Efficacy of tyrosine kinase inhibitors on a mouse chronic myeloid leukemia model and chronic myeloid leukemia stem cells

Tanaka, Yosuke; Mikami, K.; Adachi, Keito; Goyama, Susumu; Kitamura, Toshio

doi:10.1016/j.exphem.2020.09.186

Cited by 4 publications

(1 citation statement)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, similar to our results, Schemionek et al documented an increased resistance of splenic leukemic cells compared with BM leukemic cells towards imatinib ( 14 ). This may reflect the previously documented differences of susceptibility of LSCs towards the various TKIs ( 58 ). Thus, the kinetics of the CML development, the irradiation of the recipient and the TKI studied may influence the number and function of LSCs in the spleen.…”

Section: Discussionsupporting

confidence: 59%

Splenic red pulp macrophages provide a niche for CML stem cells and induce therapy resistance

et al. 2022

View full text Add to dashboard Cite

Disease progression and relapse of chronic myeloid leukemia (CML) are caused by therapy resistant leukemia stem cells (LSCs), and cure relies on their eradication. The microenvironment in the bone marrow (BM) is known to contribute to LSC maintenance and resistance. Although leukemic infiltration of the spleen is a hallmark of CML, it is unknown whether spleen cells form a niche that maintains LSCs. Here, we demonstrate that LSCs preferentially accumulate in the spleen and contribute to disease progression. Spleen LSCs were located in the red pulp close to red pulp macrophages (RPM) in CML patients and in a murine CML model. Pharmacologic and genetic depletion of RPM reduced LSCs and decreased their cell cycling activity in the spleen. Gene expression analysis revealed enriched stemness and decreased myeloid lineage differentiation in spleen leukemic stem and progenitor cells (LSPCs). These results demonstrate that splenic RPM form a niche that maintains CML LSCs in a quiescent state, resulting in disease progression and resistance to therapy.

show abstract

Section: Discussionsupporting

confidence: 59%

Splenic red pulp macrophages provide a niche for CML stem cells and induce therapy resistance

et al. 2022

View full text Add to dashboard Cite

show abstract

Effects of imidazole derivatives on cellular proliferation and apoptosis in myeloid leukemia

Nadeem,

Bibi,

Khan

et al. 2024

BMC Cancer

View full text Add to dashboard Cite

Stem Cells: Therapeutic Implications in Chemotherapy and Radiotherapy Resistance in Cancer Therapy

Tiwari

Patil

Rohiwal

2023

CSCR

View full text Add to dashboard Cite

Cancer stem cells (CSCs) are transformed form of normal stem cells within heterogeneous mixture of cancer cells. These are mainly responsible for recurrence of cancer after treatment because of their ability to develop resistance against chemo and radiotherapy due to various factors such as, activation of signalling pathways important for self-renewal, DNA repair capacity, microenvironment and expression of ABC transporters. Targeting these mechanisms as potential factors can eliminate CSCs which eventually decreases cancer recurrence. This review focuses on the characteristics of CSCs, their role in development of resistance to chemotherapy and radiotherapy along with the therapeutic potential targets for successful elimination of CSC population.

show abstract

Efficacy of tyrosine kinase inhibitors on a mouse chronic myeloid leukemia model and chronic myeloid leukemia stem cells

Cited by 4 publications

References 24 publications

Splenic red pulp macrophages provide a niche for CML stem cells and induce therapy resistance

Splenic red pulp macrophages provide a niche for CML stem cells and induce therapy resistance

Effects of imidazole derivatives on cellular proliferation and apoptosis in myeloid leukemia

Stem Cells: Therapeutic Implications in Chemotherapy and Radiotherapy Resistance in Cancer Therapy

Contact Info

Product

Resources

About