Chemokine CXC receptor 4–mediated glioma tumor tracking by bone marrow–derived neural progenitor/stem cells

Xu, Qijin; Yuan, Xiangpeng; Xu, Minlin; McLafferty, Fred S.; Hu, Jinwei; Lee, Bong Seop; Liu, Gentao; Zeng, Zhaohui; Black, Keith L.; Yu, John S.

doi:10.1158/1535-7163.mct-09-0273

Cited by 18 publications

(18 citation statements)

References 30 publications

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“…The CXCL12/CXCR4 axis is involved in several aspects of tumor progression including angiogenesis, metastasis, and survival (1,(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42). The bone marrow microenvironment facilitates the survival, differentiation, and proliferation of normal hematopoietic cells, malignant hematopoietic cells, and epithelial tumor cell bone metastasis.…”

Section: Cxcr4 and Cancermentioning

confidence: 99%

CXCL12 (SDF-1)/CXCR4 Pathway in Cancer

Teicher¹,

Fricker²

2010

Clinical Cancer Research

1,201

1,067

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Chemokines, small proinflammatory chemoattractant cytokines that bind to specific G-proteincoupled seven-span transmembrane receptors, are major regulators of cell trafficking and adhesion. The chemokine CXCL12 [stromal cell-derived factor-1 (SDF-1)] binds primarily to CXC receptor 4 (CXCR4; CD184). The binding of CXCL12 to CXCR4 induces intracellular signaling through several divergent pathways initiating signals related to chemotaxis, cell survival and/or proliferation, increase in intracellular calcium, and gene transcription. CXCR4 is expressed on multiple cell types including lymphocytes, hematopoietic stem cells, endothelial and epithelial cells, and cancer cells. The CXCL12/CXCR4 axis is involved in tumor progression, angiogenesis, metastasis, and survival. This pathway is a target for therapeutics that can block the CXCL12/CXCR4 interaction or inhibit downstream intracellular signaling.

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Section: Cxcr4 and Cancermentioning

confidence: 99%

CXCL12 (SDF-1)/CXCR4 Pathway in Cancer

Teicher¹,

Fricker²

2010

Clinical Cancer Research

1,201

1,067

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“…from the subventricular zone (SVZ) lining the lateral ventricles or from the corpus callosum, migrate toward experimental brain tumors (Assanah et al, 2006(Assanah et al, , 2009Chirasani et al, 2010;Glass et al, 2005;Walzlein et al, 2008). NPCs home in to pathologic brain tissue and possibly also to tumors due to expression of CXCR4 (Kokovay et al, 2010;Xu et al, 2009). The association of endogenous NPCs with glioblastomas may have been overlooked for many years, since it is only abundant in the young brain and since special animal models are necessary to distinguish glioblastoma cells from NPCs.…”

Section: The Interaction Of Glioblastomas With Neural Precursor Cellsmentioning

confidence: 99%

The brain tumor microenvironment

Charles

Holland

Gilbertson

et al. 2011

Glia

687

327

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High-grade brain tumors are heterogeneous with respect to the composition of bona fide tumor cells and with respect to a range of intermingling parenchymal cells. Glioblastomas harbor multiple cell types, some with increased tumorigenicity and stem cell-like capacity. The stem-like cells may be the cells of origin for tumor relapse. However, the tumor-associated parenchymal cells such as vascular cells, microglia, peripheral immune cells, and neural precursor cells also play a vital role in controlling the course of pathology. In this review, we describe the multiple interactions of bulk glioma cells and glioma stem cells with parenchymal cell populations and highlight the pathological impact as well as signaling pathways known for these types of cell-cell communication. The tumor-vasculature not only nourishes glioblastomas, but also provides a specialized niche for these stem-like cells. In addition, microglial cells, which can contribute up to 30% of a brain tumor mass, play a role in glioblastoma cell invasion. Moreover, non-neoplastic astrocytes can be converted into a reactive phenotype by the glioma microenvironment and can then secrete a number of factors which influences tumor biology. The young brain may have the capacity to inhibit gliomagenesis by the endogenous neural precursor cells, which secrete tumor suppressive factors. The factors, pathways, and interactions described in this review provide a new prospective on the cell biology of primary brain tumors, which may ultimately generate new treatment modalities. However, our picture of the multiple interactions between parenchymal and tumor cells is still incomplete. V

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“…It has previously been characterized that HSCs are recruited to intracranial glioma via tumor-secreted CXCL12 21,22 which is the ligand for CXCR4, a receptor characteristic of HSCs. 23,24 Studies have demonstrated that CXCR4 blockade inhibits bone marrowderived progenitor cell migration to glioma, indicating that CXCR4 is required for their chemotaxis to tumor.…”

Section: E994374-6mentioning

confidence: 99%

“…23,24 Studies have demonstrated that CXCR4 blockade inhibits bone marrowderived progenitor cell migration to glioma, indicating that CXCR4 is required for their chemotaxis to tumor. 21 It has been suggested that HSC-derived pericytes may be recruited by tumors to contribute to tumor vasculature. 25 This intracranial recruitment of HSCs is further increased by radiation and the hypoxic environment in the brain.…”

Section: E994374-6mentioning

confidence: 99%

Novel role of hematopoietic stem cells in immunologic rejection of malignant gliomas

et al. 2015

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Adoptive cellular therapy (ACT) after lymphodepletive conditioning can induce dramatic clinical responses, but this approach has been largely limited to melanoma due to a lack of reliable methods for expanding tumor-specific lymphocytes from the majority of other solid cancers. We have employed tumor RNA-pulsed dendritic cells (DCs) to reliably expand CD4C and CD8 C tumor-reactive T lymphocytes for curative ACT in a highly-invasive, chemotherapy-and radiation-resistant malignant glioma model. Curative treatment of established intracranial tumors involved a synergistic interaction between myeloablative (MA) conditioning, adoptively transferred tumor-specific T cells, and tumor RNApulsed DC vaccines. Hematopoietic stem cells (HSCs), administered for salvage from MA conditioning, rapidly migrated to areas of intracranial tumor growth and facilitated the recruitment of tumor-specific lymphocytes through HSCelaborated chemokines and enhanced immunologic rejection of intracranial tumors during ACT. Furthermore, HSC transplant under non-myeloablative (NMA) conditions also enhanced immunologic tumor rejection, indicating a novel role for the use of HSCs in the immunologic treatment of malignant gliomas and possibly other solid tumors.

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Chemokine CXC receptor 4–mediated glioma tumor tracking by bone marrow–derived neural progenitor/stem cells

Cited by 18 publications

References 30 publications

CXCL12 (SDF-1)/CXCR4 Pathway in Cancer

CXCL12 (SDF-1)/CXCR4 Pathway in Cancer

The brain tumor microenvironment

Novel role of hematopoietic stem cells in immunologic rejection of malignant gliomas

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