Home LiteratureArticle Details
PMID: 11337365 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Allelic loss is often the first hit in the biallelic inactivation of the p53 and DPC4 genes during pancreatic carcinogenesis.

The American journal of pathology ·Vol. 158 ·No. 5 ·2001-05-00 ·Pages 1677-83

Lüttges J, Galehdari H, Bröcker V, Schwarte-Waldhoff I, Henne-Bruns D, Klöppel G, Schmiegel W, Hahn SA

Abstract

The presumed precursor lesions of pancreatic ductal adenocarcinoma were recently classified according to their increasing grade of dysplasia and were designated as pancreatic intraepithelial neoplasia (PanIN) 1 through 3. In this study, we tested whether molecular genetic alterations can be correlated with this classification and may help to further categorize the various PanIN grades. We determined the frequencies of allelic loss at chromosomal arms 9p, 17p, and 18q in 81 microdissected duct lesions of various PanIN grades, using a combination of whole genome amplification and microsatellite analysis. In addition we examined the p53 and Dpc4 protein expression patterns by immunohistochemical analysis. In PanIN-1, we did not detect allelic losses. In PanIN-2, allelic losses were found in increasing frequency, and were particularly high in those lesions with moderate-grade dysplasia (low grade, 20, 33, and 17%, loss at 9p, 17p, and 18q, respectively; moderate grade, 46, 77, and 58%). PanIN-3 and invasive carcinomas exhibited abundant losses. Abnormal p53 and Dpc4 protein expression was only rarely identified in PanIN-2 lesions, but occurred frequently in PanIN-3 lesions and invasive carcinomas. The combined genetic and protein expression data support a model in which allelic loss is the first hit in the biallelic inactivation of the p53 and DPC4 tumor suppressor genes. In addition, our data indicate that allelic loss analysis may be useful in separating PanIN-2 lesions with low-grade dysplasia from those PanIN-2 lesions with moderate-grade dysplasia, each potentially representing a distinct progression step toward invasive carcinoma.

MeSH Terms
Alleles Chromosomes, Human, Pair 17/genetics Chromosomes, Human, Pair 18/genetics Chromosomes, Human, Pair 9/genetics DNA, Neoplasm/genetics DNA-Binding Proteins/genetics Female Humans Loss of Heterozygosity/genetics Male Microsatellite Repeats Microscopy, Confocal Middle Aged Pancreas/metabolism,pathology Pancreatic Neoplasms/genetics,pathology Smad4 Protein Trans-Activators/genetics Tumor Suppressor Protein p53/genetics
Chemicals
DNA, Neoplasm DNA-Binding Proteins SMAD4 protein, human Smad4 Protein Trans-Activators Tumor Suppressor Protein p53
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Lüttges J
Departments of Pathology and Surgery, University of Kiel, Kiel. University of Bochum, Bochum, Germany.
Galehdari H
Bröcker V
Schwarte-Waldhoff I
Henne-Bruns D
Klöppel G
Schmiegel W
Hahn S A
References (23)
23 references, click to expand
  1. Genetic progression in the pancreatic ducts.
    Am J Pathol. 2000 Jun;156(6):1821-5 PMID: 10854204
  2. Loss of expression of Dpc4 in pancreatic intraepithelial neoplasia: evidence that DPC4 inactivation occurs late in neoplastic progression.
    Cancer Res. 2000 Apr 1;60(7):2002-6 PMID: 10766191
  3. 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 Jun 1;88(11):2495-504 PMID: 10861425
  4. Molecular analysis of microdissected tumors and preneoplastic intraductal lesions in pancreatic carcinoma.
    Am J Pathol. 2000 Jul;157(1):83-92 PMID: 10880379
  5. Pancreatic intraepithelial neoplasia: a new nomenclature and classification system for pancreatic duct lesions.
    Am J Surg Pathol. 2001 May;25(5):579-86 PMID: 11342768
  6. Morphological lesions associated with human primary invasive nonendocrine pancreas cancer.
    Cancer Res. 1976 Jul;36(7 PT 2):2690-8 PMID: 1277176
  7. Relation of pancreatic duct hyperplasia to carcinoma.
    Cancer. 1979 Apr;43(4):1418-28 PMID: 445339
  8. Intraductal proliferation in the pancreas and its relationship to human and experimental carcinogenesis.
    Virchows Arch A Pathol Anat Histol. 1980;387(2):221-33 PMID: 7456311
  9. p53 and K-RAS alterations in pancreatic epithelial cell lesions.
    Oncogene. 1993 Feb;8(2):289-98 PMID: 8426738
  10. p53 mutations in pancreatic carcinoma and evidence of common involvement of homocopolymer tracts in DNA microdeletions.
    Cancer Res. 1994 Jun 1;54(11):3025-33 PMID: 8187092
  11. Overexpression of p53 protein in adenocarcinoma of the pancreas.
    Am J Clin Pathol. 1994 Jun;101(6):684-8 PMID: 8209852
  12. Expression of p53 protein in precursor lesions and adenocarcinoma of human pancreas.
    Am J Pathol. 1994 Dec;145(6):1291-5 PMID: 7992834
  13. Analysis of K-ras gene mutation in hyperplastic duct cells of the pancreas without pancreatic disease.
    Gastroenterology. 1996 Jan;110(1):227-31 PMID: 8536861
  14. DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1.
    Science. 1996 Jan 19;271(5247):350-3 PMID: 8553070
  15. Whole genome amplification using a degenerate oligonucleotide primer allows hundreds of genotypes to be performed on less than one nanogram of genomic DNA.
    Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14676-9 PMID: 8962113
  16. p16 and K-ras gene mutations in the intraductal precursors of human pancreatic adenocarcinoma.
    Cancer Res. 1997 Jun 1;57(11):2140-3 PMID: 9187111
  17. K-ras mutations and allelic loss at 5q and 18q in the development of human pancreatic cancers.
    Int J Pancreatol. 1997 Jun;21(3):205-17 PMID: 9322119
  18. Loss of chromosome 18q is an early event in pancreatic ductal tumorigenesis.
    Cancer Res. 1998 Oct 1;58(19):4222-6 PMID: 9766641
  19. Inactivation of the p16 (INK4A) tumor-suppressor gene in pancreatic duct lesions: loss of intranuclear expression.
    Cancer Res. 1998 Oct 15;58(20):4740-4 PMID: 9788631
  20. The K-ras mutation pattern in pancreatic ductal adenocarcinoma usually is identical to that in associated normal, hyperplastic, and metaplastic ductal epithelium.
    Cancer. 1999 Apr 15;85(8):1703-10 PMID: 10223563
  21. Genetic progression and divergence in pancreatic carcinoma.
    Am J Pathol. 2000 Jun;156(6):2123-33 PMID: 10854233
  22. Duct changes and K-ras mutations in the disease-free pancreas: analysis of type, age relation and spatial distribution.
    Virchows Arch. 1999 Nov;435(5):461-8 PMID: 10592048
  23. Immunohistochemical labeling for dpc4 mirrors genetic status in pancreatic adenocarcinomas : a new marker of DPC4 inactivation.
    Am J Pathol. 2000 Jan;156(1):37-43 PMID: 10623651
Article Info
Journal
The American journal of pathology
Abbr.
Am J Pathol
ISSN
0002-9440
Published
2001-05-00
Pages
1677-83
Language
English
Region
United States
NLM ID
0370502
PMCID
PMC1891939
Subset
IM
Corrections
CommentIn
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: product@genelibs.com