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STAT5: From Pathogenesis Mechanism to Therapeutic Approach in Acute Leukemia

Journal

LABORATORY MEDICINE
Volume 51, Issue 4, Pages 345-351

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/labmed/lmz074

Keywords

STAT5; acute leukemia; leukemogenesis; mutation; cell signaling; drug resistance

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Background: Based on the results of multiple studies, multiple signaling pathways is a major cause of resistence to chemotherapy in leukemia cells. Signal transducer and activator of transcription 5 (STAT5) is among these factors; it plays an essential role in proliferation of leukemic cells. Methods: We obtained the materials used in our study via PubMed search from 19% through 2019. The key search terms included degrees STAT5, acute leukemia: leukemogenesis, and mutation. Results: On activation, STAT5 not only inhibits apoptosis of leukemic cells via activating the B-cell lymphoma 2 (BCL-2) gene but also inhibits resistance to chemotherapy by enhancing human telomerase reverse transcriptase (hTERT) expression and maintaining telomere length in cells. It has also been shown that a number of mutations in the STAT5 gene and in related genes alter the expression of STAT5. Conclusion: The identification of STAT5 and the factors activated in its up- or downstream expression, affecting its function, contribute to better treatments such as targeted therapy rather than chemotherapy, improving the quality of life patients.

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