Literatur
-
1
Rozenblum E, Schutte M, Goggins M. et al .
Tumor-suppressive pathways in pancreatic carcinoma.
Cancer Research.
1997;
57
1731-1734
-
2
Almoguera C, Shibata D, Forrester K. et al .
Most human carcinomas of the exocrine pancreas contain mutant c-K-ras genes.
Gell.
1988;
53
549-554
-
3
Caldas C, Kern S E.
K-ras mutation and pancreatic adenocarcinoma.
International Journal of Pancreatology.
1995;
18
1-6
-
4
Shirasawa S, Furuse M, Yokoyama N. et al .
Altered growth of human colon cancer cell lines disrupted at activated K-ras.
Science.
1993;
260
85-86
-
5
Quaife C J, Pinkert C A, Ornitz D M. et al .
Pancreatic neoplasia induced by ras expression in acinar cells of transgenic mice.
Cell.
1987;
48
1023-1034
-
6
Wagner M, Greten F R, Weber C K. et al .
A murine tumor progression model for pancreatic cancer recapitulating the genetic alterations of the human disease.
Genes & Development.
2001;
15
286-93
-
7
Johnson L, Mercer K, Greenbaum D. et al .
Somatic activation of the k-ras oncogene causes early onset lung cancer in mice.
Nature.
2001;
11
2468-2481
-
8
Caldas C, Hahn S A, da Costa L T. et al .
Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma.
Nature Genetics.
1994;
8
27-32
-
9
Serrano M, Lee H, Chin L. et al .
Role of the INK4a locus in tumor suppression and cell mortality.
Cell.
1996;
85
27-37
-
10
Schutte M, Hruban R H, Geradts J. et al .
Abrogation of the Rb/p16 tumor-suppressive pathway in virtually all pancreatic carcinomas.
Cancer Research.
1997;
7; 57
3126-3130
-
11
Gruis N A, van der Velden P A, Sandkuijl L A. et al .
Homozygotes for CDKN2 (p16) germline mutation in Dutch familial melanoma kindreds.
Nature Genetics.
1995;
10
351-353
-
12
Goldstein A M. et al .
Increased risk of pancreatic cancer in melanoma-prone kindreds with p16INK4 mutations.
New England Journal of Medicine.
1995;
333
970-974
-
13
Whelam A J, Bartsch D, Goodfellow P J.
Brief report: a familial syndrome of pancreatic cancer and melanoma with a mutation in the CDKN2 tumor-suppressor gene.
New England Journal of Medicine.
1995;
333
975-977
-
14
Lynch H T, Fitzsimmons M L, Smyrk T C. et al .
Familial pancreatic cancer: clinicopathologic study of 18 nulear families.
American Journal of Gastroenterology.
1990;
85
54-60
-
15
Levine A J.
p53, the cellular gatekeeper for growth and division.
Gell.
1997;
88
323-331
-
16
Barton C M, Staddon S L, Hughes C M. et al .
Abnormalities of the p53 tumour suppressor gene in human pancreatic cancer.
British Journal of Cancer.
1991;
64
1076-1082
-
17
Redston M S, Caldas C, Seymour A B. et al .
p53 mutations in pancreatic canrcinoma and evidence of common involvement of homocopolymer tracts in DNA microdeletions.
Cancer Research.
1998;
54
3025-3033
-
18
Strong L C, Stine M, Norsted T L.
Cancer in survivors of childhood soft tissue sarcoma and their relatives.
J. Natl. Cancer Inst.
1987;
79
1213-1220
-
19
Li F P, Fraumeni J F Jr, Mulvihill J J. et al .
A cancer family syndrome in twenty-four kindreds.
Cancer Research.
1988;
48
5358-5362
-
20
Wrana J L.
Regulation of Smad activity.
Gell.
2000;
100
189-192
-
21
Hahn S A, Schutte M, Hoque A T. et al .
DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1.
Science.
1996;
271
350-353
-
22
Scharte-Waldhoff l, Volpert O V, Bouck N P.
et al. Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis. Proceedings of the National Academy of Sciences.
USA.
2000;
97
9624-9629
-
23
Tascilar M, Skinner H G, Rosty C. et al .
The Smad4 protein and prognosis of pancreatic ductal adenocarcinoma.
Clinical Cancer Research.
2001;
7
4115-4121
-
24
Kinzler K, Vogelstein B.
Lessions from hereditary colorectal cancer.
Gell.
1996;
87
159-170
-
25
Longegger D S, Shinozuka H, Dekker A.
Focal acinar cell dysplasia in human pancreas.
Cancer.
1980;
45
534-540
-
26 Klöppel G. Pathology of nonendocrine pancreatic tumors,. New York; Raven Press 1993: 871-898
-
27
Pour P M, Weide L, Liu G. et al .
Experimental evidence for the origin of ductal-type adenocarcinoma from the islets of Langerhans American Journal of Pathology.
1997;
150
2167-2180
-
28
Willentz R E, Geradts J, Maynard R. et al .
Inactivation of the p16 (INK4A) tumor-suppressor gene in pancreatic duct lesions: loss of intranuclear expression.
Cancer Research.
1998;
58
4740-4744
-
29
Hruban R H, Wilentz R E, Goggins M. et al .
Pathology of incipient pancreatic cancer.
Annals of Oncology.
1999;
10
S9-S11
-
30
Hruban R H, Wilentz R E, Kern S E.
Genetic progression in the pancreatic ducts.
American Journal of Pathology.
2000;
156
1821-1825
-
31
Wilentz R E, lacobuzio-Donahue C A, Argani P. et al .
Loss of expression of Dpc4 in pancreatic intraepitheial neoplasia: evidence that DPC4 inactivation occurs late in neoplastic progression.
Cancer Research.
2000;
60
2002-2006
-
32
Hruban R H, Adsay N V, Albores-Saavedra J. et al .
Pancreatic intraepithelial neplasia: a new nomenclature and classification System for pancreatic duct lesions.
Am. J. Surg. Path.
2001;
25
579-586
-
33
Kern S, Hruban R, Hollingsworth M A. et al .
A white paper: the product of a pancreas cancer think tank.
Cancer Research.
2001;
61
4923-4932
-
34
Sommers S C, Murphy S A, Warren S.
Pancreatic duct hyperplasia and cancer.
Gastroenterology.
1954;
27
629-640
-
35
Cubilla A L, Fitzgerald P J.
Morphological lesions associated with human primary invasive nonendocrine pancreatic cancer.
Cancer Research.
1976;
36
2690-2698
-
36
Furukawa T, Chiba R, Kobari M. et al .
Varying grades of epithelial atypia in the pancreatic ducts of humans: classification based on morphometry and multivariate analysis and correlated with positive reactions of carcinoembryonic antigen.
Archivs of Pathology & Laboratory Medicine.
1994;
118
227-234
-
37
Kozuka S, Sassa R, Taki T. et al .
Relation of pancreatic duct hyperplasia to carcinoma.
Cancer.
1979;
43
1418-1428
-
38
Klöppel G, Bommer G, Rückert K. et al .
Intraductal proliferation in the pancreas and its relationship to human and experimental carcinogenesis.
Virchows Archiv.
1980;
387
221-233
-
39
Moskaluk C A, Hruban R H, Kern.
SE p16 and K-ras gene mutations in the intraductal precursors of human pancreatic adenocarcinoma.
Cancer Research.
1997;
57
2140-2143
-
40
Goggins M, Schutte M, Lu J. et al .
Germline BRCA2 gene mutations in patients with apparently sporadic pancreatic and biliary adenocarcinomas.
Cancer Research.
58
5360-5364
-
41
DiGuiseppe J A, Hruban R H, Offerhaus G JA. et al .
Detection of K-ras mutations in mucinous pancreatic duct hyperplasia from a patient with a family history of pancreatic caarcinoma.
American Journal of Pathology.
1994;
144
889-895
-
42
Yamano M, Fujii H, Takagaki T. et al .
Genetic progression and divergence in pancreatic carcinoma.
American Journal of Pathology.
2000;
156
2123-2133
-
43
Day J D, DiGuiseppe J A, Yeo C J. et al .
Immunhistochemical evaluation of HER-2/neu oncogene expression in pancreatic adenocarcinoma and pancreatic intraepithelial neoplasmas.
Hum. Pathol.
1996;
27
119-124
-
44
DiGuiseppe J A, Hruban R H, Goodman S N. et al .
Overepxression of p53 protein in adenocarcinoma of the pancreas.
American Journal of Clinical Pathology.
1994;
101
684-688
-
45
Lüttges J, Galehdari H, Bröcker V. et al .
Allelic loss is often the first hit in the biallelic inactivation of the p53 and DPC4 genes during pancreatic carcinogenesis.
American Journal of Pathology.
2001;
158
1677-1683
-
46
Brat D J, Lillemoe K D, Yeo C J. et al .
Progression of pancreatic intraductal neoplasias (high-grade PanlN) to infiltating adenocarcinoma of the pancreas.
American Journal of Surgical Pathology.
1998;
22
163-169
-
47
Brockie E, Anand A, Albores-Saavedra J.
Progession of atypical ductal hyperplasia/carcinoma in situ of the pancreas to invasive adenocarcinoma.
Ann. Diag. Pathol.
1998;
2
286-292
-
48
Tada M, Ohashi M, Shiratori Y. et al .
Analysis of K-ras gene mutation in hyperplastic duct cells of the pancreas without pancreatic disease.
Gastroenterology.
1996;
110
227-31
-
49
Lüttges J, Schlehe B, Menke M AOH. et al .
The K-ras mutation pattern in pancreatic ductal adenocarcinoma is usually identical to that in associated normal, hyperplastic and metaplastic duct epithelium.
Cancer.
1999;
85
1703-1710
-
50
Lüttges J, Diederichs A, Menke M AOH. et al .
Ductal lesions in patients with chronic pancreatitis show K-ras mutations in a frequency similar to that in the normal pancreas and lack nuclear immunoreactivity for p53.
Cancer.
2000;
88
2495-2504
-
51
Apple S K, Hecht J R, Lewin D N. et al .
Immunhistochemical evaluation of K-ras, p53, and HER-2/neu expression in hyperplastic, dysplastic, and carcinomatous lesions of the pancreas: evidence for multistep carcinogenesis.
Hum. Pathol.
1999;
30
123-129
-
52
Boschman C R, Stryker S, Reddy J K. et al .
Expression of p53 protein in precursor lesions and adenocarcinoma of human pancreas.
American Journal of Pathology.
1994;
145
1291-1295
-
53
Heimöller E, Dietmaier W, Zirngibl H. et al .
Molecular analysis of microdissected tumors and preneoplastic intraductal lesions in pancreatic carcinoma.
American Journal of Pathology.
2000;
157
83-92
Prof. Dr. Roland M. Schmid
Direktor der II. Medizinischen Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München
Isamninger Straße 22
81675 München