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p27(KIP1) and PTEN cooperate in myeloproliferative neoplasm tumor suppression in mice

Journal article
Authors Jingchen Shao
Susann Li
Lars Palmqvist
Linda Fogelstrand
S. Y. Wei
Kiran Busayavalasa
Kui Liu
Viktor Liu
Published in Experimental Hematolgy & Oncology
Volume 5
ISSN 2162-3619
Publication year 2016
Published at Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Department of Chemistry and Molecular Biology
Language en
Links dx.doi.org/10.1186/s40164-016-0047-...
Keywords PTEN, p27(KIP1), Myeloproliferative neoplasms, prostate-cancer, p27 expression, t-cell, leukemia, abnormalities, tumorigenesis, activation, cdkn1b, Oncology
Subject categories Clinical Medicine

Abstract

PTEN acts as a phosphatase for PIP3 and negatively regulates the PI3K/AKT pathway, and p27(KIP1) is a cyclin-dependent kinase inhibitor that regulates the G1 to S-phase transition by binding to and regulating the activity of cyclin-dependent kinases. Genetic alterations of PTEN or CDKN1B (p27(KIP1)) are common in hematological malignancies. To better understand how mutations in these two genes might cooperate in leukemogenesis, we inactivated both genes in the hematological compartment in mice. Here, we show that the combined inactivation of Pten and Cdkn1b results in a more severe myeloproliferative neoplasm phenotype associated with lower hemoglobin, enlarged spleen and liver, and shorter lifespan compared to inactivation of Pten alone. More severe anemia and increased myeloid infiltration and destruction of the spleen contributed to the earlier death of these mice, and elevated p-AKT, cyclin D1, and cyclin D3 might contribute to the development of this phenotype. In conclusion, PTEN and p27(KIP1) cooperate in tumor suppression in the hematological compartment.

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