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S100 Proteins in Acute Myeloid Leukemia

Authors :
Annette K. Brenner
Øystein Bruserud
Source :
Neoplasia: An International Journal for Oncology Research, Vol 20, Iss 12, Pp 1175-1186 (2018)
Publication Year :
2018
Publisher :
Elsevier, 2018.

Abstract

The S100 protein family contains 20 functionally expressed members, which are commonly dysregulated in cancer. Their wide range of functions includes cell proliferation, cell differentiation, regulation of transcription factors, inflammation, chemotaxis, and angiogenesis. S100 proteins have in several types of cancer proven to be biomarkers for disease progression and prognosis. Acute myeloid leukemia (AML) is a highly heterogeneous and aggressive disease in which immature myeloblasts replace normal hematopoietic cells in the bone marrow. This review focuses on the S100 protein family members, which commonly are dysregulated in AML, and on the consequences of their dysregulation in the disorder. Like in other cancers, it appears as if S100 proteins are potential biomarkers for leukemogenesis. Furthermore, several S100 members seem to be involved in maintaining the leukemic phenotype. For these reasons, specific S100 proteins might serve as prognostic biomarkers, especially in the patient subset with intermediate/undetermined risk, and as potential targets for patient-adjusted therapy. Because the question of the most suitable candidate S100 biomarkers in AML still is under discussion, because particular AML subgroups lead to specific S100 signatures, and because downstream effects and the significance of co-expression of potential S100 binding partners in AML are not fully elucidated yet, we conclude that a panel of S100 proteins will probably be best suited for prognostic purposes.

Details

Language :
English
ISSN :
14765586 and 55628397
Volume :
20
Issue :
12
Database :
Directory of Open Access Journals
Journal :
Neoplasia: An International Journal for Oncology Research
Publication Type :
Academic Journal
Accession number :
edsdoj.55628397400641cbb4bd8ef77bdb2516
Document Type :
article
Full Text :
https://doi.org/10.1016/j.neo.2018.09.007