2023
DOI: 10.3390/cells12131798
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SHIP1 Is Present but Strongly Downregulated in T-ALL, and after Restoration Suppresses Leukemia Growth in a T-ALL Xenotransplantation Mouse Model

Abstract: Acute lymphoblastic leukemia (ALL) is the most common cause of cancer-related death in children. Despite significantly increased chances of cure, especially for high-risk ALL patients, it still represents a poor prognosis for a substantial fraction of patients. Misregulated proteins in central switching points of the cellular signaling pathways represent potentially important therapeutic targets. Recently, the inositol phosphatase SHIP1 (SH2-containing inositol 5-phosphatase) has been considered as a tumor sup… Show more

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Cited by 2 publications
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“…Furthermore, the mutation V684E was found in AML, which lies in the phosphatase domain of SHIP1 and was shown to reduce the catalytic effect of the protein, which in turn raises AKT activity [15]. The possible role of SHIP1 as a tumor suppressor in T-ALL cells is suggested on the basis of a strong downregulation of SHIP1 in T-ALL cells with upregulated PI3K/AKT signaling [18]. In CML, the BCR/ABL fusion transcript reduces the expression of SHIP1, which indicates a role for SHIP1 as a tumor suppressor in CML [19].…”
Section: Ship1 In Hematopoietic Cancermentioning
confidence: 99%
“…Furthermore, the mutation V684E was found in AML, which lies in the phosphatase domain of SHIP1 and was shown to reduce the catalytic effect of the protein, which in turn raises AKT activity [15]. The possible role of SHIP1 as a tumor suppressor in T-ALL cells is suggested on the basis of a strong downregulation of SHIP1 in T-ALL cells with upregulated PI3K/AKT signaling [18]. In CML, the BCR/ABL fusion transcript reduces the expression of SHIP1, which indicates a role for SHIP1 as a tumor suppressor in CML [19].…”
Section: Ship1 In Hematopoietic Cancermentioning
confidence: 99%