Telomeres are shortened in acinar-to-ductal metaplasia lesions associated with pancreatic intraepithelial neoplasia but not in isolated acinar-to-ductal metaplasias

[1]  M. Hebrok,et al.  Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice. , 2010, The Journal of clinical investigation.

[2]  L. Tanoue Cancer Statistics, 2009 , 2010 .

[3]  R. DePinho,et al.  Telomeres and telomerase in cancer. , 2010, Carcinogenesis.

[4]  A. D. De Marzo,et al.  Dual‐label centromere and telomere FISH identifies human, rat, and mouse cell contribution to Multispecies recombinant urogenital sinus xenografts , 2009, The Prostate.

[5]  A. Jemal,et al.  Cancer Statistics, 2009 , 2009, CA: a cancer journal for clinicians.

[6]  R. Hruban,et al.  KRAS2 Mutations in Human Pancreatic Acinar-Ductal Metaplastic Lesions Are Limited to Those with PanIN: Implications for the Human Pancreatic Cancer Cell of Origin , 2009, Molecular Cancer Research.

[7]  G. Feldmann,et al.  Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice , 2008, Proceedings of the National Academy of Sciences.

[8]  R. Hruban,et al.  Multiple genes are hypermethylated in intraductal papillary mucinous neoplasms of the pancreas , 2008, Modern Pathology.

[9]  G. Parmigiani,et al.  Core Signaling Pathways in Human Pancreatic Cancers Revealed by Global Genomic Analyses , 2008, Science.

[10]  R. Hruban,et al.  CpG island methylation profile of pancreatic intraepithelial neoplasia , 2008, Modern Pathology.

[11]  Michael Goggins,et al.  Update on pancreatic intraepithelial neoplasia. , 2008, International journal of clinical and experimental pathology.

[12]  R. Hruban,et al.  Genome-Wide Allelotypes of Familial Pancreatic Adenocarcinomas and Familial and Sporadic Intraductal Papillary Mucinous Neoplasms , 2007, Clinical Cancer Research.

[13]  R. Hruban,et al.  Tumorigenesis and Neoplastic Progression Acinar Cells Contribute to the Molecular Heterogeneity of Pancreatic Intraepithelial Neoplasia , 2007 .

[14]  S. Leach,et al.  A case of mistaken identity? Nonductal origins of pancreatic "ductal" cancers. , 2007, Cancer cell.

[15]  M. Barbacid,et al.  Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. , 2007, Cancer cell.

[16]  J. Cameron,et al.  Multifocal Neoplastic Precursor Lesions Associated With Lobular Atrophy of the Pancreas in Patients Having a Strong Family History of Pancreatic Cancer , 2006, The American journal of surgical pathology.

[17]  Christine A Iacobuzio-Donahue,et al.  Identifying allelic loss and homozygous deletions in pancreatic cancer without matched normals using high-density single-nucleotide polymorphism arrays. , 2006, Cancer research.

[18]  E. Fishman,et al.  Screening for early pancreatic neoplasia in high-risk individuals: a prospective controlled study. , 2006, Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association.

[19]  E. Furth,et al.  Pathology of genetically engineered mouse models of pancreatic exocrine cancer: consensus report and recommendations. , 2006, Cancer research.

[20]  R. Hruban,et al.  Genome-wide aberrations in pancreatic adenocarcinoma. , 2005, Cancer genetics and cytogenetics.

[21]  R. Hruban,et al.  Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice. , 2005, Cancer cell.

[22]  E. Blackburn,et al.  Telomeres and telomerase: their mechanisms of action and the effects of altering their functions , 2005, FEBS letters.

[23]  Michio Shimizu,et al.  An Illustrated Consensus on the Classification of Pancreatic Intraepithelial Neoplasia and Intraductal Papillary Mucinous Neoplasms , 2004, The American journal of surgical pathology.

[24]  R. Hruban,et al.  Large-Scale Allelotype of Pancreaticobiliary Carcinoma Provides Quantitative Estimates of Genome-Wide Allelic Loss , 2004, Cancer Research.

[25]  E. Petricoin,et al.  Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. , 2003, Cancer cell.

[26]  F. Brembeck,et al.  The mutant K-ras oncogene causes pancreatic periductal lymphocytic infiltration and gastric mucous neck cell hyperplasia in transgenic mice. , 2003, Cancer research.

[27]  J. Hicks,et al.  Telomere shortening is an early somatic DNA alteration in human prostate tumorigenesis. , 2002, Cancer research.

[28]  Scott E Kern,et al.  Telomere shortening is nearly universal in pancreatic intraepithelial neoplasia. , 2002, The American journal of pathology.

[29]  L. Chin,et al.  Telomere dysfunction provokes regional amplification and deletion in cancer genomes. , 2002, Cancer cell.

[30]  R. Hruban,et al.  Aberrant methylation of preproenkephalin and p16 genes in pancreatic intraepithelial neoplasia and pancreatic ductal adenocarcinoma. , 2002, The American journal of pathology.

[31]  R. Hruban,et al.  Aberrant Methylation of the 5' CpG Island of TSLC1 Is Common in Pancreatic Ductal Adenocarcinoma and Is First Manifest in High-Grade PanINs , 2002, Cancer biology & therapy.

[32]  J. Hackett,et al.  Balancing instability: dual roles for telomerase and telomere dysfunction in tumorigenesis , 2002, Oncogene.

[33]  D. Gisselsson,et al.  Telomere dysfunction triggers extensive DNA fragmentation and evolution of complex chromosome abnormalities in human malignant tumors , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[34]  R. DePinho,et al.  Telomere dysfunction and evolution of intestinal carcinoma in mice and humans , 2001, Nature Genetics.

[35]  W. Klapper,et al.  Telomere biology in human aging and aging syndromes , 2001, Mechanisms of Ageing and Development.

[36]  R H Hruban,et al.  Pancreatic Intraepithelial Neoplasia: A New Nomenclature and Classification System for Pancreatic Duct Lesions , 2001, The American journal of surgical pathology.

[37]  W. Schmiegel,et al.  Allelic loss is often the first hit in the biallelic inactivation of the p53 and DPC4 genes during pancreatic carcinogenesis. , 2001, The American journal of pathology.

[38]  Lynda Chin,et al.  Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice , 2000, Nature.

[39]  R. Hruban,et al.  BRCA2 is inactivated late in the development of pancreatic intraepithelial neoplasia: evidence and implications. , 2000, The American journal of pathology.

[40]  R. Hruban,et al.  Loss of expression of Dpc4 in pancreatic intraepithelial neoplasia: evidence that DPC4 inactivation occurs late in neoplastic progression. , 2000, Cancer research.

[41]  Robert A. Weinberg,et al.  Creation of human tumour cells with defined genetic elements , 1999, Nature.

[42]  C. Harley,et al.  Extension of life-span by introduction of telomerase into normal human cells. , 1998, Science.

[43]  G. Klöppel,et al.  Tumors of the Pancreas , 1997 .

[44]  C. Moskaluk,et al.  p16 and K-ras gene mutations in the intraductal precursors of human pancreatic adenocarcinoma. , 1997, Cancer research.

[45]  D. Brat,et al.  The structural basis of molecular genetic deletions. An integration of classical cytogenetic and molecular analyses in pancreatic adenocarcinoma. , 1997, The American journal of pathology.

[46]  S. Bohlander,et al.  Consistent chromosome abnormalities in adenocarcinoma of the pancreas. , 1995, Cancer research.

[47]  C B Harley,et al.  Telomeres and telomerase in aging and cancer. , 1995, Current opinion in genetics & development.

[48]  C B Harley,et al.  Specific association of human telomerase activity with immortal cells and cancer. , 1994, Science.

[49]  N. Dubrawsky Cancer statistics , 1989, CA: a cancer journal for clinicians.

[50]  S. Mujais,et al.  Uremic exocrine pancreopathy. , 1987, International Journal of Artificial Organs.

[51]  M M Grajower,et al.  Familial pancreatic cancer. , 1983, Annals of internal medicine.

[52]  Gilmore Hr,et al.  Armed Forces Institute of Pathology. , 1968, Oral surgery, oral medicine, and oral pathology.