NDLI: Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice.

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Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice.

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Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Castrillon, Diego H. Bastian, Boris C. Parsons, Ramon Depinho, Ronald A. O'hagan, Rónán C. You, Mingjian James Chin, Lynda Bosenberg, Marcus W.
Description	Author Affiliation: You MJ ( Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.);
Abstract	Dual inactivation of PTEN and INK4a/ARF tumor suppressor genes is a common feature observed in a broad spectrum of human cancer types. To validate functional collaboration between these genes in tumor suppression, we examined the biological consequences of Pten and/or Ink4a/Arf deficiency in cells and mice. Relative to single mutant controls, Ink4a/Arf-/-Pten+/- mouse embryonic fibroblast cultures exhibited faster rates of growth in reduced serum, grew to higher saturation densities, produced more colonies upon low density seeding, and showed increased susceptibility to transformation by oncogenic H-Ras. Ink4a/Arf deficiency reduced tumor-free survival and shortened the latency of neoplasias associated with Pten heterozygosity, specifically pheochromocytoma, prostatic intraepithelial neoplasia, and endometrial hyperplasia. Compound mutant mice also exhibited an expanded spectrum of tumor types including melanoma and squamous cell carcinoma. Functional synergy between Ink4a/Arf and Pten manifested most prominently in the development of pheochromocytoma, prompting an analysis of genes and loci implicated in this rare human neoplasm. The classical pheochromocytoma genes Ret, Vhl, and Nf-1 remained intact, a finding consistent with the intersection of these genes with pathways engaged by Pten and Ink4a/Arf. Notably, conventional and array-comparative genomic hybridization revealed frequent loss of distal mouse chromosome 4 in a region syntenic to human chromosome 1p that is implicated in human pheochromocytoma. This study provides genetic evidence of collaboration between Pten and Ink4a/Arf in constraining the growth and oncogenic transformation of cultured cells and in suppressing a wide spectrum of tumors in vivo.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	3
Volume Number	99
Language	English
Publisher	National Academy of Sciences
Publisher Date	2002-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Chromosome Aberrations Cyclin-Dependent Kinase Inhibitor P16 Metabolism Neoplasms Genetics Phosphoric Monoester Hydrolases Tumor Suppressor Proteins Adrenal Gland Neoplasms Pathology Animals Cell Transformation, Neoplastic Chromosome Mapping Chromosomes, Human, Pair 1 Crosses, Genetic Deficiency Genes, Tumor Suppressor Heterozygote Mice Mice, Inbred C57BL Mice, Knockout Prevention & Control Nucleic Acid Hybridization PTEN Phosphohydrolase Phenotype Pheochromocytoma Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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