Academic literature on the topic 'CXCR4 axi'
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Journal articles on the topic "CXCR4 axi"
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Rini, Brian I., Bernard Escudier, Danielle Murphy, Panpan Wang, Jamal Christo Tarazi, and Robert J. Motzer. "Angiogenic and immunomodulatory biomarkers in axitinib-treated patients (pts) with advanced renal cell carcinoma (aRCC)." Journal of Clinical Oncology 37, no. 7_suppl (March 1, 2019): 614. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.614.
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614 Background: Axitinib (axi) is approved for 2nd-line treatment of aRCC. In AXIS trial, median progression-free survival (PFS) was significantly longer in axi- vs sorafenib (sor)-treated pts (hazard ratio [HR] 0.67, 95% CI 0.54–0.81, P<0.0001). Association between mRNA/miRNA expression and clinical outcomes in a subset of axi- or sor-treated pts from AXIS was assessed. Methods: mRNA/miRNA analyses were performed on archival tumor samples. Expression was summarized for responders (complete and partial response) vs non-responders (stable and progressive disease), and for maximum percent tumor change. PFS and overall survival (OS) were analyzed by Kaplan-Meier. Results: Pt characteristics were similar between axi (n=34) and sor (n=33) arms. Association with outcomes is shown in the Table. A correlation was observed for CD68 protein and mRNA expression in axi-treated pts (R=0.4774 P=0.0043 and R=0.3985 P=0.0196, respectively). Both CXCR4 and TLR3 showed differences between treatment arms and association with PFS. TNFSF10 <median, and CD163, CSF1R and miR-221-5p ≥median were associated with shorter OS with axi vs sor ( P<0.05). Clinical trial information: NCT00678392. Conclusions: Immune-related biomarkers were associated with clinical outcomes in axi/sor-treated aRCC pts. Lower CCR7 expression was associated with better response and OS in axi-treated pts. CXCR4 and TLR3 may be predictive of response to axi. Analysis in a larger cohort is warranted.[Table: see text]
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Zheng, Lanzhi, Zhuoyi Zhang, Kang Song, Xiaoyang Xu, Yixin Tong, Jinling Wei, and Lu Jiang. "Potential biomarkers for inflammatory response in acute lung injury." Open Medicine 17, no. 1 (January 1, 2022): 1066–76. http://dx.doi.org/10.1515/med-2022-0491.
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Abstract Acute lung injury (ALI) is a severe respiratory disorder occurring in critical care medicine, with high rates of mortality and morbidity. This study aims to screen the potential biomarkers for ALI. Microarray data of lung tissues from lung-specific geranylgeranyl pyrophosphate synthase large subunit 1 knockout and wild-type mice treated with lipopolysaccharide were downloaded. Differentially expressed genes (DEGs) between ALI and wild-type mice were screened. Functional analysis and the protein–protein interaction (PPI) modules were analyzed. Finally, a miRNA-transcription factor (TF)-target regulation network was constructed. Totally, 421 DEGs between ALI and wild-type mice were identified. The upregulated DEGs were mainly enriched in the peroxisome proliferator-activated receptor signaling pathway, and fatty acid metabolic process, while downregulated DEGs were related to cytokine–cytokine receptor interaction and regulation of cytokine production. Cxcl5, Cxcl9, Ccr5, and Cxcr4 were key nodes in the PPI network. In addition, three miRNAs (miR505, miR23A, and miR23B) and three TFs (PU1, CEBPA, and CEBPB) were key molecules in the miRNA-TF-target network. Nine genes including ADRA2A, P2RY12, ADORA1, CXCR1, and CXCR4 were predicted as potential druggable genes. As a conclusion, ADRA2A, P2RY12, ADORA1, CXCL5, CXCL9, CXCR1, and CXCR4 might be novel markers and potential druggable genes in ALI by regulating inflammatory response.
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Krikun, Graciela. "The CXL12/CXCR4/CXCR7 axis in female reproductive tract disease: Review." American Journal of Reproductive Immunology 80, no. 5 (August 14, 2018): e13028. http://dx.doi.org/10.1111/aji.13028.
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Yao, Miao-En, Yi Huang, Qing-Qing Dong, Yi Lu, and Wei Chen. "The Renshen Chishao Decoction Could Ameliorate the Acute Lung Injury but Could Not Reduce the Neutrophil Extracellular Traps Formation." Evidence-Based Complementary and Alternative Medicine 2022 (August 29, 2022): 1–16. http://dx.doi.org/10.1155/2022/7784148.
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The acute lung injury (ALI) causes severe pulmonary diseases, leading to a high mortality rate. The Renshen and Chishao have protective and anti-inflammatory effects against the ALI. To explore the protective effects of the Renshen Chishao (RC) decoction against the ALI, we established the lipopolysaccharide-indued ALI model and randomly divided the mice into seven groups: control group, ALI group, high-dose RC group, middle-dose RC group, low-dose RC group, middle-dose RC group + CXCR2 antagonist group, and ALI + CXCR2 antagonist group. We estimated the lung injury by the hematoxylin and eosin staining, the neutrophil extracellular traps (NETs) formations by the immunofluorescence colocalization and enzyme-linked immunosorbent assay (ELISA), and the CXCR2/CXCL2 pathway by the flow cytometry, ELISA, and real-time polymerase chain reaction. We conducted the high-throughput sequencing and enrichment analyses to explore the potential mechanisms. The results showed that the RC decoction pathologically ameliorated the lipopolysaccharide-induced lung injury and inflammatory response but failed to reduce the circulating and lung tissue NETs formation and the blood neutrophil percent. The high-dose RC decoction increased the plasma CXCL2 level, but the RC decoction had no effects on the neutrophilic CXCR2 levels. Under the inhibition of the CXCR2, the middle-dose RC decoction still decreased the lung injury score but as yet had unobvious influence on the NETs formation. Other potential mechanisms of the RC decoction against the ALI involved the pathways of ribosome and coronavirus disease 2019 (COVID-19); the target genes of inflammatory factors, such as Ccl17, Cxcl17, Cd163, Cxcr5, and Il31ra, and lncRNAs; and the regulations of the respiratory cilia. In conclusion, the RC decoction pathologically ameliorated the lipopolysaccharide-induced lung inflammatory injury via upregulating the CXCL2/CXCR2 pathway but could not reduce the circulating or lung tissue NETs formation.
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Liu, Nanmei, Andreas Patzak, and Jinyuan Zhang. "CXCR4-overexpressing bone marrow-derived mesenchymal stem cells improve repair of acute kidney injury." American Journal of Physiology-Renal Physiology 305, no. 7 (October 1, 2013): F1064—F1073. http://dx.doi.org/10.1152/ajprenal.00178.2013.
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Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) can repair acute kidney injury (AKI), but with limited effect. We test the hypothesis that CXCR4 overexpression improves the repair ability of BMSCs and that this is related to increased homing of BMSCs and increased release of cytokines. Hypoxia/reoxygenation-pretreated renal tubular epithelial cells (HR-RTECs) were used. BMSCs, null-BMSCs, and CXCR4-BMSCs were cocultured with HR-RTECs. The number of migrating BMSCs was counted. Proliferating cell nuclear antigen (PCNA) expression, cell death, and expressions of cleaved caspase-3 and Bcl-2 in cocultured HR-RTECs were measured. Cytokeratin 18 (CK18) expression and cytokine secretions of the BMSCs cultured with HR-RTEC supernatant were detected. BMSC homing, renal function, proliferation, and cell death of tubular cells were assayed in the AKI mouse model. CXCR4-BMSCs showed a remarkable expression of CXCR4. Stromal cell-derived factor-1 in the HR-RTEC supernatant was increased. Migration of BMSCs was CXCR4-dependent. Proportions of CK18+ cells in BMSCs, null-BMSCs, and CXCR4-BMSCs showed no difference. However, CXCR4 overexpression in BMSCs stimulated secretion of bone morphogenetic protein-7, hepatocyte growth factor, and interleukin 10. The neutralizing anti-CXCR4 antibody AMD3100 abolished this. In cocultured HR-RTECs the proportions of PCNA+ cells and Bcl-2 expression were enhanced; however, the proportion of annexin V+ cells and expression of cleaved caspase-3 were reduced. The in vivo study showed increased homing of CXCR4-BMSCs in kidneys, which was associated with improved renal function, reduced acute tubular necrosis scoring, accelerated mitogenic response of tubular cells, and reduced tubular cell death. The enhanced homing and paracrine actions of BMSCs with CXCR4 overexpression suggest beneficial effects of such cells in BMSC-based therapy for AKI.
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Lukovic, Dominika, Katrin Zlabinger, Alfred Gugerell, Andreas Spannbauer, Noemi Pavo, Ljubica Mandic, Denise T. Weidenauer, et al. "Inhibition of CD34+ cell migration by matrix metalloproteinase-2 during acute myocardial ischemia, counteracted by ischemic preconditioning." F1000Research 5 (November 22, 2016): 2739. http://dx.doi.org/10.12688/f1000research.9957.1.
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Background. Mobilization of bone marrow-origin CD34+ cells was investigated 3 days (3d) after acute myocardial infarction (AMI) with/without ischemic preconditioning (IP) in relation to stromal-derived factor-1 (SDF-1α)/ chemokine receptor type 4 (CXCR4) axis, to search for possible mechanisms behind insufficient cardiac repair in the first days post-AMI. Methods. Closed-chest reperfused AMI was performed by percutaneous balloon occlusion of the mid-left anterior descending (LAD) coronary artery for 90min, followed by reperfusion in pigs. Animals were randomized to receive either IP initiated by 3x5min cycles of re-occlusion/re-flow prior to AMI (n=6) or control AMI (n=12). Blood samples were collected at baseline, 3d post-AMI, and at 1-month follow-up to analyse chemokines and mobilized CD34+ cells. To investigate the effect of acute hypoxia, SDF-1α and matrix metalloproteinase (MMP)-2 in vitro were assessed, and a migration assay of CD34+ cells toward cardiomyocytes was performed. Results. Reperfused AMI induced significant mobilisation of CD34+ cells (baseline: 260±75 vs. 3d: 668±180; P<0.001) and secretion of MMP-2 (baseline: 291.83±53.40 vs. 3d: 369.64±72.89; P=0.011) into plasma, without affecting the SDF-1α concentration. IP led to the inhibition of MMP-2 (IP: 165.67±47.99 vs. AMI: 369.64±72.89; P=0.004) 3d post-AMI, accompanied by increased release of SDF-1α (baseline: 23.80±12.36 vs. 3d: 45.29±11.31; P=0.05) and CXCR4 (baseline: 0.59±0.16 vs. 3d: 2.06±1.42; P=0.034), with a parallel higher level of mobilisation of CD34+ cells (IP: 881±126 vs. AMI: 668±180; P=0.026), compared to non-conditioned AMI. In vitro, CD34+ cell migration toward cardiomyocytes was enhanced by SDF-1α, which was completely abolished by 90min hypoxia and co-incubation with MMP-2. Conclusions. Non-conditioned AMI induces MMP-2 release, hampering the ischemia-induced increase in SDF-1α and CXCR4 by cleaving the SDF-1α/CXCR4 axis, with diminished mobilization of the angiogenic CD34+ cells. IP enforces CD34+ cell mobilization via inhibition of MMP-2.
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Lukovic, Dominika, Katrin Zlabinger, Alfred Gugerell, Andreas Spannbauer, Noemi Pavo, Ljubica Mandic, Denise T. Weidenauer, et al. "Inhibition of CD34+ cell migration by matrix metalloproteinase-2 during acute myocardial ischemia, counteracted by ischemic preconditioning." F1000Research 5 (December 20, 2016): 2739. http://dx.doi.org/10.12688/f1000research.9957.2.
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Background. Mobilization of bone marrow-origin CD34+ cells was investigated 3 days (3d) after acute myocardial infarction (AMI) with/without ischemic preconditioning (IP) in relation to stromal-derived factor-1 (SDF-1α)/ chemokine receptor type 4 (CXCR4) axis, to search for possible mechanisms behind insufficient cardiac repair in the first days post-AMI. Methods. Closed-chest reperfused AMI was performed by percutaneous balloon occlusion of the mid-left anterior descending (LAD) coronary artery for 90min, followed by reperfusion in pigs. Animals were randomized to receive either IP initiated by 3x5min cycles of re-occlusion/re-flow prior to AMI (n=6) or control AMI (n=12). Blood samples were collected at baseline, 3d post-AMI, and at 1-month follow-up to analyse chemokines and mobilized CD34+ cells. To investigate the effect of acute hypoxia, SDF-1α and matrix metalloproteinase (MMP)-2 in vitro were assessed, and a migration assay of CD34+ cells toward cardiomyocytes was performed. Results. Reperfused AMI induced significant mobilisation of CD34+ cells (baseline: 260±75 vs. 3d: 668±180; P<0.001) and secretion of MMP-2 (baseline: 291.83±53.40 vs. 3d: 369.64±72.89; P=0.011) into plasma, without affecting the SDF-1α concentration. IP led to the inhibition of MMP-2 (IP: 165.67±47.99 vs. AMI: 369.64±72.89; P=0.004) 3d post-AMI, accompanied by increased release of SDF-1α (baseline: 23.80±12.36 vs. 3d: 45.29±11.31; P=0.05) and CXCR4 (baseline: 0.59±0.16 vs. 3d: 2.06±1.42; P=0.034), with a parallel higher level of mobilisation of CD34+ cells (IP: 881±126 vs. AMI: 668±180; P=0.026), compared to non-conditioned AMI. In vitro, CD34+ cell migration toward cardiomyocytes was enhanced by SDF-1α, which was completely abolished by 90min hypoxia and co-incubation with MMP-2. Conclusions. Non-conditioned AMI induces MMP-2 release, hampering the ischemia-induced increase in SDF-1α and CXCR4 by cleaving the SDF-1α/CXCR4 axis, with diminished mobilization of the angiogenic CD34+ cells. IP might influence CD34+ cell mobilization via inhibition of MMP-2.
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Lukovic, Dominika, Katrin Zlabinger, Alfred Gugerell, Andreas Spannbauer, Noemi Pavo, Ljubica Mandic, Denise T. Weidenauer, et al. "Inhibition of CD34+ cell migration by matrix metalloproteinase-2 during acute myocardial ischemia, counteracted by ischemic preconditioning." F1000Research 5 (February 6, 2017): 2739. http://dx.doi.org/10.12688/f1000research.9957.3.
Full textAbstract:
Background. Mobilization of bone marrow-origin CD34+ cells was investigated 3 days (3d) after acute myocardial infarction (AMI) with/without ischemic preconditioning (IP) in relation to stromal-derived factor-1 (SDF-1α)/ chemokine receptor type 4 (CXCR4) axis, to search for possible mechanisms behind insufficient cardiac repair in the first days post-AMI. Methods. Closed-chest reperfused AMI was performed by percutaneous balloon occlusion of the mid-left anterior descending (LAD) coronary artery for 90min, followed by reperfusion in pigs. Animals were randomized to receive either IP initiated by 3x5min cycles of re-occlusion/re-flow prior to AMI (n=6) or control AMI (n=12). Blood samples were collected at baseline, 3d post-AMI, and at 1-month follow-up to analyse chemokines and mobilized CD34+ cells. To investigate the effect of acute hypoxia, SDF-1α and matrix metalloproteinase (MMP)-2 in vitro were assessed, and a migration assay of CD34+ cells toward cardiomyocytes was performed. Results. Reperfused AMI induced significant mobilisation of CD34+ cells (baseline: 260±75 vs. 3d: 668±180; P<0.001) and secretion of MMP-2 (baseline: 291.83±53.40 vs. 3d: 369.64±72.89; P=0.011) into plasma, without affecting the SDF-1α concentration. IP led to the inhibition of MMP-2 (IP: 165.67±47.99 vs. AMI: 369.64±72.89; P=0.004) 3d post-AMI, accompanied by increased release of SDF-1α (baseline: 23.80±12.36 vs. 3d: 45.29±11.31; P=0.05) and CXCR4 (baseline: 0.59±0.16 vs. 3d: 2.06±1.42; P=0.034), with a parallel higher level of mobilisation of CD34+ cells (IP: 881±126 vs. AMI: 668±180; P=0.026), compared to non-conditioned AMI. In vitro, CD34+ cell migration toward cardiomyocytes was enhanced by SDF-1α, which was completely abolished by 90min hypoxia and co-incubation with MMP-2. Conclusions. Non-conditioned AMI induces MMP-2 release, hampering the ischemia-induced increase in SDF-1α and CXCR4 by cleaving the SDF-1α/CXCR4 axis, with diminished mobilization of the angiogenic CD34+ cells. IP might influence CD34+ cell mobilization via inhibition of MMP-2.
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Waller, Ned, Arshed Quyyumi, Douglas Vaughan, Thomas Moss, Wai S. Chan, Robert Preti, and Andrew L. Pecora. "CD34+CXCR4+ Cell Therapy (AMR-001) for Myocardial Infarction: Preliminary Processing and Product Results of a Phase I Dose Escalation Study." Blood 110, no. 11 (November 16, 2007): 773. http://dx.doi.org/10.1182/blood.v110.11.773.773.
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Abstract Background: Approximately 20% of patients suffering a ST segment elevated acute myocardial infarction (AMI) have progressive peri-infarct zone myocardial cell death causing ventricular remodeling and poor cardiac outcomes in spite of large vessel revascularization and medical management. Neo-angiogenesis occurs when VEGF levels peak and endothelial precursors are mobilized and recruited to the infarct site. Stromal cell derived factor-1 (SDF-1), the ligand for the CXCR4 receptor, is expressed by CD34+ cells and plays a role in cell homing to areas of ischemic damage. CD34+ CXCR4+ cells home to areas of ischemia, rich in SDF-1, including infarcted myocardium and are capable of inducing neo-angiogenesis. Natural neoangiogenesis is present but insufficient following AMI, suggesting that direct administration of CD34+ CXCR4+ progenitors could mitigate peri-infarct zone myocardial cell death and improve ventricular function. Methods: In this phase I study, patients with an ST segment (AMI) are enrolled in cohorts of 5 to receive one of four doses (5, 10, 15, 20 x 106 of bone marrow derived CD34+ cells. Cells are harvested using a mini-bone marrow harvest (MMH) technique, acquired by Isolex selection and administered by infusion via the infarct related artery 5 to 10 day following successful coronary artery stenting post AMI. The first 10 subjects accrued as subjects on this phase 1 study included 9 males and 1 female, with a median age of 52 years (range 36–70). Results: The first ten patients (of 20 planned) underwent a MMH under conscious sedation without incident. Adequate numbers of viable, enriched CD34+ cells were obtained following Isolex selection for treatment of subjects enrolled at the first two dose cohorts (5 x 106 and 10 x 106 CD34+ cells). The mean fraction of cells expressing CD34 in the marrow product was 0.75%, with a mean recovery of 40% following Isolex selection (Table). Conclusions: Our study demonstrates the feasibility of collecting up to 409 ml of bone marrow using a MMH technique in the immediate post AMI setting, with yields up to 86 x 106 CD34+ cells. All patient cells expressed CXCR4 and had in vitro migratory capacity. However the lower than expected percentage of TNC expressing CD34 (compared with 9 healthy age matched individuals (1.49% vs. 0.75%) and a low % recovery following Isolex selection may limit successful upper (>10 x 106) cohort treatments. VEGf-2 expression on enriched CD34+ cells was variable. Processing and Product Results (N=10) mean (median) range *N=7 (technical loss of 3 samples);** N=9 (technical loss of 1 sample) MMH marrow volume (ml) 395 (396) 377 – 409 Harvest TNC content (x 109) 6.65 ( 6.73) 3.85 – 8.59 Harvest CD34+ content (x 106) 45.3 (50.2) 16.9 – 86.7 Harvest CD34+ % of TNC 0.75% (0.72%) 0.54% – 1.06% Selected CD34+ content (x 106) 17.8 (16.5) 8.4 – 28.9 Selected % CD34+ recovery 40.3% (41.9%) 30.2 – 49.7 Selected %CD34+ viability 97.1% (98.0 %) 96% – 99% Selected % CD34+ purity 82.5% (84.%) 70% – 91% Total processing time (hours) 14.2 (14.0) 11 – 17 SDF-1 induced migration (% of CD34+ cells) 20.2% (17.0%) 9.5% – 35.4% CXCR-4 expression(% of CD34+ cells)* 58.7% (52.0%) 44% – 78% VEGF-2 expression (% of CD34+ cells)** 0.82% (0.86%) 0% – 2.39%
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Zuk, A., M. Gershenovich, Y. Ivanova, R. T. MacFarland, S. P. Fricker, and S. Ledbetter. "CXCR4 antagonism as a therapeutic approach to prevent acute kidney injury." American Journal of Physiology-Renal Physiology 307, no. 7 (October 1, 2014): F783—F797. http://dx.doi.org/10.1152/ajprenal.00685.2013.
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We examined whether antagonism of the CXCR4 receptor ameliorates the loss of renal function following ischemia-reperfusion. CXCR4 is ubiquitously expressed on leukocytes, known mediators of renal injury, and on bone marrow hematopoietic stem cells (HSCs). Plerixafor (AMD3100, Mozobil) is a small-molecule CXCR4 antagonist that mobilizes HSCs into the peripheral blood and also modulates the immune response in in vivo rodent models of asthma and rheumatoid arthritis. Treatment with plerixafor before and after ischemic clamping ameliorated kidney injury in a rat model of bilateral renal ischemia-reperfusion. Serum creatinine and blood urea nitrogen were significantly reduced 24 h after reperfusion, as were tissue injury and cell death. Plerixafor prevented the renal increase in the proinflammatory chemokines CXCL1 and CXCL5 and the cytokine IL-6. Flow cytometry of kidney homogenates confirmed the presence of significantly fewer leukocytes with plerixafor treatment; additionally, myeloperoxidase activity was reduced. AMD3465, a monocyclam analog of plerixafor, was similarly renoprotective. Four weeks postreperfusion, long-term effects included diminished fibrosis, inflammation, and ongoing renal injury. The mechanism by which CXCR4 inhibition ameliorates AKI is due to modulation of leukocyte infiltration and expression of proinflammatory chemokines/cytokines, rather than a HSC-mediated effect. The data suggest that CXCR4 antagonism with plerixafor may be a potential option to prevent AKI.
Dissertations / Theses on the topic "CXCR4 axi"
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BIONDI, MARTA. "Enhancing AML CAR CIK therapeutic potency increasing the localization of engineered cells in the malignant niche and its selectivity by LSCs specific targeting." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/365153.
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La terapia CAR-T rappresenta un approccio promettente, ma ha riportato una ridotta efficacia nella leucemia mieloide acuta (AML), a causa dell’eterogeneità del tumore, dell’assenza di antigeni target AML-specifici e del ruolo del microambiente leucemico nella protezione dei blasti e delle cellule staminali leucemiche (LSC). La nicchia midollare, nella quale risiedono le LSC, è coinvolta in attività che promuovono la progressione leucemica e sopprimono l’ematopoiesi sana. Quindi ipotizziamo che bersagliare le LSC nascoste nella nicchia potesse migliorare l’efficacia delle CAR-T. Per testare la nostra ipotesi, abbiamo agito su due fronti: 1) promuovere una migrazione efficiente delle CAR-T nella nicchia midollare, 2) selezionare un antigene target ristretto ai blasti leucemici e alle LSC. Prima, abbiamo proposto una strategia per guidare le cellule CD33.CAR CIK (Cytokine-Induced Killer), una sottopopolazione di cellule T effettrici, verso la nicchia leucemica. La chemochina CXCL12, rilasciata dalle cellule mesenchimali stromali (MSC), nella nicchia midollare, e il suo recettore CXCR4, sono coinvolti nella regolazione della migrazione dei leucociti all’interno della nicchia. Quindi, abbiamo ipotizzato che sfruttare questo asse potesse migliorare la capacità di homing delle CD33.CAR-CIK nella nicchia e favorire l’eradicazione della leucemia. Tuttavia i protocolli di manipolazione ex vivo delle CD33.CAR-CIK riducono l’espressione di CXCR4, compromettendo la capacità delle cellule infuse di raggiungere la nicchia. Quindi per implementare la capacità di homing delle CD33.CAR-CIK nel microambiente midollare, abbiamo sviluppato delle CD33.CAR-CIK overesprimenti CXCR4, nella sua forma wild-type o iperattiva mutata. Le CIK ingegnerizzate con i costrutti CD33.CAR-CXCR4 hanno mostrato un consistente aumento dell’espressione di CXCR4, senza riportare alterazioni fenotipiche e nelle funzioni effettrici CAR-associate. Inoltre, rispetto alle CD33.CAR-CIK, le cellule CD33.CAR-CXCR4WT -CIK ed in particolare le CD33.CAR-CXCR4MUT-CIK hanno dimostrato non solo una superiore risposta chemotattica in vitro verso il CXCL12 ed i surnatanti delle MSC, ma anche un aumentato homing in vivo. In seguito, per promuovere lo sviluppo di un approccio CAR-T più efficace e sicuro, abbiamo proposto di re-indirizzare il CAR verso un antigene espresso selettivamente dalle cellule AML, ma assente sulle cellule staminali ematopoietiche (HSC). TIM-3 è un immune checkpoint, svolge un ruolo centrale nella regolazione delle risposte immunitarie nell’AML e costituisce un marcatore selettivo per le LSC, senza essere espresso dalle HSC. Abbiamo disegnato un CAR di terza generazione diretto contro TIM-3, utilizzando la porzione scFv derivante da un anticorpo monoclonale anti-TIM-3. In vitro, le TIM-3.CAR-CIK hanno dimostrato di eliminare sia le linee AML che i blasti primari, senza dare tossicità verso le cellule TIM-3+ sane, come le CIK attivate, i monociti e le cellule NK. Inoltre, le TIM-3.CAR-CIK hanno eliminato in maniera selettiva le LSC (CD34+ CD38-). Infine, le TIM-3.CAR-CIK hanno mantenuto le loro capacità effettrici nonostante multiple ristimolazioni in vitro, gettando le basi per lo studio di questo costrutto in vivo. Complessivamente, entrambi gli approcci, uno implementando l’homing delle CAR-CIK alla nicchia midollare e l’altro conferendo una superiore selettività, potrebbero migliorare l’efficacia della terapia CAR-T nel contesto dell’AML.Chimeric Antigen Receptor (CAR) T-cell therapy has produced remarkable clinical responses in patients affected by acute lymphoblastic leukemia. Unfortunately, CAR T-cells have not been equally successful in acute myeloid leukemia (AML) due to tumor heterogeneity, lack of truly AML-restricted target antigens and the role of leukemia microenvironment in blasts protection and leukemia stem cells (LSCs) maintenance. Specifically, the bone marrow (BM) niche, where LSCs reside, is involved in leukemia promoting activities whilst suppressing normal hematopoiesis. Therefore, we hypothesized that targeting LSCs at their location may enhance the potency and selectivity of CAR-T cells. To address this issue, we have designed two aims: 1) promote rapid and efficient localization of CAR T-cells within the BM niche, 2) select a leukemia-restricted antigen to specifically target AML blasts and LSCs. First, we proposed to harness CD33.CAR-redirected Cytokine-Induced Killer (CIK) cells, an alternative effector T-cell population with acquired NK-like cytotoxic activity as well as minimal alloreactivity, to selectively route their activity to leukemia transformed niche. The chemokine ligand 12 (CXCL12), released by mesenchymal stromal cells (MSCs) within the medullary niche, and its chemokine receptor 4 (CXCR4) are two pivotal players regulating leukocytes trafficking to the BM. In AML, CXCL12 interacts with CXCR4 overexpressed on blasts, promoting their migration and homing in the niche. Hence, taking advantage of this axis might facilitate CD33.CAR-CIK cells homing to the BM and therefore leukemia eradication. However, ex vivo manipulation protocols of CD33.CAR-CIK cells consistently downregulate CXCR4 expression and may affect the capacity of adoptively infused cells to migrate to BM and exert their anti-leukemic action. Therefore, to improve CD33.CAR-CIKs homing in the BM microenvironment we have developed CD33.CAR-CIK cells overexpressing CXCR4, in its wild-type or hyperactive mutant form. Notably, CIK cells engineering with CD33.CAR-CXCR4 constructs led to a consistent increase in CXCR4 expression, without altering CIK cells phenotype and CAR-related effector functions. Interestingly, compared to conventional CD33.CAR-CIK cells, CD33.CAR-CXCR4WT and especially CD33.CAR-CXCR4MUT-CIK cells demonstrated significantly superior in vitro chemotactic response toward CXCL12 and MSC-derived supernatants, and greater in vivo BM homing ability and persistence. Furthermore, to develop an effective anti-AML CAR T-cell therapy, it is fundamental to identify a LSC-specific marker, sparing the normal counterpart of hematopoietic stem cells (HSCs). T-cell immunoglobulin and mucin protein 3 (TIM-3) is an immune checkpoint molecule, it plays a central role in immune responses in AML and it is an LSC-specific marker, lacking expression on HSCs. Therefore, we designed a third-generation anti-TIM-3.CAR using the single-chain fragment variable (scFv) derived from an antagonistic ligand-blocking anti-TIM-3 antibody. In vitro, TIM-3.CAR-CIK cells efficiently killed both AML cell lines and primary AML blasts, but not normal TIM-3+ activated CIK cells, monocytes and NK-cells. Notably, we observed selective elimination of primary LSC-enriched population (CD34+ CD38-). Furthermore, TIM-3.CAR-CIK cells maintained their effector functions despite multiple in vitro restimulations, setting the basis for further exploration in in vivo models. Overall, both approaches, one improving CAR-CIK cells homing to the transformed niche and the other conferring superior safety and selectivity, might improve the efficacy of anti-AML CAR-CIK therapy.
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SOLARI, AGNESE. "CXCR4/CXCR7-CXCL11/CXCL12 AXIS PROMOTES MALIGNANT PHENOTYPE IN PUTATIVE STEM CELLS FROM HUMAN MENINGIOMAS." Doctoral thesis, Università degli studi di Genova, 2019. http://hdl.handle.net/11567/946169.
Full textAbstract:
Meningioma is the most frequent primary tumor of the central nervous system. The
greatest percentage of meningiomas is benign tumors (WHO grade I). However,
although surgical and radiotherapy techniques have significantly improved over the
years, some meningiomas, independently from the grading, are refractory to
multimodality therapies, and recur and/or undergo malignant transformation,
representing an unsolved therapeutic challenge. Therefore, beside histopathologic
benign appearance, biologically aggressive meningiomas need to be molecularly
characterized, to identify novel therapeutic targets.
In malignant tumors, recurrence is mainly ascribed to the presence of cancer stem
cells (CSCs) which are expression of tumor cell heterogeneity, and sustain
tumorigenesis, metastasization and drug resistance.
CSCs are characterized by stem cell marker expression, self-renewal, and ability to
differentiate into tumor-specific cell types. Recently, CSCs and their functional role
have been also studied in benign tumors, including meningioma. A range of genes
and proteins have been proposed to identify meningioma stem-like cells, among
them CD105, a transmembrane glycoprotein, involved in angiogenesis and in the
progression of a variety of tumors. Stemness, as well as cancer cell aggressive
behavior, is a cell property strictly linked to tumor microenvironment: reciprocal
interactions between growth factors, cytokines and chemokines released by both
CSCs and other cell types forming the niche, modulate each other to sustain tumor
growth. Chemokine signaling, and the CXCL11/CXCL12-CXCR4/CXCR7 system in
particular, drives cell proliferation and migration in several solid tumors. On these
premises, this study is focused on the isolation and characterization of stem-like
cells from post-surgical samples of human meningiomas, delving deeply into the
role of this subpopulation in meningioma aggressive behavior. Moreover, we
analyzed the contribution of CXCR4-7 receptors in the regulation of their biological
properties. Twenty-eight primary cell cultures have been obtained from 35
meningiomas, and maintained in stem cell-permissive culture conditions to enrich
in CSCs. Putative meningioma stem cells rapidly grow, form meningospheres and
express stem markers, such as Sox2, NANOG, CD133 and Oct-4. Conversely, CD105
was not differentially expressed between stem-like cells and their “non-stem”
counterpart, cells grown in serum-containing medium. Moreover, stem-like cells
displayed high migratory capacity and in vitro angiogenic activity, supporting their
malignant phenotype. Meningioma stem-like cells displayed a distinct chemokinereceptor
profile from “non-stem” cell population, and selectively respond to in vitro
CXCL11 and CXCL12 stimulation enhancing proliferation, migration and vascular
mimicry. Pharmacological inhibition of individual CXCR4 or CXCR7 significantly
impaired CXCL12- and CXCL11-induced proliferation, chemotaxis and vessel-like
structure formation, therefore suggesting that these activities are mediated by both
receptors. We speculated that these receptors act as heterodimers, formed upon
ligand activation and that the blockade of one of them results in a complete
inhibition of biological effects.
Overall our results, collected from a large number of meningioma cell cultures
derived from different patients, allow the identification of a tumor subpopulation
endowed with comm
on stem cell-like features, and suggest that both CXCR4 and
CXCR7 signaling sustains meningioma stem cell phenotype. Prospectively, the
isolation and culture of stem-like cells directly from the meningioma tissues will
allow to test new therapeutic compounds to block meningioma growth and
invasiveness, in particular for those tumors showing an unpredictable aggressive
behavior. In this context, we propose that the CXCR4-7 chemokinergic system might
represent a relevant pharmacological target.
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Mikami, Sakae. "Blockade of CXCL12/CXCR4 axis ameliorates murine experimental colitis." Kyoto University, 2009. http://hdl.handle.net/2433/124258.
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Howard, Cory M. "Characterization of the CXCR4-LASP1-eIF4F Axis in Triple-Negative Breast Cancer." University of Toledo Health Science Campus / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=mco1596298549051863.
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Das, Avik. "Ischemic stroke in type II diabetic mice: Deregulation of SDF-1a/CXCR4 axis." Wright State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=wright1247594137.
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Rondeau, Vincent. "Rôle de la désensibilisation de CXCR4 dans la spécification lympho-myéloïde des progéniteurs hématopoïétiques multipotents. Lymphoid differentiation of hematopoietic stem cells requires efficient Cxcr4 desensitization New method to obtain lymphoid progenitors CXCR4-driven mitochondrial metabolic pathways shape the lympho-myeloid fate of hematopoietic multipotent progenitors." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASQ022.
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Les cellules souches et progéniteurs hématopoïétiques (CSPHs), incluant les progéniteurs multipotents (MPPs), sont responsables de la production des cellules immunes circulantes. Ils résident dans la moelle osseuse (MO) au sein de structures spécialisées, les niches endostéale et (péri)-vasculaire, qui régulent la spécification et l'engagement lymphoïde versus myéloïde des CSPHs. Dans la MO, le couple formé par la chimiokine CXCL12 et l’un de ses récepteurs, CXCR4, exerce un rôle clé dans la régulation de la rétention et la quiescence des CSPHs. Ces processus sont dérégulés dans le Syndrome WHIM (SW), une maladie immuno-hématologique rare liée à des mutations autosomiques dominantes du gène codant CXCR4, qui altèrent la désensibilisation du récepteur et conduisent à un gain de fonction en réponse à CXCL12. Cliniquement, le SW se caractérise notamment par une profonde leucopénie circulante qui affecte les lignages lymphoïde et myéloïde et dont les mécanismes restent à déterminer. Grâce à un modèle murin génétiquement modifié du SW et à l'accès à des prélèvements biologiques de patients atteints du SW, nous avons testé l'hypothèse que la lymphopénie circulante associée au SW résultait de défauts hématopoïétiques dans la MO. Nous avons révélé un rôle clé de la désensibilisation de CXCR4 dans la différenciation lymphoïde des CSPHs et identifié les MPPs comme étant le stade défectueux dans le SW. La divergence entre les lignages lymphoïde et myeloïde se produit précisément à ce stade au sein duquel règne une hétérogénéité : les MPP2/3 sont biaisés myéloïde et les MPP4 sont orientés lymphoïde. Notre compréhension de la façon dont les signaux extrinsèques (niches) et intrinsèques aux MPPs déterminent leur devenir lymphoïde versus myéloïde est encore parcellaire. Dans ce contexte, l’objectif de ma thèse a été de déterminer si et comment la signalisation de CXCR4 régule la dépendance énergétique des MPPs et à comprendre comment les voies métaboliques façonnent leur spécification lympho-myéloïde. Dans la MO des souris porteuses de la mutation gain de fonction de Cxcr4, nous avons observé une diminution du nombre de MPP4 qui contrastait avec l'augmentation des MPP2/3. L’analyse de prélèvements médullaires de patients a également permis de rapporter une diminution de la fréquence des progéniteurs lymphoïdes et une augmentation de celle des progéniteurs myéloïdes. Chez la souris mutantes, ce biais myéloïde du compartiment de MPPs s'avèrait associé à une expansion anormale et une reprogrammation moléculaire et métabolique des MPP4. Fait marquant, un traitement chronique par l’AMD3100, un antagoniste de CXCR4, permettait de normaliser le nombre de MPP4 dans la MO, de restaurer leurs propriétés métaboliques, et de corriger la lymphopénie des souris mutantes. Par conséquent, nos résultats suggèrent que l’axe CXCL12/CXCR4 est requis au maintien du potentiel lymphoïde des MPP4 au travers de la modulation de leur activité métabolique mitochondrialeHematopoietic stem and progenitor cells (HSPCs), including the multipotent progenitors (MPPs), are responsible for replenishing immune cells. They reside in bone marrow (BM) endosteal and (peri)-vascular niches, which provide all cellular and molecular components required for their lifelong maintenance and fate. Among them, the CXCL12 chemokine and one of its receptor, CXCR4, exert a dominant role in promoting HSPC retention and quiescence. These processes are deregulated in the WHIM Syndrome (WS), a rare immunodeficiency caused by inherited heterozygous autosomal gain-of-function CXCR4 mutations that affect homologous desensitization of the receptor. Clinically, WS is notably characterized by severe, chronic circulating lymphopenia whose mechanisms remain to be elucidated. Using a mouse model carrying a naturally occurring WS-linked Cxcr4 mutation as well as human BM and blood samples, we explored the possibility that the lymphopenia in WS originates from defects at the HSPC level in BM. We reported that Cxcr4 desensitization is required for lymphoid differentiation of HSPCs and further identified the MPP stage as defective in mutant mice. The divergence between lymphoid and myeloid lineages occurs at the MPP stage, which is composed of distinct subpopulations, i.e., MPP2 and MPP3 are reported as distinct myeloid-biased MPP subsets that operate together with lymphoid-primed MPP4 to control blood leukocyte production. Our understanding of how cell-extrinsic niche-related and cell-intrinsic cues drive the lymphoid versus myeloid fate decision of MPPs is still fragmentary. Therefore, my PhD project aimed at determining whether and how CXCR4 signaling regulates bioenergetics demands of MPPs and at understanding how these metabolic pathways shape the lympho-myeloid fate of MPPs. We unraveled a myeloid skewing of the HSPC compartment in BM of WS mice and patients. In mutant mice, this partly relied on the contraction of the MPP4 pool and on cell-autonomous molecular and metabolic changes that reprogramed MPP4 away from lymphoid differentiation. Interestingly, chronic treatment with the CXCR4 antagonist AMD3100 normalized mitochondrial metabolism and fate of MPP4, while correcting circulating lymphopenia in WS mice. This study provides evidence that CXCR4 signaling acts as an essential gatekeeper for integrity of the mitochondrial machinery, which in turn controls lymphoid potential of MPP4
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Goh, Poh. "Roles of protein kinase C and arrestin in migration of cells via CXCR4/CXCL12 signalling axis." Thesis, University of East Anglia, 2018. https://ueaeprints.uea.ac.uk/67806/.
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Aim: The chemokine system not only coordinates leukocyte migration in immunity and inflammation, but it is also implicated in the pathogenesis of many human diseases, including cancer. The expression of chemokines and their receptors is altered in many malignancies and leads to aberrant chemokine receptor signalling. Emerging evidence indicates that the tumour microenvironment has critical roles in all aspects of cancer biology, including growth, angiogenesis, metastasis and progression. One of the important representatives of this system are the chemokine ligand CXCL12 and its receptor, CXCR4 as they are most commonly found on human and murine cancer cells. Our aims are to study and understand if there are any differences in activation of signalling molecules in the downstream signalling cascades in CXC- chemokine receptors in different cell types, and to identify the importance of different effector proteins in migration of cells; the two proteins of interest include Protein Kinase C (PKC) and arrestins. Methodology: Experimentation was undertaken in MCF-7 breast cancer cells and Jurkat leukemic T-lymphocytes which both naturally express the chemokine receptor CXCR4. Small molecule inhibition and protein overexpression was used in chemotaxis and calcium release assays to measure cellular responses. Immunocytochemistry was used to determine the effect of protein blocking and protein overexpression on receptor internalisation, protein localisation and the formation of cellular structures associated with migration. Results: Inhibition of PKC has no effect on Jurkat cell migration, but it blocks MCF-7 cell migration showing that there is a difference in the usage of PKC in different cell types. Arrestin 3 is important for migration in both suspension Jurkat cells and adherent breast cancer MCF-7 cells. Conclusion: Our study shows that CXCL12-induced migration may be arrestin 3 mediated. We have also shown that activation of signalling molecules needed for CXCL12-induced migration can differ between different cell lines. Overall, the research in this thesis has identified potential signalling molecules that can be targeted to interfere with migration of cells.
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Kato, Itaru. "Identification of hepatic niche harboring human acute lymphoblastic leukemic cells via the SDF-1/CXCR4 axis." Kyoto University, 2012. http://hdl.handle.net/2433/157438.
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Swidenbank, Isabella. "The role of the CXCR4-CXCL12 chemokine axis in melanoma metastasis to the normal and fibrotic liver." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2612.
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Malignant melanoma represents the most aggressive form of skin cancer. Although early stage disease is treatable through surgical excision alone, late stage tumours frequently metastasise to the liver, at which point treatment options remain limited. Migration of melanoma towards metastatic sites has been shown to be associated with the CXCR4-CXCL12 chemokine axis. The chemokine receptor CXCR4 is expressed by melanoma cells and the chemokine CXCL12 is secreted by the liver. Expression of CXCL12 has been shown to be increased in liver fibrosis and therefore it was hypothesized that cells involved in liver damage may promote melanoma metastasis to this organ. CXCR4 and CXCL12 expression in melanoma and liver cells in vitro and in vivo was examined by RT-PCR, Western blotting and immunohistochemical staining. Chemotaxis assays were performed to test the ability of AMD11070 to inhibit migration of melanoma cells. Quantitative RT-PCR and Western blotting determined the influence of different fibrosis models (Carbon tetrachloride (CCl4), Bile Duct Ligation (BDL) and Methapyrilene (MP)) on CXCL12 expression. Furthermore, the migration of melanoma was examined in animal models of liver injury. Results showed that melanoma cells and different liver cell types (myofibroblasts and biliary epithelial cells) express both CXCR4 and CXCL12. CXCR4 expression in melanoma promoted migration of tumour cells towards CXCL12 secreting liver cells and AMD11070 inhibited this. CXCR4 and CXCL12 proteins of varying sizes were observed in vivo suggesting that post translational modifications of these proteins may occur. CXCL12 expression increased in three models of chronic liver injury; CCl₄, BDL and MP. In an animal model, murine melanoma cells metastasized to the lungs and to both the fibrotic and normal liver. These findings suggest that the reduction of liver cells secreting CXCL12 may help to reduce melanoma metastasis to this organ.
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Chow, Yan Ching Ken. "Role and Molecular Basis of the CXCL12-signalling Axis in the Pathogenesis of WHIM syndrome and the carcinogenesis associated with human papillomavirus (HPV) infection." Paris 7, 2008. http://www.theses.fr/2008PA077129.
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Le syndrome WHIM (SW) est un déficit rare caractérisé par une leuco-neutropénie (e. X. Myélokathexis) et la profusion des verrues cutanées et de carcinomes ano-génitaux due au Papillomavirus Humain (HPV). Il est associé à des dysfonctions du chimiorécepteur CXCR4 en réponse à son ligand SDF-1/CXCL12, qui sont souvent liées à des mutations hétérozygotes de CXCR4 conduisant à la troncation de l'extrémité C-terminale du récepteur impliquée dans le recrutement de l'arrestine (βarr) pour le processus de désensibilisation. Le récepteur muté (e. X. CXCR4¹º¹³) qui n'est donc plus désensibilisé et présente un gain de fonction confère aux leucocytes des patients des réponses exacerbées à CXCL12 dont nous proposons qu'elles contribuent à la pathogenèse du SW. Dans cette thèse, nous montrons que ces dysfonctions impliquent une association inattendue entre CXCR4¹º¹³ et βarr2. Cette interaction se traduit par une activation accrue et prolongée des voies de signalisation dépendantes de βarr2 en aval du récepteur et également de l' intégrité de la troisième boucle intracellulaire de CXCR4¹º¹³. Nous identifions que CXCR4¹º¹³ forme des dimères avec son homologue sauvage au sein desquels une association possible renforcée entre barr2 et CXCR4¹º¹³ pourrait contribuer aux réponses exacerbées à CXCL12. L'expression anormale de CXCL12 que nous avions identifiée dans les lésions dues à HPV provenant d'individus souffrants ou non du SW et le rôle critique de cette chimiokine dans le développement de nombreux cancers suggèrent l'implication de cet axe de signalisation dans la pathogénie virale. Dans les kératinocytes immortalisés par HPV à haut-risque, nous observons une expression anormale de CXCL12 et de ses deux récepteurs que nous caractérisons comme étant dépendante des protéines virales HPV-E6/7 et nécessaire à la prolifération et la migration des kératinocytes. Dans le contexte du SW, ce processus en coopération avec l'activation incontrôlée de CXCR4¹º¹³ pourrait contribuer à la maîignisation des lésions ano-génitales alors même que nous y avons identifié la seule présence d'HPV à faible potentiel cancérogène (bas-risque)The WHIM syndrome (WS) is a rare immunodeficiency characterised by severe leukoneutropenia (e. G. Myelokathexis) and profuse human papillomavirus (HPV)-associated skin lesions and malignant ano-genital cohdyloma. The disease links to dysfunctions of the CXCR4 chemokine receptor in response to its ligand SDF-1/CXCL12, and associates in many cases to heterozygous mutations causing truncation in the cytoplasmic tail of the receptor that is important for the β-arrestin (βarr)-mediated receptor desensitisation process. Such truncated receptor (e. G. CXCR4¹º¹³) displays no desensitisation and thus manifests a gain of function in response to CXCL12 in leukocytes derived from WS patients, which likely contribute to the pathogenesis of the disorder. In this study, we demonstrated that such dysfunctions are in fact dependent on an unexpected interaction between βarr2 and CXCR4¹º¹³. Upon CXCL12 stimulation, the CXCR4¹º¹³receptor displays an augmented and prolonged |3arr2-dépendent signalling that relies on the integrity of the third intracellular loop of the receptor. We have also observed the existence of CXCR4wt/CXCR4¹º¹³ heterodimer from which the possible enhanced parr2/CXCR4¹º¹³ interaction may contribute to the augmented response of the receptor to CXCL12. With the abnormal expression of CXCL12 we observed in HPV-induced lesions derived from both WS and non-WS patients, and the critical role of the chemokine in tumor growth and metastasis, we speculate on the existence of an HPV/CXCL12 interplay that could be crucial for the viral-mediated pathogenesis. Using keratinocytes immortalised by the subgenomic fragment of high-risk HPV, we showed an HPV-E6/7-dependent expression of CXCL12 and its receptors and the critical role of this signalling axis in the prolifération and motility of these cells. In WS, such HPV/CXCL12-interplay may synergise with the hyperfunctioning of CXCR4, and contribute to the malignant development of ano-genital condyloma that is unusually associated with low-risk HPV - the only viral subtype we identified in these lesions
Conference papers on the topic "CXCR4 axi"
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Costello, Christine M., Brian McCullagh, Katherine Howell, John A. Belperio, Michael P. Keane, Sean P. Gaine, and Paul McLoughlin. "A Role For The CXCL12/CXCR7/CXCR4 Axis In Pulmonary Hypertension." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3399.
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Balthazar, L., M. Cebo, J. Rheinlaender, D. Rath, M. Gawaz, T. E. Schäffer, M. Lämmerhofer, and M. Chatterjee. "Platelet Lipidome and Lipid Induced Thromboinflammatory Actions are Influenced by the CXCL12-CXCR4-CXCR7 Axis." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680094.
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Balthazar, L., M. Cebo, J. Rheinlaender, D. Rath, M. Gawaz, T. E. Schäffer, M. Lämmerhofer, and M. Chatterjee. "Platelet Lipidome and Lipid Induced Thromboinflammatory Actions are Influenced by the CXCL12-CXCR4-CXCR7 Axis." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680195.
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D'Alterio, Crescenzo, Antonio Avallone, Paolo Delrio, Fabiana Tatangelo, Biagio Pecori, Elena Di Gennaro, Rosario Vincenzo Iaffaioli, Paolo Muto, Gerardo Botti, and Stefania Scala. "Abstract 1145: CXCR4-CXCL12-CXCR7 axis predicts prognosis in locally advanced-Chemo Radiotherapy (CRT) treated rectal cancer patients." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1145.
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Clements, D., LM Markwick, and SR Johnson. "The CXCR4/CXCL12 Axis in Lymphangioleiomyomatosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4350.
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Cho, Byung Sik, Zhihong Zeng, Hong Mu, Teresa McQueen, Marina Protopopova, Jorge Cortes, Joe Marszalek, et al. "Abstract 4768: Novel peptidic CXCR4 antagonist LY2510924 disrupts the SDF-1α/CXCR4 axis resulting in anti-AML efficacyin vivo." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4768.
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Yu, Minghuan, and Mary A. Kosir. "Abstract 5276: CXCL7/CXCR2 axis and invasion." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5276.
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Petty, JM, CC Lenox, E. Burg, A. Panoskaltsis-Mortari, and BT Suratt. "Modulation of the Marrow CXCR4/SDF-1 Axis during Lung Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4019.
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Singh, Seema, Sudha Talwar, Sanjeev Srivastava, Sarah Braune, Laurie B. Owen, and Ajay P. Singh. "Abstract 5378: Targeting CXCL12/CXCR4 signaling axis for pancreatic cancer therapy." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5378.
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Jungbauer, F., C. Aderhold, N. Rotter, A. Lammert, B. Kramer, B. Kuhlin, C. Thorn, and K. Hörmann. "The SDF1-CXCR4-axis in HPV-positive and HPV-negative HNSCC." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640057.
Full textReports on the topic "CXCR4 axi"
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Yu, Xiuping. Wnt/beta-Catenin, Foxa2, and CXCR4 Axis Controls Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada609497.
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Yu, Xiuping. Wnt/Beta-Catenin, Foxa2, and CXCR4 Axis Controls Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada591009.
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Vanhoy, Lyndsay. The SDF1-CXCR4 Axis Functions through p38-MAPK Signaling to Drive Breast Cancer Progression and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada495339.
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Vanhoy, Lyndsay. The SDF1-CXCR4 Axis Functions through p38-MAPK Signaling to Drive Breast Cancer Progression and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada517434.
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Nussloch, Gwyneth H. The CXCR/EGFR Axis in the Initiation and Progression of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada561905.
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