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a Institute for Cancer Genetics, Columbia University, New York, New York 10032, USA b Department of Internal Diseases and Hypertension, Medical University of Warsaw, 02-097 Warsaw, Poland
Key Words: PTEN • pheochromocytoma • IGF II
Address for correspondence: Janusz Puc, Ph.D., Department of Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0648. Voice: 858-534-0758; fax: 858-534-8180. e-mail: jpuc{at}ucsd.edu
PTEN, a tumor suppressor gene, is frequently mutated in a variety of human tumors. In mice, monoallelic inactivation of this gene predisposes animals to neoplasia of multiple organs. Interestingly, Pten heterozygous mice develop bilateral hyperplasia of the adrenal medulla. In this report we demonstrate that these neoplasms are hormonally active pheochromocytomas that secrete increased amounts of bioactive catecholamines: norepinephrine and epinephrine. To test a possibility that PTEN might be one of the genes responsible for human sporadic pheochromocytoma, we performed mutation analysis of DNA obtained from tumors of 29 patients. However, direct sequencing of all nine exons of the PTEN gene, including the splice junctions, revealed no mutations. Examination of protein expression by immunohistochemistry using 8 normal adrenals and 11 sporadic pheochromocytomas showed no decrease in the PTEN protein expression in the tumor tissue, but upregulation of insulin-like growth factor II, a peptide implicated in growth of adrenal tissue, was observed in four cases (36%).
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