2014
DOI: 10.1182/blood-2013-12-542480
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NOX-A12: mobilizing CLL away from home

Abstract: Comment on "The Spiegelmer NOX-A12, a novel CXCL12 inhibitor, interferes with chronic lymphocytic leukemia cell motility and causes chemosensitization". Hoellenriegel J, Zboralski D, Maasch C, Rosin NY, Wierda WG, Keating MJ, Kruschinski A, Burger JA.\ud Blood. 2014 Feb 13;123(7):1032-9. doi: 10.1182/blood-2013-03-493924. Epub 2013 Nov 25

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Cited by 28 publications
(21 citation statements)
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References 7 publications
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“…NOX-A12 214, 215 is a 45-nt L-form RNA aptamer known as a Spiegelmer®, developed against chemokine (C-X-C motif) ligand 12 (CXCL-12). Also known as stromal cell-derived factor-1 (SDF-1) 216218 , CXCL-12 plays important roles in tumor proliferation, new blood vessel formation, and metastasis.…”
Section: Clinical Development Of Aptamer-based Therapeuticsmentioning
confidence: 99%
“…NOX-A12 214, 215 is a 45-nt L-form RNA aptamer known as a Spiegelmer®, developed against chemokine (C-X-C motif) ligand 12 (CXCL-12). Also known as stromal cell-derived factor-1 (SDF-1) 216218 , CXCL-12 plays important roles in tumor proliferation, new blood vessel formation, and metastasis.…”
Section: Clinical Development Of Aptamer-based Therapeuticsmentioning
confidence: 99%
“…This strategy for the inhibition of inflammation is comparable to the recently developed CellJammer and NOX A12 aptamer approaches and is an alternative method for small molecule chemokine receptor antagonists to inhibit chemokine function. 41,[44][45][46][47][48][49][50] In the CellJammer and NOX A12 approaches, chemokine mutants with increased GAGbinding affinity and abrogated GPCR signalling or aptamers that mask the GAG-binding site of a chemokine are used, respectively. This results in antagonists which potently compete with active chemokines For each group, micrographs were taken of ear sections of different mice (n ≥ 4 mice/group).…”
Section: Discussionmentioning
confidence: 99%
“…Their product NOX-A12 functions as a CXCL12 inhibitor and enabled the release of CXCL12 from the surface of tumor stromal cells and blocked its interaction with cell surface receptors CXCR4 and CXCR7. This mechanism facilitated the mobilization of CXCR4-expressing tumor cells from their tissue niches to areas, where they become easily accessible by NK cells or T cells (134, 135). Using tumor spheroids, increased mobilization of T and NK cells toward tumor cells in the tumor microenvironment was demonstrated.…”
Section: Tumor Disruptive Technology Aiding Nk Tumor Recognitionmentioning
confidence: 99%