Acinar-ductal-carcinoma sequence in transforming growth factor-α transgenic mice

Roland M. Schmid; Günther Klöppel; Guido Adler; Martin Wagner

doi:10.1111/j.1749-6632.1999.tb09526.x

Acinar-ductal-carcinoma sequence in transforming growth factor-α transgenic mice

Roland M. Schmid, Günther Klöppel, Guido Adler, Martin Wagner

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30 Scopus citations

Abstract

Transgenic mice overexpressing transforming growth factor-α (TGF-α) display an expansion of intrapancreatic fibroblasts and a progressive accumulation of extracellular matrix. This massive fibrosis is associated with an increase in pancreatic size and weight. In parallel, tubular complexes appear that are composed of acinar cells with a decreased height. These acinar cells lose zymogen granules and become transitional cells, which subsequently gain duct cell features. In animals older than one year dysplastic lesions develop, which originate from tubular complexes. Occasionally these dysplastic foci transform to papillary and cystic pancreatic carcinoma. These tumors are positive for the duct specific antigen Duct-1 and carbonic anhydrase activity indicative of ductal differentiation. Tumors overexpress the epidermal growth factor (EGF)-receptor and p53, but lack K-ras mutations. These data suggest an acinar-ductal-carcinoma sequence in TGF-α transgenic mice.

Original language	English
Pages (from-to)	219-230
Number of pages	12
Journal	Annals of the New York Academy of Sciences
Volume	880
DOIs	https://doi.org/10.1111/j.1749-6632.1999.tb09526.x
State	Published - 1999
Externally published	Yes

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title = "Acinar-ductal-carcinoma sequence in transforming growth factor-α transgenic mice",

abstract = "Transgenic mice overexpressing transforming growth factor-α (TGF-α) display an expansion of intrapancreatic fibroblasts and a progressive accumulation of extracellular matrix. This massive fibrosis is associated with an increase in pancreatic size and weight. In parallel, tubular complexes appear that are composed of acinar cells with a decreased height. These acinar cells lose zymogen granules and become transitional cells, which subsequently gain duct cell features. In animals older than one year dysplastic lesions develop, which originate from tubular complexes. Occasionally these dysplastic foci transform to papillary and cystic pancreatic carcinoma. These tumors are positive for the duct specific antigen Duct-1 and carbonic anhydrase activity indicative of ductal differentiation. Tumors overexpress the epidermal growth factor (EGF)-receptor and p53, but lack K-ras mutations. These data suggest an acinar-ductal-carcinoma sequence in TGF-α transgenic mice.",

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AU - Schmid, Roland M.

AU - Klöppel, Günther

AU - Adler, Guido

AU - Wagner, Martin

PY - 1999

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N2 - Transgenic mice overexpressing transforming growth factor-α (TGF-α) display an expansion of intrapancreatic fibroblasts and a progressive accumulation of extracellular matrix. This massive fibrosis is associated with an increase in pancreatic size and weight. In parallel, tubular complexes appear that are composed of acinar cells with a decreased height. These acinar cells lose zymogen granules and become transitional cells, which subsequently gain duct cell features. In animals older than one year dysplastic lesions develop, which originate from tubular complexes. Occasionally these dysplastic foci transform to papillary and cystic pancreatic carcinoma. These tumors are positive for the duct specific antigen Duct-1 and carbonic anhydrase activity indicative of ductal differentiation. Tumors overexpress the epidermal growth factor (EGF)-receptor and p53, but lack K-ras mutations. These data suggest an acinar-ductal-carcinoma sequence in TGF-α transgenic mice.

AB - Transgenic mice overexpressing transforming growth factor-α (TGF-α) display an expansion of intrapancreatic fibroblasts and a progressive accumulation of extracellular matrix. This massive fibrosis is associated with an increase in pancreatic size and weight. In parallel, tubular complexes appear that are composed of acinar cells with a decreased height. These acinar cells lose zymogen granules and become transitional cells, which subsequently gain duct cell features. In animals older than one year dysplastic lesions develop, which originate from tubular complexes. Occasionally these dysplastic foci transform to papillary and cystic pancreatic carcinoma. These tumors are positive for the duct specific antigen Duct-1 and carbonic anhydrase activity indicative of ductal differentiation. Tumors overexpress the epidermal growth factor (EGF)-receptor and p53, but lack K-ras mutations. These data suggest an acinar-ductal-carcinoma sequence in TGF-α transgenic mice.

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Acinar-ductal-carcinoma sequence in transforming growth factor-α transgenic mice

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