Ron

p53 and Pten control Neural and Glioma Stem/Progenitor Cell Renewal and Differentiation

Here we showed that concomitant central nervous system (CNS)-specific deletion of p53 and Pten in the mouse CNS generates a penetrant acute-onset high-grade malignant glioma phenotype with notable clinical, pathological and molecular resemblance to primary glioblastoma multiforme in humans.  Read the Abstract Download the PDF

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Chromosomally Unstable Mouse Tumours have Genomic Alterations Similar to Diverse Human Cancers

In this study, we engineered lymphoma-prone mice with chromosomal instability to assess the usefulness of mouse models in cancer gene discovery and the extent of cross-species overlap in cancer-associated copy number aberrations. We determined that murine and human tumors have common biological processes driven by orthologous genetic events during their malignant evolution. These findings encourage

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Activated Kras and Ink4a/Arf Deficiency cooperate to produce Metastatic Pancreatic Ductal Adenocarcinoma

We assessed the cooperative interactions of two signature mutations in mice engineered to sustain pancreas-specific Pre-mediated activation of a mutant Kras allele and deletion of a conditional Ink4a/Arf tumor suppressor allele. Our findings in the mouse provided experimental support for the widely accepted model of human pancreatic adenocarcinoma in which activated KRAS initiates PanIN lesions, and the INK4A/ARF tumor suppressors

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Malignant Glioma: Genetics and Biology of a Grave Matter

Review article: Malignant brain tumors strike deep into the psyche of those receiving and those delivering the diagnosis. Malignant gliomas, the most common subtype of primary brain tumors, are aggressive, highly invasive, and neurologically destructive tumors considered to be among the deadliest of human cancers. Read the Abstract Download the PDF

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The Age of Cancer

A striking link exists between advanced age and increased incidence of cancer. Here I review how several of the age-related molecular and physiological changes might act in concert to promote cancer, and in particular epithelial carcinogenesis. Experimental data indicate that the aged, cancer-prone phenotype might represent the combined pathogenetic effects of mutation load, epigenetic regulation,

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Telomere Dysfunction promotes Non-reciprocal Translocations and Epithelial Cancers in Mice

This paper provides evidence that telomere attrition in aging telomerase-deficient p53 mutant mice promotes the development of epithelial cancers by a process of fusion-bridge breakage that leads to the formation of complex non-reciprocal translocations—a classical cytogenetic feature of human carcinomas.  Read the Abstract Download the PDF

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