Concepts in B cell acute lymphoblastic leukemia pathogenesis.
| Autor: | Garcia C; Department of Pediatrics, University of Colorado Anschutz Medical Campus, 12800 East 19th Avenue, Aurora, CO 80045, United States., Miller-Awe MD; Department of Pediatrics, University of Colorado Anschutz Medical Campus, 12800 East 19th Avenue, Aurora, CO 80045, United States., Witkowski MT; Department of Pediatrics, University of Colorado Anschutz Medical Campus, 12800 East 19th Avenue, Aurora, CO 80045, United States. |
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| Jazyk: | angličtina |
| Zdroj: | Journal of leukocyte biology [J Leukoc Biol] 2024 Jun 28; Vol. 116 (1), pp. 18-32. |
| DOI: | 10.1093/jleuko/qiae015 |
| Abstrakt: | B cell acute lymphoblastic leukemia (B-ALL) arises from genetic alterations impacting B cell progenitors, ultimately leading to clinically overt disease. Extensive collaborative efforts in basic and clinical research have significantly improved patient prognoses. Nevertheless, a subset of patients demonstrate resistance to conventional chemotherapeutic approaches and emerging immunotherapeutic interventions. This review highlights the mechanistic underpinnings governing B-ALL transformation. Beginning with exploring normative B cell lymphopoiesis, we delineate the influence of recurrent germline and somatic genetic aberrations on the perturbation of B cell progenitor differentiation and protumorigenic signaling, thereby facilitating the neoplastic transformation underlying B-ALL progression. Additionally, we highlight recent advances in the multifaceted landscape of B-ALL, encompassing metabolic reprogramming, microbiome influences, inflammation, and the discernible impact of socioeconomic and racial disparities on B-ALL transformation and patient survival. Competing Interests: Conflict of interest statement. The authors declare no competing interests relevant to the material presented in this review article. (© The Author(s) 2024. Published by Oxford University Press on behalf of Society for Leukocyte Biology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.) |
| Databáze: | MEDLINE |
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