Michael G Goggins

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. 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
  2. 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
  3. ncbi request reprint Molecular markers of early pancreatic cancer
    Michael Goggins
    The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Department of Pathology, 720 Rutland Avenue, Baltimore, MD 21205 2196, USA
    J Clin Oncol 23:4524-31. 2005
  4. ncbi request reprint Genome-wide aberrations in pancreatic adenocarcinoma
    Norma J Nowak
    Cancer Genetics, Roswell Park Cancer Institute, State University of New York at Buffalo, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Cancer Genet Cytogenet 161:36-50. 2005
  5. ncbi request reprint DNA methylation alterations in the pancreatic juice of patients with suspected pancreatic disease
    Hiroyuki Matsubayashi
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
    Cancer Res 66:1208-17. 2006
  6. pmc Aberrant methylation of suppressor of cytokine signalling-1 (SOCS-1) gene in pancreatic ductal neoplasms
    N Fukushima
    Department of Pathology, The Johns Hopkins Medical Institutions, 632 Ross Building, 720 Rutland Ave, Baltimore, MD 21205 2196, USA
    Br J Cancer 89:338-43. 2003
  7. pmc Loss of E-cadherin expression and outcome among patients with resectable pancreatic adenocarcinomas
    Seung Mo Hong
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Mod Pathol 24:1237-47. 2011
  8. pmc Telomeres are shortened in acinar-to-ductal metaplasia lesions associated with pancreatic intraepithelial neoplasia but not in isolated acinar-to-ductal metaplasias
    Seung Mo Hong
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Mod Pathol 24:256-66. 2011
  9. pmc Unlike pancreatic cancer cells pancreatic cancer associated fibroblasts display minimal gene induction after 5-aza-2'-deoxycytidine
    Jun Yu
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The John Hopkins Medical Institutions, Baltimore, Maryland, United States of America
    PLoS ONE 7:e43456. 2012
  10. pmc Mutant GNAS detected in duodenal collections of secretin-stimulated pancreatic juice indicates the presence or emergence of pancreatic cysts
    Mitsuro Kanda
    Johns Hopkins Medical Institutions, Department of Pathology, Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, 1550 Orleans Street, Baltimore, MD 21231, USA
    Gut 62:1024-33. 2013

Research Grants

  1. THE PanINs OF PANCREATITIS,PANCREAS CANCER AND CONTROLS
    Michael Goggins; Fiscal Year: 2002
  2. Markers of Early Pancreatic Cancer
    Michael Goggins; Fiscal Year: 2007
  3. CLASSIFYING PANCREATIC CANCERS BY METHYLATOR PHENOTYPES
    Michael Goggins; Fiscal Year: 2006
  4. CLASSIFYING PANCREATIC CANCERS BY METHYLATOR PHENOTYPES
    Michael Goggins; Fiscal Year: 2005
  5. FOLATE PATHWAY POLYMORPHISMS AND PANCREATIC CANCER RISK
    Michael Goggins; Fiscal Year: 2002
  6. CLASSIFYING PANCREATIC CANCERS BY METHYLATOR PHENOTYPES
    Michael Goggins; Fiscal Year: 2004
  7. Markers of Early Pancreatic Cancer
    Michael Goggins; Fiscal Year: 2006
  8. CLASSIFYING PANCREATIC CANCERS BY METHYLATOR PHENOTYPES
    Michael Goggins; Fiscal Year: 2003
  9. Markers of Early Pancreatic Cancer
    Michael Goggins; Fiscal Year: 2009
  10. Markers of Early Pancreatic Cancer
    Michael G Goggins; Fiscal Year: 2010

Detail Information

Publications96

  1. 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...
  2. 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...
  3. ncbi request reprint Molecular markers of early pancreatic cancer
    Michael Goggins
    The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Department of Pathology, 720 Rutland Avenue, Baltimore, MD 21205 2196, USA
    J Clin Oncol 23:4524-31. 2005
    ....
  4. ncbi request reprint Genome-wide aberrations in pancreatic adenocarcinoma
    Norma J Nowak
    Cancer Genetics, Roswell Park Cancer Institute, State University of New York at Buffalo, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Cancer Genet Cytogenet 161:36-50. 2005
    ..These findings should greatly facilitate further research in understanding the pathogenesis of this lethal disease, and could lead to the identification of novel therapeutic targets and biomarkers for early detection...
  5. ncbi request reprint DNA methylation alterations in the pancreatic juice of patients with suspected pancreatic disease
    Hiroyuki Matsubayashi
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
    Cancer Res 66:1208-17. 2006
    ..The detection and quantification of aberrantly methylated DNA in pancreatic juice is a promising approach to the diagnosis of pancreatic cancer...
  6. pmc Aberrant methylation of suppressor of cytokine signalling-1 (SOCS-1) gene in pancreatic ductal neoplasms
    N Fukushima
    Department of Pathology, The Johns Hopkins Medical Institutions, 632 Ross Building, 720 Rutland Ave, Baltimore, MD 21205 2196, USA
    Br J Cancer 89:338-43. 2003
    ..These results indicate that loss of SOCS-1 gene is associated with transcriptional silencing and may have growth-promoting effects, and that its methylation is a useful marker of pancreatic cancer...
  7. pmc Loss of E-cadherin expression and outcome among patients with resectable pancreatic adenocarcinomas
    Seung Mo Hong
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Mod Pathol 24:1237-47. 2011
    ..02). Among patients undergoing pancreaticoduodenectomy for pancreatic ductal adenocarcinoma, partial loss of tumoral E-cadherin expression is an independent predictor of poor outcome...
  8. pmc Telomeres are shortened in acinar-to-ductal metaplasia lesions associated with pancreatic intraepithelial neoplasia but not in isolated acinar-to-ductal metaplasias
    Seung Mo Hong
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Mod Pathol 24:256-66. 2011
    ..These results indicate that isolated acinar-to-ductal metaplasias are not a precursor to PanIN, and support the hypothesis that PanIN-associated acinar-to-ductal metaplasias arise secondary to PanIN lesions...
  9. pmc Unlike pancreatic cancer cells pancreatic cancer associated fibroblasts display minimal gene induction after 5-aza-2'-deoxycytidine
    Jun Yu
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The John Hopkins Medical Institutions, Baltimore, Maryland, United States of America
    PLoS ONE 7:e43456. 2012
    ..Aberrant DNA methylation is an important cause of transcriptional alterations in cancer cells but it is not known how important DNA methylation alterations are to CAF behavior...
  10. pmc Mutant GNAS detected in duodenal collections of secretin-stimulated pancreatic juice indicates the presence or emergence of pancreatic cysts
    Mitsuro Kanda
    Johns Hopkins Medical Institutions, Department of Pathology, Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, 1550 Orleans Street, Baltimore, MD 21231, USA
    Gut 62:1024-33. 2013
    ..Better approaches are needed to characterise these lesions. In this study we evaluated the utility of detecting mutant DNA in secretin-stimulated pancreatic juice...
  11. pmc ABO blood group and other genetic variants associated with pancreatic cancer
    Anne Marie Lennon
    Department of Medicine, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, MD 21205 2196, USA
    Genome Med 2:39. 2010
    ..1...
  12. pmc Markers of pancreatic cancer: working toward early detection
    Michael Goggins
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Clin Cancer Res 17:635-7. 2011
    ..Because early-stage pancreatic cancer is generally asymptomatic, the only reliable way to detect it is by targeting individuals at increased risk for pancreatic screening...
  13. pmc Identifying molecular markers for the early detection of pancreatic neoplasia
    Michael Goggins
    Department of Pathology, Medicine, and Oncology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Semin Oncol 34:303-10. 2007
    ..As we continue to characterize the genetic, epigenetic, and proteomics alterations that occur in pancreatic cancers and their percursors, better diagnostic markers of pancreatic cancer are expected to follow...
  14. pmc Widespread activation of the DNA damage response in human pancreatic intraepithelial neoplasia
    Jan Bart M Koorstra
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Mod Pathol 22:1439-45. 2009
    ..Loss of p53 function appears to be a critical determinant for bypassing this checkpoint and the subsequent progression to invasive adenocarcinoma...
  15. ncbi request reprint Sensitive and quantitative detection of KRAS2 gene mutations in pancreatic duct juice differentiates patients with pancreatic cancer from chronic pancreatitis, potential for early detection
    Chanjuan Shi
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 7:353-360. 2008
    ..LigAmp quantification of mutant KRAS2 in pancreatic juice differentiates pancreatic adenocarcinoma from chronic pancreatitis, and may be a useful early detection tool for pancreatic cancer...
  16. ncbi request reprint Biomarker discovery from pancreatic cancer secretome using a differential proteomic approach
    Mads Grønborg
    Department of Biological Chemistry, McKusick Nathans Institute of Genetic Medicine, The Johns Hopkins University, Baltimore, Maryland 21205, USA
    Mol Cell Proteomics 5:157-71. 2006
    ..28 was obtained, confirming previously reported poor associations between RNA and protein expression studies...
  17. pmc Aberrant MicroRNA-155 expression is an early event in the multistep progression of pancreatic adenocarcinoma
    Ji Kon Ryu
    Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Baltimore, MD, USA
    Pancreatology 10:66-73. 2010
    ..Misexpression of microRNAs (miRNAs) is commonly encountered in invasive neoplasia; however, miRNA abnormalities in PanIN lesions have not been documented...
  18. pmc Epigenetic silencing of MicroRNA miR-107 regulates cyclin-dependent kinase 6 expression in pancreatic cancer
    Kwang Hyuck Lee
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Pancreatology 9:293-301. 2009
    ....
  19. pmc Mucin 16 (cancer antigen 125) expression in human tissues and cell lines and correlation with clinical outcome in adenocarcinomas of the pancreas, esophagus, stomach, and colon
    Mirte M Streppel
    Department of Pathology, Johns Hopkins University, Baltimore, MD 21231 2410, USA
    Hum Pathol 43:1755-63. 2012
    ..We propose that mucin 16 may function as a prognostic marker and therapeutic target in the future...
  20. ncbi request reprint LigAmp for sensitive detection of single-nucleotide differences
    Chanjuan Shi
    Department of Pathology, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, Maryland 21205, USA
    Nat Methods 1:141-7. 2004
    ..Preliminary evidence indicates that reactions can be multiplexed. This assay may find applications in the diagnosis of genetic disorders and the management of patients with cancer and infectious diseases...
  21. pmc MicroRNA miR-155 is a biomarker of early pancreatic neoplasia
    Nils Habbe
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Cancer Biol Ther 8:340-6. 2009
    ..Misexpression of microRNAs (miRNAs) is commonly observed in pancreatic adenocarcinoma. In contrast, miRNA abnormalities in pancreatic cancer precursor lesions have not been documented...
  22. pmc Whole-exome sequencing of neoplastic cysts of the pancreas reveals recurrent mutations in components of ubiquitin-dependent pathways
    Jian Wu
    Ludwig Center for Cancer Genetics and Howard Hughes Medical Institutions, Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 108:21188-93. 2011
    ..These results highlight the essential role of ubiquitin ligases in these neoplasms and have important implications for the diagnosis and treatment of patients with cystic tumors...
  23. ncbi request reprint Gene expression profiling identifies markers of ampullary adenocarcinoma
    N Tjarda Van Heek
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 2196, USA
    Cancer Biol Ther 3:651-6. 2004
    ..001). Measurement of markers of ampullary cancer such as osteopontin may aid in the early detection and differential diagnosis of patients with periampullary lesions...
  24. pmc Clinicopathological correlates of activating GNAS mutations in intraductal papillary mucinous neoplasm (IPMN) of the pancreas
    Marco Dal Molin
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Ann Surg Oncol 20:3802-8. 2013
    ..The purpose of this study was to explore clinicopathological correlates of GNAS mutational status in resected IPMNs...
  25. ncbi request reprint Comprehensive proteomic analysis of human pancreatic juice
    Mads Grønborg
    McKusick Nathans Institute of Genetic Medicine and Department of Biological Chemistry, Johns Hopkins University, Baltimore, Maryland 21205, USA
    J Proteome Res 3:1042-55. 2004
    ..The proteins identified in this study could be directly assessed for their potential as biomarkers for pancreatic cancer by quantitative proteomics methods or immunoassays...
  26. pmc Molecular determinants of retinoic acid sensitivity in pancreatic cancer
    Sonal Gupta
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Clin Cancer Res 18:280-9. 2012
    ..To identify a predictive molecular "signature" for sensitivity to retinoic acid in pancreatic cancer...
  27. ncbi request reprint Serum macrophage inhibitory cytokine 1 as a marker of pancreatic and other periampullary cancers
    Jens Koopmann
    Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA
    Clin Cancer Res 10:2386-92. 2004
    ..In this study, we evaluated serum macrophage inhibitory cytokine-1 (MIC-1) as a marker of pancreatic cancer...
  28. 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...
  29. pmc In vivo and in vitro propagation of intraductal papillary mucinous neoplasms
    Hirohiko Kamiyama
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Lab Invest 90:665-73. 2010
    ..Patient origin was confirmed using DNA fingerprinting. Most non-invasive IPMNs grow in NOG mice. We successfully established one IPMN cell line, and plan to use it to clarify the molecular pathogenesis of IPMNs...
  30. pmc Elevated microRNA miR-21 levels in pancreatic cyst fluid are predictive of mucinous precursor lesions of ductal adenocarcinoma
    Ji Kon Ryu
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Pancreatology 11:343-50. 2011
    ..Deregulated microRNA (miRNAs) expression is widespread in pancreatic cancer. We assessed whether aberrant miRNAs in pancreatic cyst fluid could be used as potential biomarkers for cystic precursor lesions of pancreatic cancer...
  31. pmc CpG island methylation profile of pancreatic intraepithelial neoplasia
    Norihiro Sato
    Departments of Pathology, Oncology and Medicine, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD, USA
    Mod Pathol 21:238-44. 2008
    ..001), Reprimo (P=0.01), and LHX1 (P=0.03). These results suggest that aberrant CpG island hypermethylation begins in early stages of PanINs, and its prevalence progressively increases during neoplastic progression...
  32. 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
    ....
  33. ncbi request reprint Early detection of pancreatic carcinoma
    Christophe Rosty
    Department of Pathology, Johns Hopkins Medical Institutions, 720 Rutland Avenue, Baltimore, MD 21205 2196, USA
    Hematol Oncol Clin North Am 16:37-52. 2002
    ....
  34. ncbi request reprint Loss of Stk11/Lkb1 expression in pancreatic and biliary neoplasms
    Fikret Sahin
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Mod Pathol 16:686-91. 2003
    ..Immunohistochemical analysis for Stk11 expression may be a valid surrogate for genetic analysis of STK11 gene mutations in cancers...
  35. 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...
  36. pmc Systemic administration of polymeric nanoparticle-encapsulated curcumin (NanoCurc) blocks tumor growth and metastases in preclinical models of pancreatic cancer
    Savita Bisht
    The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Mol Cancer Ther 9:2255-64. 2010
    ..NanoCurc is a promising new formulation that is able to overcome a major impediment for the clinical translation of curcumin to cancer patients by improving systemic bioavailability, and by extension, therapeutic efficacy...
  37. pmc New markers of pancreatic cancer identified through differential gene expression analyses: claudin 18 and annexin A8
    Zarir E Karanjawala
    The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21231 2410, USA
    Am J Surg Pathol 32:188-96. 2008
    ..New markers to distinguish benign reactive glands from infiltrating ductal adenocarcinoma of the pancreas are needed...
  38. 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...
  39. 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...
  40. ncbi request reprint Epigenetic down-regulation of CDKN1C/p57KIP2 in pancreatic ductal neoplasms identified by gene expression profiling
    Norihiro Sato
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Clin Cancer Res 11:4681-8. 2005
    ..Although our knowledge of the clinical and pathologic features of IPMNs is increasing, the molecular mechanisms underlying these neoplasms remain poorly understood...
  41. ncbi request reprint Expression and prognostic significance of 14-3-3sigma and ERM family protein expression in periampullary neoplasms
    Steven R Hustinx
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
    Cancer Biol Ther 4:596-601. 2005
    ..4; 0.9-2.2, p = 0.14). Aberrant expression of 14-3-3sigma may contribute to the outcome of patients with pancreatic ductal adenocarcinoma...
  42. pmc Overexpression of smoothened activates the sonic hedgehog signaling pathway in pancreatic cancer-associated fibroblasts
    Kimberly Walter
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Clin Cancer Res 16:1781-9. 2010
    ..Our aim is to identify signaling pathways involved in tumor-stromal cell interactions in human pancreatic cancer...
  43. ncbi request reprint Age- and disease-related methylation of multiple genes in nonneoplastic duodenum and in duodenal juice
    Hiroyuki Matsubayashi
    Department of Pathology, Division of Biostatistics, Johns Hopkins Medical Institutions, 720 Rutland Avenue, Baltimore, MD 21205, USA
    Clin Cancer Res 11:573-83. 2005
    ....
  44. ncbi request reprint Gene expression profiles in pancreatic intraepithelial neoplasia reflect the effects of Hedgehog signaling on pancreatic ductal epithelial cells
    Nijaguna B Prasad
    Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Cancer Res 65:1619-26. 2005
    ..These data show frequent up-regulation of foregut markers in early PanIN lesions and suggest that PanIN development may involve Hedgehog-mediated conversion to a gastric epithelial differentiation program...
  45. pmc Pdx1 expression in pancreatic precursor lesions and neoplasms
    Jason Y Park
    Department of Pathology, University of Texas Southwestern Medical Center, Dallas, 75235, USA
    Appl Immunohistochem Mol Morphol 19:444-9. 2011
    ....
  46. pmc Importance of age of onset in pancreatic cancer kindreds
    Kieran A Brune
    Department of Pathology, Sol Goldman Pancreatic Cancer Research Center at Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD 21231, USA
    J Natl Cancer Inst 102:119-26. 2010
    ..Young-onset cancer is a hallmark of many familial cancer syndromes, yet the implications of young-onset disease in predicting risk of pancreatic cancer among familial pancreatic cancer (FPC) kindred members remain unclear...
  47. doi request reprint Familial pancreatic cancer: from genes to improved patient care
    Ralph H Hruban
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Hospital, Weinberg Building 2242, 401 North Broadway, Baltimore, MD 21231, USA
    Expert Rev Gastroenterol Hepatol 1:81-8. 2007
    ..This review focuses on the genetic basis for the familial aggregation of pancreatic cancer, with emphasis placed on the implications of the genetic alterations on clinical patient care...
  48. pmc Pancreatic cancer associated fibroblasts display normal allelotypes
    Kimberly Walter
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 7:882-8. 2008
    ..The aim of this study was to determine if pancreatic cancer associated fibroblasts display similar genetic alterations...
  49. pmc Elevated cancer mortality in the relatives of patients with pancreatic cancer
    Li Wang
    1Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21231, USA
    Cancer Epidemiol Biomarkers Prev 18:2829-34. 2009
    ..Our results show that relatives of pancreatic cancer patients are at higher risk of developing cancers at other sites and highlight the importance of complete family history in clinical risk assessment...
  50. 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...
  51. 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...
  52. pmc Aberrant methylation of preproenkephalin and p16 genes in pancreatic intraepithelial neoplasia and pancreatic ductal adenocarcinoma
    Noriyoshi Fukushima
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 2196, USA
    Am J Pathol 160:1573-81. 2002
    ....
  53. ncbi request reprint Expression of the caudal-type homeodomain transcription factors CDX 1/2 and outcome in carcinomas of the ampulla of Vater
    Donna E Hansel
    MBBS, Department of Surgery, The Johns Hopkins University School of Medicine, 720 Rutland Ave, Ross 771, Baltimore, MD 21205, USA
    J Clin Oncol 23:1811-8. 2005
    ..We assessed the expression of these putative intestinal epithelial-specific transcription factors and their influence on patient outcome...
  54. 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...
  55. ncbi request reprint Epigenetic inactivation of TFPI-2 as a common mechanism associated with growth and invasion of pancreatic ductal adenocarcinoma
    Norihiro Sato
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
    Oncogene 24:850-8. 2005
    ..We thus conclude that epigenetic inactivation of TFPI-2 is a common mechanism that contributes to the aggressive phenotype of pancreatic ductal adenocarcinoma...
  56. ncbi request reprint Gene expression profiling of tumor-stromal interactions between pancreatic cancer cells and stromal fibroblasts
    Norihiro Sato
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 2196, USA
    Cancer Res 64:6950-6. 2004
    ..Thus, COX-2 inhibitors can decrease the invasive properties of pancreatic cancer cells acquired through tumor-stromal interactions...
  57. ncbi request reprint Evaluation of osteopontin as biomarker for pancreatic adenocarcinoma
    Jens Koopmann
    Department of Pathology and Surgery, Johns Hopkins Medical Institutions, Baltimore, MD, USA
    Cancer Epidemiol Biomarkers Prev 13:487-91. 2004
    ..One candidate tumor marker recently identified by global gene expression analysis of pancreatic cancer is the secreted glycophosphoprotein osteopontin (OPN). In this study, we evaluate OPN as a serum marker of pancreatic adenocarcinoma...
  58. ncbi request reprint Screening for pancreatic neoplasia in high-risk individuals: an EUS-based approach
    Marcia Irene Canto
    Department of Medicine Gastroenterology, Johns Hopkins Medical Institution, Baltimore, MD 21205, USA
    Clin Gastroenterol Hepatol 2:606-21. 2004
    ..We prospectively evaluated the feasibility of screening for pancreatic neoplasia in high-risk individuals...
  59. pmc Gene expression profiling identifies genes associated with invasive intraductal papillary mucinous neoplasms of the pancreas
    Norihiro Sato
    Departments of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 2196, USA
    Am J Pathol 164:903-14. 2004
    ..0001). Our findings suggest that preoperative assessment of gene expression profiles may be able to differentiate invasive from noninvasive IPMNs...
  60. ncbi request reprint Identification of maspin and S100P as novel hypomethylation targets in pancreatic cancer using global gene expression profiling
    Norihiro Sato
    1Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD, USA
    Oncogene 23:1531-8. 2004
    ..Thus, our present results confirm that DNA hypomethylation is a frequent epigenetic event in pancreatic cancer, and suggest that gene expression profiling may help to identify potential targets affected by this epigenetic alteration...
  61. 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
    ....
  62. ncbi request reprint Frequent hypomethylation of multiple genes overexpressed in pancreatic ductal adenocarcinoma
    Norihiro Sato
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA
    Cancer Res 63:4158-66. 2003
    ..These results indicate that gene hypomethylation is a frequent epigenetic event in pancreatic cancer and is commonly associated with the overexpression of affected genes...
  63. 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...
  64. ncbi request reprint Gene expression alterations in the non-neoplastic parenchyma adjacent to infiltrating pancreatic ductal adenocarcinoma
    Noriyoshi Fukushima
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21205 2196, USA
    Mod Pathol 18:779-87. 2005
    ....
  65. ncbi request reprint An illustrated consensus on the classification of pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasms
    Ralph H Hruban
    Department of Pathology, The Johns Hopkins Medical Institutions, 401 N Broadway, Weinberg 2242, Baltimore, MD 21231 2410, USA
    Am J Surg Pathol 28:977-87. 2004
    ..We present a consensus classification of the precursor lesions in the pancreatic ducts, PanINs and IPMNs...
  66. ncbi request reprint Differentiating pancreatic lesions by microarray and QPCR analysis of pancreatic juice RNAs
    Carmelle D Rogers
    Department of Pathology, The Sol Goldman Center for Pancreatic Cancer Research, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 5:1383-9. 2006
    ..We hypothesized that gene expression alterations indicative of pancreatic cancer can be detected by profiling the RNA of pancreatic juice...
  67. ncbi request reprint Screening for early pancreatic neoplasia in high-risk individuals: a prospective controlled study
    Marcia Irene Canto
    Depatment of Medicine Gastroenterology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Clin Gastroenterol Hepatol 4:766-81; quiz 665. 2006
    ..This study screened for early pancreatic neoplasia and compared the pancreatic abnormalities in high-risk individuals and control subjects...
  68. pmc Prevalence of the alternative lengthening of telomeres telomere maintenance mechanism in human cancer subtypes
    Christopher M Heaphy
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Am J Pathol 179:1608-15. 2011
    ..These findings may have therapeutic consequences, because ALT-positive cancers are predicted to be resistant to anti-telomerase therapies...
  69. pmc Hilar cholangiocarcinoma: tumor depth as a predictor of outcome
    Mechteld C de Jong
    Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Arch Surg 146:697-703. 2011
    ..The American Joint Committee on Cancer staging system for hilar cholangiocarcinoma may be inaccurate because the bile duct lacks discrete tissue boundaries...
  70. 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...
  71. 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...
  72. pmc Linkage analysis of chromosome 4 in families with familial pancreatic cancer
    Alison P Klein
    The Sol Goldman Pancreatic Research Center, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 6:320-3. 2007
    ....
  73. pmc Differential expression of multiple genes in association with MADH4/DPC4/SMAD4 inactivation in pancreatic cancer
    Dengfeng Cao
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Hospital Baltimore, MD, USA
    Int J Clin Exp Pathol 1:510-7. 2008
    ..Further investigations to validate and to determine the significance of these candidate target genes in pancreatic carcinogenesis and progression are warranted...
  74. pmc Genetic and epigenetic alterations of familial pancreatic cancers
    Kieran Brune
    Department of Pathology, Medicine, Oncology, Johns Hopkins Medical Institutions, The Sol Goldman Pancreatic Cancer Research Center, 1550 Orleans Street, CRB2, Room 342, Baltimore, MD 21231, USA
    Cancer Epidemiol Biomarkers Prev 17:3536-42. 2008
    ..The aim of this study was to compare the prevalence of common genetic and epigenetic alterations in sporadic and familial pancreatic ductal adenocarcinomas...
  75. ncbi request reprint Genome-wide allelotypes of familial pancreatic adenocarcinomas and familial and sporadic intraductal papillary mucinous neoplasms
    Tadayoshi Abe
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Clin Cancer Res 13:6019-25. 2007
    ..Identifying the genomic losses that occur in pancreatic neoplasms, particularly those that occur in familial and precursor neoplasms, may help localize the genes responsible for pancreatic cancer susceptibility...
  76. pmc Absence of germline BRCA1 mutations in familial pancreatic cancer patients
    Jennifer E Axilbund
    Department of Oncology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University, Baltimore, Maryland, USA
    Cancer Biol Ther 8:131-5. 2009
    ....
  77. ncbi request reprint Methylation of cyclin D2 is observed frequently in pancreatic cancer but is also an age-related phenomenon in gastrointestinal tissues
    Hiroyuki Matsubayashi
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, 21205 2196, USA
    Clin Cancer Res 9:1446-52. 2003
    ..We investigated the methylation of cyclin D2 in aging and pancreatic neoplastic development, and the utility of cyclin D2 methylation as a marker of pancreatic adenocarcinoma...
  78. ncbi request reprint Aberrant methylation of the 5' CpG island of TSLC1 is common in pancreatic ductal adenocarcinoma and is first manifest in high-grade PanlNs
    Marnix Jansen
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA
    Cancer Biol Ther 1:293-6. 2002
    ..We conclude that epigenetic silencing of TSLC1 expression through 5' CpG island associated methylation is common in pancreatic adenocarcinoma and is a late event in pancreatic neoplastic development...
  79. ncbi request reprint The role of epigenetic alterations in pancreatic cancer
    Norihiro Sato
    Department of Pathology, The Johns Hopkins Medical Institutions, The Sol Goldman Center for Pancreatic Cancer Research, 342 Cancer Research Building 2, 1550 Orleans St, Baltimore, MD 21231, USA
    J Hepatobiliary Pancreat Surg 13:286-95. 2006
    ..In this review, we briefly summarize recent research findings in the field of pancreatic cancer epigenetics and discuss their biological and clinical implications...
  80. 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...
  81. pmc Palladin is overexpressed in the non-neoplastic stroma of infiltrating ductal adenocarcinomas of the pancreas, but is only rarely overexpressed in neoplastic cells
    Safia N Salaria
    The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231 2410, USA
    Cancer Biol Ther 6:324-8. 2007
    ..This hypothesis was based on reverse transcriptase-polymerase chain reaction analyses of bulk pancreatic tissue, yet pancreatic cancer is a complex admixture of neoplastic epithelial cells and desmoplastic stroma...
  82. 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...
  83. ncbi request reprint p16 Inactivation in pancreatic intraepithelial neoplasias (PanINs) arising in patients with chronic pancreatitis
    Christophe Rosty
    Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA
    Am J Surg Pathol 27:1495-501. 2003
    ..This alteration, common to pancreatic cancer-associated PanINs, may contribute to the predisposition of patients with chronic pancreatitis to develop pancreatic ductal adenocarcinoma...
  84. pmc KRAS2 mutations in human pancreatic acinar-ductal metaplastic lesions are limited to those with PanIN: implications for the human pancreatic cancer cell of origin
    Chanjuan Shi
    The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 212312, USA
    Mol Cancer Res 7:230-6. 2009
    ..Isolated AMD lesions are genetically distinct from those associated with PanINs, and the latter may represent retrograde extension of the neoplastic PanIN cells or less likely are precursors to PanIN...
  85. 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...
  86. pmc Genome-wide profiling of methylated promoters in pancreatic adenocarcinoma
    Noriyuki Omura
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Biol Ther 7:1146-56. 2008
    ..Many genes undergo aberrant methylation in human cancers, and microarray platforms enable more comprehensive profiling of aberrant DNA methylation patterns...
  87. ncbi request reprint Identification of hepatocarcinoma-intestine-pancreas/pancreatitis-associated protein I as a biomarker for pancreatic ductal adenocarcinoma by protein biochip technology
    Christophe Rosty
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205 2196, USA
    Cancer Res 62:1868-75. 2002
    ..Taken together, these data suggest that pancreatic juice measurement of HIP/PAP-I may help to identify patients with pancreatic adenocarcinoma...
  88. ncbi request reprint Epigenetic alterations in intraductal papillary mucinous neoplasms of the pancreas
    Norihiro Sato
    Department of Pathology, The Johns Hopkins Medical Institutions, The Sol Goldman Center for Pancreatic Cancer Research, 342 Cancer Research Building 2, 1550 Orleans St, Baltimore, MD 21231, USA
    J Hepatobiliary Pancreat Surg 13:280-5. 2006
    ..Further studies of epigenetic alterations in IPMN will shed light on the molecular pathogenesis of this unique neoplasm and lead to the identification of epigenetic markers that can be applied in the clinical setting...
  89. pmc Pancreatic cancers epigenetically silence SIP1 and hypomethylate and overexpress miR-200a/200b in association with elevated circulating miR-200a and miR-200b levels
    Ang Li
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University, Baltimore, Maryland 21231, USA
    Cancer Res 70:5226-37. 2010
    ..The elevated serum levels of miR-200a and miR-200b in most patients with pancreatic cancer could have diagnostic utility...
  90. pmc Prognostic significance of tumorigenic cells with mesenchymal features in pancreatic adenocarcinoma
    Zeshaan A Rasheed
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    J Natl Cancer Inst 102:340-51. 2010
    ..Aldehyde dehydrogenase (ALDH) activity can identify tumor-initiating cells and normal stem cells from several human tissues. We examined the prognostic significance and functional features of ALDH expression in pancreatic adenocarcinoma...
  91. 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...
  92. ncbi request reprint Characterization of gene expression in mucinous cystic neoplasms of the pancreas using oligonucleotide microarrays
    Noriyoshi Fukushima
    Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
    Oncogene 23:9042-51. 2004
    ..Some of the genes identified as overexpressed in these neoplasms may be useful as markers that can distinguish MCNs from non-neoplastic pancreatic cystic lesions...
  93. pmc Serum fatty acid synthase as a marker of pancreatic neoplasia
    Kim Walter
    Department of Pathology, Johns Hopkins University, Baltimore, MD 21231, USA
    Cancer Epidemiol Biomarkers Prev 18:2380-5. 2009
    ..In conclusion, serum FAS levels are elevated in patients with pancreatic cancer and IPMNs and are associated with neoplastic overexpression of FAS...
  94. pmc Rapid characterization of candidate biomarkers for pancreatic cancer using cell microarrays (CMAs)
    Min Sik Kim
    McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Proteome Res 11:5556-63. 2012
    ..Our results demonstrate the utility of CMAs as a useful resource for rapid screening of molecules of interest and suggest that CMAs can become a universal standard platform in cancer research...
  95. ncbi request reprint A proteomic analysis of human bile
    Troels Zakarias Kristiansen
    McKusick Nathans Institute of Genetic Medicine and Department of Biological Chemistry, Johns Hopkins University, Baltimore, MD 21205, USA
    Mol Cell Proteomics 3:715-28. 2004
    ..In combination with "tagging" approaches for differential proteomics, our method could be used for identification of cancer biomarkers from any body fluid...

Research Grants11

  1. THE PanINs OF PANCREATITIS,PANCREAS CANCER AND CONTROLS
    Michael Goggins; Fiscal Year: 2002
    ..abstract_text> ..
  2. Markers of Early Pancreatic Cancer
    Michael Goggins; Fiscal Year: 2007
    ..We will also determine the diagnostic utility of combining the results of the markers derived from these 3 Aims. ..
  3. CLASSIFYING PANCREATIC CANCERS BY METHYLATOR PHENOTYPES
    Michael Goggins; Fiscal Year: 2006
    ..Aim #4: Determine if functional DNA methylation differences exist between CIMP+ compared to CIMP- pancreatic carcinomas. ..
  4. CLASSIFYING PANCREATIC CANCERS BY METHYLATOR PHENOTYPES
    Michael Goggins; Fiscal Year: 2005
    ..Aim #4: Determine if functional DNA methylation differences exist between CIMP+ compared to CIMP- pancreatic carcinomas. ..
  5. FOLATE PATHWAY POLYMORPHISMS AND PANCREATIC CANCER RISK
    Michael Goggins; Fiscal Year: 2002
    ..abstract_text> ..
  6. CLASSIFYING PANCREATIC CANCERS BY METHYLATOR PHENOTYPES
    Michael Goggins; Fiscal Year: 2004
    ..Aim #4: Determine if functional DNA methylation differences exist between CIMP+ compared to CIMP- pancreatic carcinomas. ..
  7. Markers of Early Pancreatic Cancer
    Michael Goggins; Fiscal Year: 2006
    ..We will also determine the diagnostic utility of combining the results of the markers derived from these 3 Aims. ..
  8. CLASSIFYING PANCREATIC CANCERS BY METHYLATOR PHENOTYPES
    Michael Goggins; Fiscal Year: 2003
    ..Aim #4: Determine if functional DNA methylation differences exist between CIMP+ compared to CIMP- pancreatic carcinomas. ..
  9. Markers of Early Pancreatic Cancer
    Michael Goggins; Fiscal Year: 2009
    ..We will also determine the diagnostic utility of combining the results of the markers derived from these 3 Aims. ..
  10. Markers of Early Pancreatic Cancer
    Michael G Goggins; Fiscal Year: 2010
    ..We will also determine the diagnostic utility of combining the results of the markers derived from these 3 Aims. ..