Bone marrow niche-derived extracellular matrix-degrading enzymes influence the progression of B-cell acute lymphoblastic leukemia

Verma, Divij; Zanetti, Costanza; Godavarthy, Parimala Sonika; Kumar, Rahul; Minciacchi, Valentina R.; Pfeiffer, Jakob; Metzler, Markus; Lefort, Sylvain; Maguer-Satta, Véronique; Nicolini, Franck E.; Burroni, Barbara; Fontenay, Michaëla; Krause, Daniela

doi:10.1038/s41375-019-0674-7

Cited by 48 publications

(36 citation statements)

References 51 publications

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“…Blasts may affect the osteoblastic niche, leading to the loss of osteoblastic cells and an impaired function of normal HSCs [ 60 ]. They contribute to the remodeling of the extracellular matrix (ECM) through secretion of matrix metalloproteinase-9 (MMP-9) [ 66 ]. Interestingly, overexpression of C-X-C chemokine receptor type 4 (CXCR4) on leukemic cells is associated with extra-medullary organs involvement and poor patients’ outcome [ 67 ].…”

Section: Bone Marrow Niche As a Sanctuary Site Supporting Acute Lymentioning

confidence: 99%

“…Together with IL-7, CXCL12 stimulates proliferation of both T- and BCP-ALL [ 73 , 74 ]. Other cytokines (IL-1, IFN-γ, and TNF-α) and the soluble HLA-G in the bone marrow microenvironment may also contribute to T-ALL recurrence by inducing immunotolerance [ 66 , 75 ]. Recently, tunneling nanotubes were identified as a mechanism of the crosstalk between ALL cells and MSCs within the niche.…”

Section: Bone Marrow Niche As a Sanctuary Site Supporting Acute Lymentioning

confidence: 99%

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Mechanisms of Immune Evasion in Acute Lymphoblastic Leukemia

Pastorczak

Domka

Fidyt

et al. 2021

Cancers

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Acute lymphoblastic leukemia (ALL) results from a clonal expansion of abnormal lymphoid progenitors of B cell (BCP-ALL) or T cell (T-ALL) origin that invade bone marrow, peripheral blood, and extramedullary sites. Leukemic cells, apart from their oncogene-driven ability to proliferate and avoid differentiation, also change the phenotype and function of innate and adaptive immune cells, leading to escape from the immune surveillance. In this review, we provide an overview of the genetic heterogeneity and treatment of BCP- and T-ALL. We outline the interactions of leukemic cells in the bone marrow microenvironment, mainly with mesenchymal stem cells and immune cells. We describe the mechanisms by which ALL cells escape from immune recognition and elimination by the immune system. We focus on the alterations in ALL cells, such as overexpression of ligands for various inhibitory receptors, including anti-phagocytic receptors on macrophages, NK cell inhibitory receptors, as well as T cell immune checkpoints. In addition, we describe how developing leukemia shapes the bone marrow microenvironment and alters the function of immune cells. Finally, we emphasize that an immunosuppressive microenvironment can reduce the efficacy of chemo- and immunotherapy and provide examples of preclinical studies showing strategies for improving ALL treatment by targeting these immunosuppressive interactions.

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Section: Bone Marrow Niche As a Sanctuary Site Supporting Acute Lymentioning

confidence: 99%

Section: Bone Marrow Niche As a Sanctuary Site Supporting Acute Lymentioning

confidence: 99%

Mechanisms of Immune Evasion in Acute Lymphoblastic Leukemia

Pastorczak

Domka

Fidyt

et al. 2021

Cancers

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“…Consistently, matrix metalloproteinase-9 (MMP-9) produced by leukemia cells facilitated tumor progression via remodeling of the ECM of the BM microenvironment. This is supported by the fact that MMP-9-deficiency in the BM microenvironment reduced leukemia-initiating cells and prolonged survival of mice with BCR-ABL1-positive B-cell acute lymphoblastic leukemia (B-ALL; Verma et al, 2020 ).…”

Section: Evidence Of Stromal Cell Programming By Tumor Microenvironmementioning

confidence: 96%

Tumor Microenvironment Uses a Reversible Reprogramming of Mesenchymal Stromal Cells to Mediate Pro-tumorigenic Effects

Kamdje

Etet

Tagne

et al. 2020

Front. Cell Dev. Biol.

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The role of mesenchymal stromal cells (MSCs) in the tumor microenvironment is well described. Available data support that MSCs display anticancer activities, and that their reprogramming by cancer cells in the tumor microenvironment induces their switch toward pro-tumorigenic activities. Here we discuss the recent evidence of pro-tumorigenic effects of stromal cells, in particular (i) MSC support to cancer cells through the metabolic reprogramming necessary to maintain their malignant behavior and stemness, and (ii) MSC role in cancer cell immunosenescence and in the establishment and maintenance of immunosuppression in the tumor microenvironment. We also discuss the mechanisms of tumor microenvironment mediated reprogramming of MSCs, including the effects of hypoxia, tumor stiffness, cancer-promoting cells, and tumor extracellular matrix. Finally, we summarize the emerging strategies for reprogramming tumor MSCs to reactivate anticancer functions of these stromal cells.

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“…Similarly, LTβR deficiency reduced the number of leukemic stem cells and prolonged their survival in a murine model of chronic myeloid leukemia, supporting the idea that LTβR signaling in hematopoietic and leukemic stem cells mediates similar effects. Interestingly, leukemic-cell-derived TNF induced matrix metalloproteinase 9 (MMP-9) expression by the bone marrow microenvironment through TNFR1, thus contributing to acute lymphoblastic B-cell leukemia progression [ 34 ]. LTβR signaling may also modulate the leukemic microenvironment: inactivation of LTβR results in a significant delay in leukemia onset in TEL-JAK2 mice, which spontaneously develop T-cell leukemia, presumably due to the loss of LTβR signaling in thymic stromal cells [ 99 ].…”

Section: Tnf/lt and Hematological Malignanciesmentioning

confidence: 99%

Dual Role of TNF and LTα in Carcinogenesis as Implicated by Studies in Mice

Gubernatorova

Polinova

Petropavlovskiy

et al. 2021

Cancers

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Tumor necrosis factor (TNF) and lymphotoxin alpha (LTα) are two related cytokines from the TNF superfamily, yet they mediate their functions in soluble and membrane-bound forms via overlapping, as well as distinct, molecular pathways. Their genes are encoded within the major histocompatibility complex class III cluster in close proximity to each other. TNF is involved in host defense, maintenance of lymphoid tissues, regulation of cell death and survival, and antiviral and antibacterial responses. LTα, known for some time as TNFβ, has pleiotropic functions including control of lymphoid tissue development and homeostasis cross talk between lymphocytes and their environment, as well as lymphoid tissue neogenesis with formation of lymphoid follicles outside the lymph nodes. Along with their homeostatic functions, deregulation of these two cytokines may be associated with initiation and progression of chronic inflammation, autoimmunity, and tumorigenesis. In this review, we summarize the current state of knowledge concerning TNF/LTα functions in tumor promotion and suppression, with the focus on the recently uncovered significance of host–microbiota interplay in cancer development that may explain some earlier controversial results.

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Bone marrow niche-derived extracellular matrix-degrading enzymes influence the progression of B-cell acute lymphoblastic leukemia

Cited by 48 publications

References 51 publications

Mechanisms of Immune Evasion in Acute Lymphoblastic Leukemia

Mechanisms of Immune Evasion in Acute Lymphoblastic Leukemia

Tumor Microenvironment Uses a Reversible Reprogramming of Mesenchymal Stromal Cells to Mediate Pro-tumorigenic Effects

Dual Role of TNF and LTα in Carcinogenesis as Implicated by Studies in Mice

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