STMN1 is highly expressed and contributes to clonogenicity in acute promyelocytic leukemia cells

Vicari, Hugo Passos; Coelho-Silva, Juan Luiz; Pereira-Martins, Diego A; Lucena-Araújo, Antonio R.; Lima, Keli; Silva, Jean Carlos Lipreri da; Scheucher, Priscila Santos; Koury, Luisa Corrêa de Araujo; Melo, Raul A de; Bittencourt, Rosane; Pagnano, Kátia Bórgia Barbosa; Nunes, Éllen Almeida; Fagundes, Evandro M.; Kerbauy, Fábio R.; Figueiredo-Pontes, Lorena Lôbo de; Costa-Lotufo, Letı́cia V.; Rego, Eduardo Magalhães; Traina, Fabı́ola; Machado-Neto, João Agostinho

doi:10.1007/s10637-021-01197-0

Cited by 7 publications

(1 citation statement)

References 39 publications

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“…Comparative analysis of Dx blast cells with healthy BM cells identified a set of overexpressed genes in the heterogenous T-ALL blasts. These included genes that impact microtubule dynamics and cell cycle progression ( STMN1 ) 51 , cancer stemness ( SOX4 ) 52 , cell development and proliferation ( HES4 ) 53 , cell adhesion ( CD99 ) 54 , and a novel gene with unknown function ( ARMH1/C1orf228 ). Overexpression of some of the blast signature genes was significantly associated with poorer event free survival in patients with T-ALL, consistent with modulation of key pathways related to tumor cell growth, proliferation, and migration.…”

Section: Discussionmentioning

confidence: 99%

Pediatric T-cell acute lymphoblastic leukemia blast signature and MRD associated immune environment changes defined by single cell transcriptomics analysis

Bhasin

Thomas

Summers

et al. 2023

Sci Rep

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Different driver mutations and/or chromosomal aberrations and dysregulated signaling interactions between leukemia cells and the immune microenvironment have been implicated in the development of T-cell acute lymphoblastic leukemia (T-ALL). To better understand changes in the bone marrow microenvironment and signaling pathways in pediatric T-ALL, bone marrows collected at diagnosis (Dx) and end of induction therapy (EOI) from 11 patients at a single center were profiled by single cell transcriptomics (10 Dx, 5 paired EOI, 1 relapse). T-ALL blasts were identified by comparison with healthy bone marrow cells. T-ALL blast-associated gene signature included SOX4, STMN1, JUN, HES4, CDK6, ARMH1 among the most significantly overexpressed genes, some of which are associated with poor prognosis in children with T-ALL. Transcriptome profiles of the blast cells exhibited significant inter-patient heterogeneity. Post induction therapy expression profiles of the immune cells revealed significant changes. Residual blast cells in MRD+ EOI samples exhibited significant upregulation (P < 0.01) of PD-1 and RhoGDI signaling pathways. Differences in cellular communication were noted in the presence of residual disease in T cell and hematopoietic stem cell compartments in the bone marrow. Together, these studies generate new insights and expand our understanding of the bone marrow landscape in pediatric T-ALL.

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