The Regulation of Normal and Leukemia Stem Cells

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 1877

Special Issue Editor


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Guest Editor
Key Laboratory of Stem Cells and Tissue Engineering (Ministry of Education), Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China
Interests: cellular and molecular mechanisms behind hematopoietic stem cells; leukemic stem cells; microenvironment

Special Issue Information

Dear Colleagues,

Normal and leukemia stem cells are crucial to understanding the function of the hematopoietic system and the development of leukemia. Normal hematopoietic stem cells (HSCs) are responsible for the continuous regeneration of the blood system, while leukemia stem cells (LSCs) are the origin cells of leukemia, possessing chemoresistance and disease relapse capacity. The in-depth exploration of the characteristics and regulatory mechanisms of these stem cells is of great significance for the development of novel treatment strategies and the enhancement of outcomes for leukemia patients. This Special Issue will highlight the current understanding of both the cellular and molecule mechanisms involved in normal and leukemia stem cells in normal and diseased states.

This Special Issue, entitled “The Regulation of Normal and Leukemia Stem Cells”, will foreground recent advances in haematopoiesis research. We encourage the submission of reviews and experimental articles, and look forward to receiving your contributions.

Prof. Dr. Meng Zhao
Guest Editor

Manuscript Submission Information

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Keywords

  • hematopoietic stem cells
  • leukemia stem cells
  • niche
  • leukemia
  • metabolism
  • drug resistance
  • immune evasion

Published Papers (1 paper)

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Research

16 pages, 6119 KiB  
Article
Venetoclax Overcomes Sorafenib Resistance in Acute Myeloid Leukemia by Targeting BCL2
by Xi Xu, Weiwei Ma, Guo Qiu, Li Xuan, Chong He, Tian Zhang, Jian Wang and Qifa Liu
Biology 2023, 12(10), 1337; https://doi.org/10.3390/biology12101337 - 16 Oct 2023
Viewed by 1624
Abstract
Sorafenib, a kinase inhibitor, has shown promising therapeutic efficacy in a subset of patients with acute myeloid leukemia (AML). However, despite its clinical effectiveness, sorafenib resistance is frequently observed in clinical settings, and the mechanisms underlying this resistance as well as effective strategies [...] Read more.
Sorafenib, a kinase inhibitor, has shown promising therapeutic efficacy in a subset of patients with acute myeloid leukemia (AML). However, despite its clinical effectiveness, sorafenib resistance is frequently observed in clinical settings, and the mechanisms underlying this resistance as well as effective strategies to overcome it remain unclear. We examined both single-cell and bulk transcription data in sorafenib-resistant and control AML patients and integrated a sorafenib resistance gene signature to predict the sensitivity of AML cells and the clinical outcomes of AML patients undergoing sorafenib therapy. In addition, our drug sensitivity analysis of scRNA-seq data using deconvolution methods showed that venetoclax was effective in targeting sorafenib-resistant AML cells. Mechanistically, sorafenib was found to activate the JAK-STAT3 pathway and upregulate BCL2 expression in sorafenib-resistant AML cells. This upregulation of BCL2 expression rendered the cells vulnerable to the BCL2 inhibitor venetoclax. In conclusion, we developed a platform to predict sorafenib resistance and clinical outcomes in AML patients after therapy. Our findings suggest that the combination of sorafenib and venetoclax could be an effective therapeutic strategy for AML treatment. Full article
(This article belongs to the Special Issue The Regulation of Normal and Leukemia Stem Cells)
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