TGFα Transgenic Mice

  title={TGF$\alpha$ Transgenic Mice},
  author={Florian R. Greten and Martin Wagner and Christoph K. Weber and Ulrich Zechner and Guido Adler and Roland M. Schmid},
  pages={363 - 368}
Pancreatic cancer is a devastating disease with a fatal prognosis due to late diagnosis and resistance to radiation and chemotherapy. The average survival after diagnosis is still 3 to 8 months. In the last few years genetic alterations in cancer-causing genes have been identified in tumors and putative premalignant lesions using microdissection techniques. However, the functional consequence of these genetic alterations for pancreatic growth and differentiation is unknown. TGFα overexpressed… 
Modeling Pancreatic Cancer In Vivo: From Xenograft and Carcinogen-Induced Systems to Genetically Engineered Mice
Generation of mice that develop spontaneous pancreatic cancer from a targeted genetic mutation is a valuable research tool, considering the broad spectrum of genes and cell targets that can be used, producing a variety of neoplastic lesions and cancer that can reflect many aspects of human pancreatic ductal adenocarcinoma.
Mouse Models of Pancreatic Cancer
Pancreatic ductal adenocarcinoma (PDAC) is a disease characterized by aggressive tumor biology, desmoplasia and chemoresistance. Given the insidious nature of its onset, multiple models have been
Apoptosis: Targets in Pancreatic Cancer
This review will focus on the role of apoptotic proteins contributing to pancreatic cancer development and progression and will demonstrate possible targets to influence this deadly disease.
The mutant K-ras oncogene causes pancreatic periductal lymphocytic infiltration and gastric mucous neck cell hyperplasia in transgenic mice.
How mutant K-ras signaling modulates important molecular events in the initiating events of pancreatic and gastric carcinogenesis is defined.
Challenges and advances in mouse modeling for human pancreatic tumorigenesis and metastasis
This review summarizes the currently available animal models for pancreatic cancer and the advances in pancreaticcancer animal modeling, and compares and contrast the advantages and disadvantages of three major categories of these models: carcinogen-induced; xenograft and allograft; and genetically engineered mouse models.
Recent developments of transgenic and xenograft mouse models of pancreatic cancer for translational research
These newly developed in vivo model systems provide powerful tools likely to boost preclinical evaluation and bench-to-bedside transition of novel therapeutic approaches directed against this dire malady.
Current Update of Cytokines in Pancreatic Cancer: Pathogenic Mechanisms, Clinical Indication, and Therapeutic Values
How cytokines act to create a microenvironment conducive to tumor cell survival and growth, discussed how cytokines affect proliferation, invasion, metastasis, and apoptosis in pancreatic cancer cells, and how this knowledge has been applied either to target cytokines or use them therapeutically are examined.
Characterization of pancreatic lesions from MT-tgfα, Ela-myc and MT-tgfα/Ela-myc single and double transgenic mice
The short latency for tumor development, the variety of tumor morphology and the liver metastases seen in Ela- myc and MT-tgfα/Ela-myc mice make these animals good models for investigating new therapeutic and preventive strategies for pancreatic cancer.
Progressive metaplastic and dysplastic changes in mouse pancreas induced by cyclooxygenase-2 overexpression.
The progressive nature of the metaplastic/dysplastic changes observed in this model make it a valuable tool for examining the transition from chronic inflammation to neoplasia.


A murine tumor progression model for pancreatic cancer recapitulating the genetic alterations of the human disease.
This study describes a tumor progression model for ductal pancreatic cancer in mice overexpressing TGF-alpha and concludes that genetic events are critical for pancreatic tumor formation in mice.
Pancreatic tumor pathogenesis reflects the causative genetic lesion.
It is demonstrated that the initial oncogenic alteration can influence the pattern of subsequent tumor pathogenesis and, given that human exocrine pancreatic tumors are predominantly ductal adenocarcinomas, support the suggestion that transformed acinar cells may contribute to the genesis of this serious disease in man.
Interaction between murine germline mutations in p53 and APC predisposes to pancreatic neoplasia but not to increased intestinal malignancy.
Surprisingly, given the proposed role for loss of function mutations of the p53 gene in the development of human colorectal cancer, there is no evidence for either an increase in the rate of adenoma formation in APC +/-, p53 -/- animals, or an increased rate of progression to malignancy compared with APC + p53 +/+ mice.
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Observations indicate that a normal p53 gene is dispensable for embryonic development, that its absence predisposes the animal to neoplastic disease, and that an oncogenic mutant form of p53 is not obligatory for the genesis of many types of tumours.
Cooperative tumorigenic effects of germline mutations in Rb and p53
The phenotypic effects of combined germline mutations in these two tumour suppressor genes Rb and p53 are described to indicate that mutations in Rband p53 can cooperate in the transformation of certain cell types in the mouse.
Allelotype of pancreatic adenocarcinoma.
The first allelotype of pancreatic adenocarcinoma is assembled, a survey for allelic loss among each chromosomal arm, using seven cryostat-dissected neoplasms, with a value similar to that seen previously in colorectal carcinoma.