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P‐Akt expression distinguishes two types of malignant rhabdoid tumors
Author(s) -
Charboneau Aubri,
Chai Jingjing,
Jordan Jennifer,
Funkhouser William,
Judkins Alexander,
Biegel Jaclyn,
Weissman Bernard
Publication year - 2006
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.20737
Subject(s) - protein kinase b , suppressor , cancer research , tumor suppressor gene , pi3k/akt/mtor pathway , biology , phosphorylation , medicine , gene , signal transduction , carcinogenesis , microbiology and biotechnology , genetics
Highly aggressive pediatric malignant rhabdoid tumors (MRT) arise in the kidney and central nervous system (CNS) with no curative treatment available. Multiple studies have shown that inactivation of the SNF5 tumor suppressor gene occurs in virtually all MRTs. However, few studies have addressed whether additional genetic events may contribute to MRT development. In this report, we demonstrate that phosphorylated Akt (P‐Akt) is expressed in a subpopulation of cells in at least 10% of primary rhabdoid tumors as well as at high levels in three MRT cell lines. Similar to other high P‐Akt expressing tumor cell lines, MRTs have decreased sensitivity to p21 induced growth arrest. Therefore, P‐Akt expression may distinguish between two types of MRTs. Because drugs directed against the PI3‐K/Akt have shown promise in clinical trials for other tumor types, they may prove useful for treatment of patients with P‐Akt positive MRTs. P‐Akt expression also provides a potential mechanistic link between these pediatric tumors and adult malignancies. J. Cell. Physiol. 209: 422–427, 2006. © 2006 Wiley‐Liss, Inc.