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Pim1 Kinase Cooperates with Hormone Treatment to Promote Bladder and Ureteral Urothelial Hyperplasia

Autor Narlik-Grassow, Maja; Blanco-Aparicio, Carmen; Cecilia, Yolanda; Pérez, Marco; Muñoz-Galván, Sandra ; Cañamero, Marta; Renner, Oliver; Carnero, Amancio
Palabras clave Pim1 kinase
Mouse models
Urothelial hyperplasia
Fecha de publicación 7-feb-2014
EditorOMICS Publishing Group
Citación Journal of Carcinogenesis and Mutagenesis 5: 161 (2014)
ResumenThe Pim serine/threonine kinases have been shown to be overexpressed in cancer. Elevated levels of Pim1 kinase were demonstrated in human leukemia and lymphomas, as well as in solid tumors such as pancreatic, prostate and bladder cancers, and have been proposed as a prognostic marker. Although the Pim kinases have been identified as oncogenes in transgenic mouse models, they have only weak transforming abilities on their own. However, they have been shown to greatly enhance the ability of other genes or chemical carcinogens to induce tumors. To explore the role of Pim1 in bladder and ureteral urothelial cancer, we generated a conditional Pim1 transgenic mouse model and found that prostate specific antigen-(PSA)-driven Cre expression lead to transgene expression in the bladder upon (testosterone/estrogen) hormone treatment. We then explored the effect of Pim1 overexpression on hormone treatment, either alone or in combination with Pten haploinsufficiency. We found that Pim1 overexpression increased the severity of bladder and ureteral urothelial hyperplasias in both backgrounds, leading to pyelonephritis in transgenic animals. Our data suggest that Pim1 might contribute to progression, rather than initiation, and that the hyperplasias also contribute to the development of pyelonephritis.
Descripción This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Versión del editorhttp://dx.doi.org/10.4172/2157-2518.1000161
URI http://hdl.handle.net/10261/95227
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