Either IL-7 activation of JAK-STAT or BEZ inhibition of PI3K-AKT-mTOR pathways dominates the single-cell phosphosignature of


Journal

Haematologica
ISSN: 1592-8721
Titre abrégé: Haematologica
Pays: Italy
ID NLM: 0417435

Informations de publication

Date de publication:
01 06 2022
Historique:
received: 17 03 2021
pubmed: 22 10 2021
medline: 3 6 2022
entrez: 21 10 2021
Statut: epublish

Résumé

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive cancer arising from lymphoblasts of T-cell origin. While TALL accounts for only 15% of childhood and 25% of adult ALL, 30% of patients relapse with a poor outcome. Targeted therapy of resistant and high-risk pediatric T-ALL is therefore urgently needed, together with precision medicine tools allowing the testing of efficacy in patient samples. Furthermore, leukemic cell heterogeneity requires drug response assessment at the single-cell level. Here we used single-cell mass cytometry to study signal transduction pathways such as JAK-STAT, PI3K-AKT-mTOR and MEK-ERK in 16 diagnostic and five relapsed T-ALL primary samples, and investigated the in vitro response of cells to Interleukin-7 (IL-7) and the inhibitor BEZ-235. T-ALL cells showed upregulated activity of the PI3K-AKT-mTOR and MEK-ERK pathways and increased expression of proliferation and translation markers. We found that perturbation induced by the ex vivo administration of either IL-7 or BEZ-235 reveals a high degree of exclusivity with respect to the phospho-protein responsiveness to these agents. Notably, these response signatures were maintained from diagnosis to relapse in individual patients. In conclusion, we demonstrated the power of mass cytometry single-cell profiling of signal transduction pathways in T-ALL. Taking advantage of this advanced approach, we were able to identify distinct clusters with different responsiveness to IL-7 and BEZ-235 that can persist at relapse. Collectively our observations can contribute to a better understanding of the complex signaling network governing T-ALL behavior and its correlation with influence on the response to therapy.

Identifiants

pubmed: 34670357
doi: 10.3324/haematol.2021.278796
pmc: PMC9152963
doi:

Substances chimiques

Interleukin-7 0
MTOR protein, human EC 2.7.1.1
Proto-Oncogene Proteins c-akt EC 2.7.11.1
TOR Serine-Threonine Kinases EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1293-1310

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Auteurs

Daniela Kuzilková (D)

Childhood Leukaemia Investigation Prague, Czech Republic; Department of Pediatric Hematology and Oncology, 2nd Faculty of Medicine, Charles University Prague, Czech Republic.

Cristina Bugarin (C)

Fondazione Tettamanti, Clinica Pediatrica Università degli Studi Milano Bicocca, Monza (MB), Italy.

Katerina Rejlova (K)

Childhood Leukaemia Investigation Prague, Czech Republic; Department of Pediatric Hematology and Oncology, 2nd Faculty of Medicine, Charles University Prague, Czech Republic.

Axel R Schulz (AR)

German Rheumatism Research Center Berlin (DRFZ), a Leibniz Institute, Berlin, Germany.

Henrik E Mei (HE)

German Rheumatism Research Center Berlin (DRFZ), a Leibniz Institute, Berlin, Germany.

Maddalena Paganin (M)

Pediatric Hematology, Oncology and Stem Cell Transplant Division, Women and Child Health Department, University of Padova, Padova, Italy.

Alessandra Biffi (A)

Pediatric Hematology, Oncology and Stem Cell Transplant Division, Women and Child Health Department, University of Padova, Padova, Italy.

Andrea Biondi (A)

Fondazione Tettamanti, Clinica Pediatrica Università degli Studi Milano Bicocca, Monza (MB), Italy. andrea.biondi@unimib.it.

Tomas Kalina (T)

Childhood Leukaemia Investigation Prague, Czech Republic; Department of Pediatric Hematology and Oncology, 2nd Faculty of Medicine, Charles University Prague, Czech Republic.

Giuseppe Gaipa (G)

Fondazione Tettamanti, Clinica Pediatrica Università degli Studi Milano Bicocca, Monza (MB), Italy.

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