The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Constitutive phosphoinositide 3-kinase/Akt activation represents a favorable prognostic factor in de novo acute myelogenous leukemia patients
Abstract
The phosphoinositide 3-kinase (PI3K/Akt) pathway is activated in acute myelogenous leukemia (AML) and is promising for targeted inhibition. Ninety-two patients with primary AML were analyzed for PI3K/Akt constitutive activation. Fifty percent of the patients presented with constitutive PI3K activation (PI3K +). No difference was observed between PI3K + and PI3K − groups concerning age, sex, white blood cell count, lactate dehydrogenase (LDH) level, bone marrow blast cells, French-American-British (FAB) classification, cytogenetics, RAS or nucleophosmin (NPM) mutations. Slightly more FLT3-ITD was detected in the PI3K − group (P = .048). The complete remission rate was similar between the 2 groups. With a median follow-up of 26 months, we observed for PI3K + and PI3K − patients, respectively, 56% and 33% overall survival (P = .001) and 72% and 41% relapse-free survival (P = .001). Constitutive PI3K/Akt activity is a favorable prognosis factor in AML, even after adjustment for FLT3-ITD, and may confer a particular sensitivity to chemotherapy. A better understanding of the downstream effectors of the PI3K/Akt pathway is needed before targeting in AML.
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“Several reports point to hyperactivation of PI3K signaling in AML, and activated AKT is commonly associated with poor overall survival of patients with AML as well as with a less complete response (CR) rate to chemotherapy (18–23).”
From Loss of Dnmt3a impairs hematopoietic homeostasis and myeloid cell skewing via the PI3Kinase pathway (2023) · cites this paper as [21]
In the citing paper
“Several reports point to hyperactivation of PI3K signaling in AML, and activated AKT is commonly associated with poor overall survival of patients with AML as well as with a less complete response (CR) rate to chemotherapy (18–23).”
From Loss of Dnmt3a impairs hematopoietic homeostasis and myeloid cell skewing via the PI3Kinase pathway (2023) · cites this paper as [21]
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Cites
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Cited by
Crossing paths: interactions between the cell death machinery and growth factor survival signals
Brumatti, G., Salmanidis, M., & Ekert, P. G. (2010) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-010-0288-8 · Cited by 85
Loss of Dnmt3a impairs hematopoietic homeostasis and myeloid cell skewing via the PI3Kinase pathway
Palam, L. R., Ramdas, B., Pickerell, K., Pasupuleti, S. K., Kanumuri, R., Cesarano, A., Szymanski, M., Selman, B., Dave, U. P., Sandusky, G., et al. (2023) · JCI Insight · doi:10.1172/jci.insight.163864 · Cited by 13
Metadata
- Authors
- Tamburini, J., Elie, C., Bardet, V., Chapuis, N., Park, S., Broët, P., Cornillet-Lefebvre, P., Lioure, B., Ugo, V., Blanchet, O., Ifrah, N., Witz, F., Dreyfus, F., Mayeux, P., Lacombe, C., & Bouscary, D.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2007-08-01
- Volume
- 110
- Issue
- 3
- Pages
- 1025-1028
- ISSN
- 0006-4971
- 1528-0020
- Cited by
- 120
- References
- 1
- Language
- en
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