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Pim kinases in hematological malignancies: where are we now and where are we going?
- Source :
- Journal of Hematology & Oncology
- Publication Year :
- 2014
-
Abstract
- The proviral insertion in murine (PIM) lymphoma proteins are a serine/threonine kinase family composed of three isoformes: Pim-1, Pim-2 and Pim-3. They play a critical role in the control of cell proliferation, survival, homing and migration. Recently, overexpression of Pim kinases has been reported in human tumors, mainly in hematologic malignancies. In vitro and in vivo studies have confirmed their oncogenic potential. Indeed, PIM kinases have shown to be involved in tumorgenesis, to enhance tumor growth and to induce chemo-resistance, which is why they have become an attractive therapeutic target for cancer therapy. Novel molecules inhibiting Pim kinases have been evaluated in preclinical studies, demonstrating to be effective and with a favorable toxicity profile. Given the promising results, some of these compounds are currently under investigation in clinical trials. Herein, we provide an overview of the biological activity of PIM-kinases, their role in hematologic malignancies and future therapeutic opportunities. Electronic supplementary material The online version of this article (doi:10.1186/s13045-014-0095-z) contains supplementary material, which is available to authorized users.
- Subjects :
- Cancer Research
medicine.medical_specialty
Review
Pim kinases, Target therapy, Hematologic malignancies
Target therapy
Serine
Mice
Proto-Oncogene Proteins c-pim-1
In vivo
hemic and lymphatic diseases
Internal medicine
medicine
Animals
Humans
Protein Kinase Inhibitors
Molecular Biology
Pim inhibitors
Pim kinases
Hematology
Cell growth
business.industry
Biological activity
medicine.disease
In vitro
Lymphoma
Oncology
Hematologic Neoplasms
Immunology
Cancer research
Hematologic malignancies
business
Homing (hematopoietic)
Subjects
Details
- Language :
- English
- Database :
- OpenAIRE
- Journal :
- Journal of Hematology & Oncology
- Accession number :
- edsair.doi.dedup.....2afd536a171e25e003146fbd08f7163c