Integrin-α9 overexpression underlies the niche-independent maintenance of leukemia stem cells in acute myeloid leukemia

Niibori-Nambu, Akiko; Wang, Chelsia Qiuxia; Chin, Desmond Wai Loon; Chooi, Jing Yuan; Hosoi, Hiroki; Sonoki, Takashi; Tham, Cheng-Yong; Nah, Giselle Sek Suan; Cirovic, Branko; Tan, Darren Qiancheng; Takizawa, Hitoshi; Sashida, Goro; Goh, Yufen; Tng, Jiaqi; Fam, Wee Nih; Fullwood, Melissa Jane; Suda, Toshio; Yang, Henry; Tergaonkar, Vinay; Taniuchi, Ichiro; Li, Shang; Chng, Wee Joo; Osato, Motomi

doi:10.1016/j.gene.2024.148761

Gene

2024

DOI: 10.1016/j.gene.2024.148761

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Integrin-α9 overexpression underlies the niche-independent maintenance of leukemia stem cells in acute myeloid leukemia

Akiko Niibori-Nambu,

Chelsia Qiuxia Wang,

Desmond Wai Loon Chin

et al.

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Divergent Processing of Cell Stress Signals as the Basis of Cancer Progression: Licensing NFκB on Chromatin

Vlahopoulos

2024

IJMS

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Inflammation is activated by diverse triggers that induce the expression of cytokines and adhesion molecules, which permit a succession of molecules and cells to deliver stimuli and functions that help the immune system clear the primary cause of tissue damage, whether this is an infection, a tumor, or a trauma. During inflammation, short-term changes in the expression and secretion of strong mediators of inflammation occur, while long-term changes occur to specific groups of cells. Long-term changes include cellular transdifferentiation for some types of cells that need to regenerate damaged tissue, as well as death for specific immune cells that can be detrimental to tissue integrity if they remain active beyond the boundaries of essential function. The transcriptional regulator NFκB enables some of the fundamental gene expression changes during inflammation, as well as during tissue development. During recurrence of malignant disease, cell stress-induced alterations enable the growth of cancer cell clones that are substantially resistant to therapeutic intervention and to the immune system. A number of those alterations occur due to significant defects in feedback signal cascades that control the activity of NFκB. Specifically, cell stress contributes to feedback defects as it overrides modules that otherwise control inflammation to protect host tissue. NFκB is involved in both the suppression and promotion of cancer, and the key distinctive feature that determines its net effect remains unclear. This paper aims to provide a clear answer to at least one aspect of this question, namely the mechanism that enables a divergent response of cancer cells to critical inflammatory stimuli and to cell stress in general.

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Divergent Processing of Cell Stress Signals as the Basis of Cancer Progression: Licensing NFκB on Chromatin

Vlahopoulos

2024

IJMS

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Integrin-α9 overexpression underlies the niche-independent maintenance of leukemia stem cells in acute myeloid leukemia

Cited by 1 publication

References 73 publications

Divergent Processing of Cell Stress Signals as the Basis of Cancer Progression: Licensing NFκB on Chromatin

Divergent Processing of Cell Stress Signals as the Basis of Cancer Progression: Licensing NFκB on Chromatin

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