A constitutively active epidermal growth factor receptor cooperates with disruption of G1 cell-cycle arrest pathways to induce glioma-like lesions in mice

Article Abstract:

Avian retroviral receptors have been used to study the relationship between gliomagenesis and mutation in epidermal growth factor receptor (EGFR). Lesions similar to human gliomas can be induced through expression of a mutant form of EGFR in glial lineage cells. Tumors appear to develop more efficiently from cells in the glial lineage that are immature. Additional mutations seem to be necessary for EGFR-induced gliomagenesis, mutations occurring in genes that encode proteins active in pathways of cell-cycle arrest.

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Lung adenocarcinomas induced in mice by mutant EGF receptors found in human lung cancers respond to a tyrosine kinase inhibitor or to down-regulation of the receptors

Article Abstract:

The role of somatic mutations in exons encoding the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) gene in the initiation and maintenance of lung cancer was studied. It was observed that with mice carrying either EGFR allele, withdrawal of doxycycline or treatment with erlotinib causes rapid tumor regression, as assessed by magnetic resonance imaging and histopathology, demonstrating that mutant EGFR is required for tumor maintenance.

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The c-myc and PyMT oncogenes induce different tumor types in a somatic mouse model for pancreatic cancer

Article Abstract:

A mouse model is generated for pancreatic cancer through the somatic delivery of oncogene-bearing avian retroviruses to mice that express TVA, the receptor for avian leucosis sarcoma virus subgroup A (ALSV-A), under the control of the elastase promoter. It is observed that specific oncogenes can induce the formation of different pancreatic tumor types in a single transgenic line, most likely from one or more types of multipotential progenitor cells.

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