FANCC and FANCG in human cancer provides a preclinical model for specific therapeutic options
    Eike Gallmeier
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, Maryland, USA
    Gastroenterology 130:2145-54. 2006
    ..How specifically to treat pancreatic and other cancers harboring Fanconi anemia gene mutations has raised great interest recently, yet preclinical studies have been hampered by the lack of well-controlled human cancer models...
  78. ncbi request reprint Role of the DPC4 tumor suppressor gene in adenocarcinoma of the ampulla of Vater: analysis of 140 cases
    Denis M McCarthy
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Mod Pathol 16:272-8. 2003
    ..Although ampullary and pancreatic adenocarcinomas share histologic and molecular features, ampullary carcinomas are less likely to show loss of Dpc4 expression or K-ras gene mutations...
  79. ncbi request reprint Targeting Fanconi anemia/BRCA2 pathway defects in cancer: the significance of preclinical pharmacogenomic models
    Eike Gallmeier
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, Maryland 21231, USA
    Clin Cancer Res 13:4-10. 2007
    ..Clinical trials are now under way...
  80. ncbi request reprint Analysis of anaphase figures in routine histologic sections distinguishes chromosomally unstable from chromosomally stable malignancies
    Elizabeth Montgomery
    Department of Pathology, Johns Hopkins University, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 2:248-52. 2003
    ....
  81. pmc Exomic sequencing identifies PALB2 as a pancreatic cancer susceptibility gene
    Sian Jones
    Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Baltimore, MD 21231, USA
    Science 324:217. 2009
    ..These results illustrate that complete, unbiased sequencing of protein-coding genes can lead to the identification of a gene responsible for a hereditary disease...
  82. ncbi request reprint Targeted deletion of MKK4 in cancer cells: a detrimental phenotype manifests as decreased experimental metastasis and suggests a counterweight to the evolution of tumor-suppressor loss
    Steven C Cunningham
    Department of Oncology, Sidney Kimmel Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Cancer Res 66:5560-4. 2006
    ....
  83. pmc Telomere shortening is nearly universal in pancreatic intraepithelial neoplasia
    N Tjarda Van Heek
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Am J Pathol 161:1541-7. 2002
    ..A critical shortening of telomere length in PanINs may predispose these noninvasive ductal lesions to accumulate progressive chromosomal abnormalities and to develop toward the stage of invasive carcinoma...
  84. ncbi request reprint History and principles of conductive media for standard DNA electrophoresis
    Jonathan R Brody
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Anal Biochem 333:1-13. 2004
    ..Such media allow for application of a higher electric field. Applications of DNA electrophoresis can now be reengineered for lower ionic strength, higher field strengths, and lower requirements for heat dissipation...
  85. ncbi request reprint Homozygous deletion of the MTAP gene in invasive adenocarcinoma of the pancreas and in periampullary cancer: a potential new target for therapy
    Steven R Hustinx
    Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA
    Cancer Biol Ther 4:83-6. 2005
    ..Thus, pancreatic cancer is a promising cancer type in which to explore novel chemotherapeutic strategies to exploit the selective loss of MTAP function...
  86. ncbi request reprint Large-scale allelotype of pancreaticobiliary carcinoma provides quantitative estimates of genome-wide allelic loss
    Christine A Iacobuzio-Donahue
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Cancer Res 64:871-5. 2004
    ..01). These findings offer new loci for investigation of the genetic alterations common to pancreaticobiliary cancers and aid the understanding of mechanisms of allelic loss in human carcinogenesis...
  87. ncbi request reprint Scrambled exons
    J M Nigro
    Oncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231
    Cell 64:607-13. 1991
    ..These results demonstrate that the splicing process does not always pair sequential exons in the order predicted from their positions in genomic DNA, thus creating a novel type of RNA product...
  88. ncbi request reprint Absence of specific cell killing of the BRCA2-deficient human cancer cell line CAPAN1 by poly(ADP-ribose) polymerase inhibition
    Eike Gallmeier
    Department of Oncology, The Sol Goldman Pancreatic Cancer Research Center, Baltimore, Maryland, USA
    Cancer Biol Ther 4:703-6. 2005
    ....
  89. pmc Hybrids of aneuploid human cancer cells permit complementation of simple and complex cancer defects
    David A Dezentje
    Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Cancer Biol Ther 8:347-55. 2009
    ..Fusing CIN cell lines to form mapped hybrids offers new tools for positional cloning or classification of simple and complex cancer phenotypes, including mechanical defects and altered drug responses...
  90. ncbi request reprint Evaluation of candidate genes MAP2K4, MADH4, ACVR1B, and BRCA2 in familial pancreatic cancer: deleterious BRCA2 mutations in 17%
    Kathleen M Murphy
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Res 62:3789-93. 2002
    ..These findings confirm the increased risk of pancreatic cancer in individuals with BRCA2 mutations and identify germ-line BRCA2 mutations as the most common inherited genetic alteration yet identified in familial pancreatic cancer...
  91. ncbi request reprint Concordant loss of MTAP and p16/CDKN2A expression in pancreatic intraepithelial neoplasia: evidence of homozygous deletion in a noninvasive precursor lesion
    Steven R Hustinx
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD, USA
    Mod Pathol 18:959-63. 2005
    ..The concordant loss of expression of both genes in PanIN lesions demonstrates that homozygous deletions of the p16 tumor suppressor gene can occur in noninvasive precursor lesions...
  92. ncbi request reprint In vivo therapeutic responses contingent on Fanconi anemia/BRCA2 status of the tumor
    Michiel S Van Der Heijden
    Department of Oncology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Clin Cancer Res 11:7508-15. 2005
    ..Defects in these genes could lead to hypersensitivity to interstrand cross-linkers in vivo and a more optimal treatment of pancreatic cancer patients based on the genetic profile of the tumor...
  93. pmc Functional defects in the fanconi anemia pathway in pancreatic cancer cells
    Michiel S Van Der Heijden
    Department of Oncology, Rm 464, Cancer Research Building, 1650 Orleans St, Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Am J Pathol 165:651-7. 2004
    ..These results support the practical exploration of crosslinking agents for non-Fanconi anemia patients that have tumors defective in the Fanconi pathway...
  94. ncbi request reprint Sodium boric acid: a Tris-free, cooler conductive medium for DNA electrophoresis
    Jonathan R Brody
    Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Biotechniques 36:214-6. 2004
  95. ncbi request reprint The genetics of FANCC and FANCG in familial pancreatic cancer
    Carmelle D Rogers
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Cancer Biol Ther 3:167-9. 2004
    ..FANCC and FANCG mutations may have low penetrance for the pancreatic cancer phenotype...
  96. pmc Beverage-agarose gel electrophoresis: an inquiry-based laboratory exercise with virtual adaptation
    Steven C Cunningham
    Department of Oncology, The Sidney Kimmel Cancer Research Center at Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    CBE Life Sci Educ 5:281-6. 2006
    ..Our findings provide a readily accessible, inexpensive, and intriguing technique for teaching electrophoresis and the progressive optimization of a laboratory technique...
  97. ncbi request reprint A double missense variation of the BUB1 gene and a defective mitotic spindle checkpoint in the pancreatic cancer cell line Hs766T
    Paula M Hempen
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD, USA
    Hum Mutat 21:445. 2003
    ..1998) supports the suggestion the missense mutations of the BUB1 gene in the Hs766T cell line may contribute to its observed mitotic checkpoint defect...
  98. ncbi request reprint MKK4 status predicts survival after resection of gastric adenocarcinoma
    Steven C Cunningham
    Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, MD 21231 1000, USA
    Arch Surg 141:1095-9; discussion 1100. 2006
    ..Lack of expression of the tumor-suppressor gene MKK4 is significantly correlated with poor survival after resection of gastric adenocarcinoma...
  99. ncbi request reprint Gene-specific selection against experimental fanconi anemia gene inactivation in human cancer
    Eike Gallmeier
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, Maryland, USA
    Cancer Biol Ther 6:654-60. 2007
    ..This would explain why certain FA gene defects, despite an apparent selection for FA pathway inactivation in cancer, are rarely observed in tumors among the general population...
  100. ncbi request reprint Hereditary factors in pancreatic cancer
    Henry T Lynch
    Department of Preventive Medicine and Public Health, Creighton University School of Medicine, 2500 California Plaza, Omaha NE 68178, USA
    J Hepatobiliary Pancreat Surg 9:12-31. 2002
    ..If changes in these putative biomarkers are observed, endoscopic retrograde cholangiopancreatography (ERCP) would be the next diagnostic step. We conclude with a discussion of ethical concerns about this research...
  101. ncbi request reprint SOS1 mutations are rare in human malignancies: implications for Noonan Syndrome patients
    Kenneth D Swanson
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, Massachusetts, USA
    Genes Chromosomes Cancer 47:253-9. 2008
    ..Our findings suggest that SOS1 is not a significant human oncogene in most cancers. Furthermore, NS patients with SOS1 mutations may not be at increased risk of developing cancer...