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Phosphatidylinositol 3‐kinase inhibition potentiates glucocorticoid response in B‐cell acute lymphoblastic leukemia

Overview of attention for article published in Journal of Cellular Physiology, September 2017
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Title
Phosphatidylinositol 3‐kinase inhibition potentiates glucocorticoid response in B‐cell acute lymphoblastic leukemia
Published in
Journal of Cellular Physiology, September 2017
DOI 10.1002/jcp.26135
Pubmed ID
Authors

Cecilia Evangelisti, Alessandra Cappellini, Mariana Oliveira, Rita Fragoso, João T. Barata, Alice Bertaina, Franco Locatelli, Carolina Simioni, Luca M. Neri, Francesca Chiarini, Annalisa Lonetti, Francesca Buontempo, Ester Orsini, Andrea Pession, Lucia Manzoli, Alberto Maria Martelli, Camilla Evangelisti

Abstract

Despite remarkable progress in polychemotherapy protocols, pediatric B-cell acute lymphoblastic leukemia (B-ALL) remains fatal in around 20% of cases. Hence, novel targeted therapies are needed for patients with poor prognosis. Glucocorticoids (GCs) are drugs commonly administrated for B-ALL treatment. Activation of the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin signaling pathway is frequently observed in B-ALL and contributes to GC-resistance. Here, we analyzed for the first time to our knowledge, the therapeutic potential of pan and isoform-selective PI3K p110 inhibitors, alone or combined with dexamethasone (DEX), in B-ALL leukemia cell lines and patient samples. We found that a pan PI3K p110 inhibitor displayed the most powerful cytotoxic effects in B-ALL cells, by inducing cell cycle arrest and apoptosis. Both a pan PI3K p110 inhibitor and a dual γ/δ PI3K p110 inhibitor sensitized B-ALL cells to DEX by restoring nuclear translocation of the GC receptor and counteracted stroma-induced DEX-resistance. Finally, gene expression analysis documented that, on one hand the combination consisting of a pan PI3K p110 inhibitor and DEX strengthened the DEX-induced up- or down-regulation of several genes involved in apoptosis, while on the other, it rescued the effects of genes that might be involved in GC-resistance. Overall, our findings strongly suggest that PI3K p110 inhibition could be a promising strategy for treating B-ALL patients by improving GC therapeutic effects and/or overcoming GC-resistance. This article is protected by copyright. All rights reserved.

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The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 49 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 49 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 10 20%
Student > Ph. D. Student 8 16%
Student > Master 6 12%
Researcher 6 12%
Student > Doctoral Student 2 4%
Other 6 12%
Unknown 11 22%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 12 24%
Medicine and Dentistry 8 16%
Agricultural and Biological Sciences 7 14%
Immunology and Microbiology 3 6%
Computer Science 2 4%
Other 4 8%
Unknown 13 27%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 14 August 2017.
All research outputs
#16,667,643
of 24,585,562 outputs
Outputs from Journal of Cellular Physiology
#3,696
of 6,084 outputs
Outputs of similar age
#203,831
of 319,997 outputs
Outputs of similar age from Journal of Cellular Physiology
#41
of 76 outputs
Altmetric has tracked 24,585,562 research outputs across all sources so far. This one is in the 32nd percentile – i.e., 32% of other outputs scored the same or lower than it.
So far Altmetric has tracked 6,084 research outputs from this source. They receive a mean Attention Score of 4.0. This one is in the 39th percentile – i.e., 39% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 319,997 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 36th percentile – i.e., 36% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 76 others from the same source and published within six weeks on either side of this one. This one is in the 46th percentile – i.e., 46% of its contemporaries scored the same or lower than it.