• 1
    Liao DJ, Wang Y, Wu J, Adsay NV, Grignon D, Khanani F, Sarkar FH. Characterization of pancreatic lesions from MT-tgf alpha, Ela-myc and MT-tgf alpha/Ela-myc single and double transgenic mice. J Carcinog 2006; 5: 19.
  • 2
    Sandgren EP, Luetteke NC, Qiu TH, Palmiter RD, Brinster RL, Lee DC. Transforming growth factor alpha dramatically enhances oncogene-induced carcinogenesis in transgenic mouse pancreas and liver. Mol Cell Biol 1993; 13: 32030.
  • 3
    Sandgren EP, Quaife CJ, Paulovich AG, Palmiter RD, Brinster RL. Pancreatic tumor pathogenesis reflects the causative genetic lesion. Proc Natl Acad Sci USA 1991; 88: 937.
  • 4
    Schaeffer BK, Terhune PG, Longnecker DS. Pancreatic carcinomas of acinar and mixed acinar/ductal phenotypes in Ela-1-myc transgenic mice do not contain c-K-ras mutations. Am J Pathol 1994; 145: 696701.
  • 5
    Scarpelli DG, Rao MS, Reddy JK. Are acinar cells involved in the pathogenesis of ductal adenocarcinoma of the pancreas? Cancer Cells 1991; 3: 275–7.
  • 6
    Grippo PJ, Nowlin PS, Demeure MJ, Longnecker DS, Sandgren EP. Preinvasive pancreatic neoplasia of ductal phenotype induced by acinar cell targeting of mutant kras in transgenic mice. Cancer Res 2003; 63: 20169.
  • 7
    De La OJ, Emerson LL, Goodman JL, Froebe SC, Illum BE, Curtis AB, Murtaugh LC. Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia. Proc Natl Acad Sci USA 2008; 105: 1890712.
  • 8
    Habbe N, Shi G, Meguid RA, Fendrich V, Esni F, Chen H, Feldmann G, Stoffers DA, Konieczny SF, Leach SD, Maitra A. Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice. Proc Natl Acad Sci USA 2008; 105: 189138.
  • 9
    Sandgren EP, Luetteke NC, Palmiter RD, Brinster RL, Lee DC. Overexpression of TGF alpha in transgenic mice: induction of epithelial hyperplasia, pancreatic metaplasia, and carcinoma of the breast. Cell 1990; 61: 112135.
  • 10
    Bockman DE, Merlino G. Cytological changes in the pancreas of transgenic mice overexpressing transforming growth factor alpha. Gastroenterology 1992; 103: 188392.
  • 11
    Wagner M, Greten FR, Weber CK, Koschnick S, Mattfeldt T, Deppert W, Kern H, Adler G, Schmid RM. A murine tumor progression model for pancreatic cancer recapitulating the genetic alterations of the human disease. Genes Dev 2001; 15: 28693.
  • 12
    Crawford HC, Scoggins CR, Washington MK, Matrisian LM, Leach SD. Matrix metalloproteinase-7 is expressed by pancreatic cancer precursors and regulates acinar-to-ductal metaplasia in exocrine pancreas. J Clin Invest 2002; 109: 143744.
  • 13
    Asano T, Yao Y, Zhu J, Li D, Abbruzzese JL, Reddy SA. The PI 3-kinase/Akt signaling pathway is activated due to aberrant Pten expression and targets transcription factors NF-kappaB and c-Myc in pancreatic cancer cells. Oncogene 2004; 23: 857180.
  • 14
    Buchholz M, Schatz A, Wagner M, Michl P, Linhart T, Adler G, Gress TM, Ellenrieder V. Overexpression of c-myc in pancreatic cancer caused by ectopic activation of NFATc1 and the Ca2+/calcineurin signaling pathway. EMBO J 2006; 25: 3714–24.
  • 15
    Koenig A, Linhart T, Schlengemann K, Reutlinger K, Wegele J, Adler G, Singh G, Hofmann L, Kunsch S, Buch T, Schafer E, Gress TM, et al. NFAT-induced histone acetylation relay switch promotes c-Myc-dependent growth in pancreatic cancer cells. Gastroenterology 2010; 138: 1189–99 e1–2.
  • 16
    Schild C, Wirth M, Reichert M, Schmid RM, Saur D, Schneider G. PI3K signaling maintains c-myc expression to regulate transcription of E2F1 in pancreatic cancer cells. Mol Carcinog 2009; 48: 114958.
  • 17
    Armengol G, Knuutila S, Lluis F, Capella G, Miro R, Caballin MR. DNA copy number changes and evaluation of MYC, IGF1R, and FES amplification in xenografts of pancreatic adenocarcinoma. Cancer Genet Cytogenet 2000; 116: 13341.
  • 18
    Holzmann K, Kohlhammer H, Schwaenen C, Wessendorf S, Kestler HA, Schwoerer A, Rau B, Radlwimmer B, Dohner H, Lichter P, Gress T, Bentz M. Genomic DNA-chip hybridization reveals a higher incidence of genomic amplifications in pancreatic cancer than conventional comparative genomic hybridization and leads to the identification of novel candidate genes. Cancer Res 2004; 64: 442833.
  • 19
    Mahlamaki EH, Barlund M, Tanner M, Gorunova L, Hoglund M, Karhu R, Kallioniemi A. Frequent amplification of 8q24, 11q, 17q, and 20q-specific genes in pancreatic cancer. Genes Chromosomes Cancer 2002; 35: 3538.
  • 20
    Schleger C, Verbeke C, Hildenbrand R, Zentgraf H, Bleyl U. c-MYC activation in primary and metastatic ductal adenocarcinoma of the pancreas: incidence, mechanisms, and clinical significance. Mod Pathol 2002; 15: 4629.
  • 21
    Grippo PJ, Sandgren EP. Highly invasive transitional cell carcinoma of the bladder in a simian virus 40 T-antigen transgenic mouse model. Am J Pathol 2000; 157: 80513.
  • 22
    Ornitz DM, Hammer RE, Messing A, Palmiter RD, Brinster RL. Pancreatic neoplasia induced by SV40 T-antigen expression in acinar cells of transgenic mice. Science 1987; 238: 18893.
  • 23
    Ge L, Meng W, Zhou H, Bhowmick N. Could stroma contribute to field cancerization? Med Hypotheses 2010; 75: 26–31.
  • 24
    Braakhuis BJ, Tabor MP, Kummer JA, Leemans CR, Brakenhoff RH. A genetic explanation of Slaughter's concept of field cancerization: evidence and clinical implications. Cancer Res 2003; 63: 172730.