Journal
BLOOD REVIEWS
Volume 43, Issue -, Pages -Publisher
CHURCHILL LIVINGSTONE
DOI: 10.1016/j.blre.2020.100671
Keywords
Chronic myeloid leukemia; Survivin; Treatment resistance; Molecular crosstalks; Therapeutic approaches
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Funding
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [CNPq-304565/2016-4]
- Fundacao de Amparo a Pesquisa do Rio de Janeiro (FAPERJ) [E-26/202-798/2017]
- Ministerio da Saude/INCA
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Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by the BCR-ABL oncoprotein, known to drive leukemogenesis by orchestrating multiple signaling pathways ultimately involved in cell survival. Despite successful response rates of CML patients to tyrosine kinase inhibitors (TKIs), resistance eventually arises due to BCR-ABL-dependent and independent mechanisms. Survivin is an inhibitor of apoptosis protein acting in the interface between apoptosis deregulation and cell cycle progression. In CML, high levels of survivin have been associated with late stages of disease and therapy resistance. In this review, we provide an overview of important aspects concerning survivin subcellular localization and expression pattern in CML patients and cell lines. Moreover, we highlight the relevance of molecular networks involving survivin for disease progression and treatment resistance. Finally, we discuss the mechanisms accounting for survivin overexpression, as well as novel therapeutic interventions that have been designed to counteract survivin-associated malignancy in CML.
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