Готові списки джерел за темами / Cxcr1-2

Добірка наукової літератури з теми "Cxcr1-2"

Автор: Grafiati
Опубліковано: 6 липня 2024

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  3. Книги
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Статті в журналах з теми "Cxcr1-2":

1

Zhang, Jing, Shouguo Huang, Lini Quan, Qiu Meng, Haiyan Wang, Jie Wang, and Jin Chen. "Determination of Potential Therapeutic Targets and Prognostic Markers of Ovarian Cancer by Bioinformatics Analysis." BioMed Research International 2021 (March 19, 2021): 1–13. http://dx.doi.org/10.1155/2021/8883800.

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This study is to study the expression of CXCRs in ovarian cancer tissues and their value in prognosis. The expressions of CXCR1-CXCR7 mRNA between ovarian tumor tissues and normal tissues and in different pathological types of ovarian tumor tissues were compared by ONCOMINE online tool. The relationship between the expression of CXCRs and clinical pathological staging was studied by GEPIA. Kaplan-Meier plotter online tool was used to analyze prognosis. Finally, GO and KEGG analyses and protein interaction network analysis were performed for CXCRs by the DAVID software to predict their function, and cBioPortal was used to identify the key functional genes. The expression of CXCR3/4/7 mRNA in ovarian cancer tissues was higher than that in normal ovarian tissues, and the expression of CXCR4 was the highest ( fold change = 306.413 , P < 0.05 ). The expression of CXCR1/2/3/4/7 mRNA in different pathological types of ovarian tumors was significantly different ( P < 0.05 ). Only CXCR5 expression level was associated with tumor staging. Survival analysis showed that high CXCR7 mRNA expression and low CXCR5/6 expression were associated with the shortening of overall survival. High CXCR4/7 expression and low CXCR5/6 expression were associated with the shortening of progression-free survival. High CXCR2/4 expression and low CXCR5/6 expression were closely related to the shortening of postprogressing survival. Protein interaction network analysis showed that GNB1, PTK2, MAPK1, PIK3CA, GNB4, GNA11, KNG1, and ARNT proteins were closely related to the CXC receptor family. CXCR3/4/7 are potential therapeutic targets, and CXCR2/4/5/6/7 are new markers for the prognosis of ovarian cancer.
2

Doroshenko, Tatyana, Yuri Chaly, Valery Savitskiy, Olga Maslakova, Anna Portyanko, Irina Gorudko, and Nikolai N. Voitenok. "Phagocytosing neutrophils down-regulate the expression of chemokine receptors CXCR1 and CXCR2." Blood 100, no. 7 (October 1, 2002): 2668–71. http://dx.doi.org/10.1182/blood.100.7.2668.

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CXC chemokines play a central role in regulation of neutrophil activation and chemotaxis. Because the chemotactic responses of neutrophils are impaired after phagocytosis, we explored the effect of phagocytic stimuli on the expression of interleukin-8 (IL-8) receptors, CXCR1 and CXCR2, in human neutrophils. After phagocytosis of opsonized yeast, the expression of CXCR1 and CXCR2 was substantially down-regulated and was accompanied by reduced Ca++responses to corresponding ligands, IL-8 and neutrophil-activating peptide–2 (NAP-2). The levels of CXCR1 and CXCR2 mRNA were constant during phagocytic stimulation of neutrophils. Confocal microscopy revealed that CXCR reduction was not via internalization. Metalloproteinase inhibitor, 1,10-phenantroline, prevented the reduction of CXCRs induced by phagocytosis, indicating that proteolytic degradation may be responsible for down-regulation. These observations suggest that down-regulation of CXCR expression may substantially reduce the responsiveness of phagocytosing neutrophils to CXC chemokines.
3

Konrad, F. M., and J. Reutershan. "CXCR2 in Acute Lung Injury." Mediators of Inflammation 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/740987.

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In pulmonary inflammation, recruitment of circulating polymorphonuclear leukocytes is essential for host defense and initiates the following specific immune response. One pathological hallmark of acute lung injury and acute respiratory distress syndrome is the uncontrolled transmigration of neutrophils into the lung interstitium and alveolar space. Thereby, the extravasation of leukocytes from the vascular system into the tissue is induced by chemokines that are released from the site of inflammation. The most relevant chemokine receptors of neutrophils are CXC chemokine receptor (CXCR) 1 and CXCR2. CXCR2 is of particular interest since several studies implicate a pivotal role of this receptor in development and promotion of numerous inflammatory disorders. CXCR2 gets activated by ELR+chemokines, including MIP-2, KC (rodents) and IL-8 (human). Since multiple ELR+CXC chemokines act on both receptors—CXCR1 and CXCR2—a pharmacologic agent blocking both receptors seems to be advantageous. So far, several CXCR1/2 antagonists have been developed and have been tested successfully in experimental studies. A newly designed CXCR1 and CXCR2 antagonist can be orally administered and was for the first time found efficient in humans. This review highlights the role of CXCR2 in acute lung injury and discusses its potential as a therapeutic target.
4

Feniger-Barish, Rotem, Dan Belkin, Alon Zaslaver, Shira Gal, Mally Dori, Maya Ran, and Adit Ben-Baruch. "GCP-2–induced internalization of IL-8 receptors: hierarchical relationships between GCP-2 and other ELR+-CXC chemokines and mechanisms regulating CXCR2 internalization and recycling." Blood 95, no. 5 (March 1, 2000): 1551–59. http://dx.doi.org/10.1182/blood.v95.5.1551.005a36_1551_1559.

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The chemotactic potencies of ELR+-CXC chemokines during acute inflammation are regulated by their binding affinities and by their ability to activate, desensitize, and internalize their specific receptors, CXCR1 and CXCR2. To gain insight into the fine mechanisms that control acute inflammatory processes, we have focused in this study on the highly potent ELR+-CXC chemokine Granulocyte Chemotactic Protein 2 (GCP-2), and on its ability to control the cell surface expression of CXCR1 and CXCR2. Although GCP-2 has been considered an effective ligand for both CXCR1 and CXCR2, our findings demonstrated that it was a potent inducer of CXCR2 internalization only. A functional hierarchy was shown to exist between GCP-2 and 2 other ELR+-CXC chemokines, IL-8 and NAP-2, in their abilities to induce CXCR1 and CXCR2 internalization, according to the following: IL-8 &gt; GCP-2 &gt; NAP-2. By the use of pertussis toxin (PTx), it was demonstrated that the actual events of Gi-coupling to CXCR2 do not have a major role in the regulation of its internalization. Rather, CXCR2 internalization was shown to be negatively controlled by induction of signaling events, as indicated by the promotion of CXCR2 internalization following exposure to wortmannin, a potent inhibitor of phosphatidylinositol (PI) 3 kinases and PI4 kinases. Furthermore, our results suggest that rab11+-endosomes participate in the trafficking of CXCR2 through the endocytic pathway, to eventually allow its recycling back to the plasma membrane. To conclude, our findings shed light on the interrelationships between GCP-2 and other ELR+-CXC chemokines, and determine the mechanisms involved in the regulation of GCP-2–induced internalization and recycling of CXCR2.
5

Smithson, Alex, Maria Rosa Sarrias, Juanjo Barcelo, Belen Suarez, Juan Pablo Horcajada, Sara Maria Soto, Alex Soriano, et al. "Expression of Interleukin-8 Receptors (CXCR1 and CXCR2) in Premenopausal Women with Recurrent Urinary Tract Infections." Clinical Diagnostic Laboratory Immunology 12, no. 12 (December 2005): 1358–63. http://dx.doi.org/10.1128/cdli.12.12.1358-1363.2005.

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ABSTRACT The migration of neutrophils through infected tissues is mediated by the CXC chemokines and its receptors (CXCR1 and CXCR2). It has been proposed that a CXCR1 deficiency could confer susceptibility to acute pyelonephritis in children. The objective of the study is to assess the surface expression of CXCR1 and CXCR2 and the existence of polymorphisms in the CXCR1 gene in premenopausal women with recurrent urinary tract infections. The study included 20 premenopausal women with recurrent urinary infections, with normal urinary tracts, and without diseases potentially associated with relapsing urinary infections and 30 controls without previous urinary infections. The levels of CXCR1 and CXCR2 expression on neutrophils were measured and analyzed by flow cytometry by measuring the mean fluorescence intensity (MFI) channel. The promoter and coding regions of the CXCR1 gene were analyzed for the presence of polymorphisms by a sequence-based typing method. Patients with recurrent urinary tract infections exhibited median levels of CXCR1 expression, determined from MFI values, similar to those of the controls. The analysis of CXCR2 showed that patients with recurrent urinary infections had lower median levels of expression, determined from the MFI values, than the controls (P = 0.002, Mann-Whitney U test). No polymorphisms were detected at the promoter or at the exon 1 region of the CXCR1 gene either in the patients or in the controls. Polymorphisms were detected at the exon 2 of CXCR1, but their frequencies did not differ between patients and controls. We have found a low level of CXCR2 expression in patients with recurrent urinary tract infections. These results suggest that a low level of CXCR2 expression may increase the susceptibilities of premenopausal women to urinary tract infections.
6

Molczyk, Caitlin, and Rakesh K. Singh. "CXCR1: A Cancer Stem Cell Marker and Therapeutic Target in Solid Tumors." Biomedicines 11, no. 2 (February 16, 2023): 576. http://dx.doi.org/10.3390/biomedicines11020576.

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Therapy resistance is a significant concern while treating malignant disease. Accumulating evidence suggests that a subset of cancer cells potentiates tumor survival, therapy resistance, and relapse. Several different pathways regulate these purported cancer stem cells (CSCs). Evidence shows that the inflammatory tumor microenvironment plays a crucial role in maintaining the cancer stem cell pool. Typically, in the case of the tumor microenvironment, inflammatory pathways can be utilized by the tumor to aid in tumor progression; one such pathway is the CXCR1/2 pathway. The CXCR1 and CXCR2 receptors are intricately related, with CXCR1 binding two ligands that also bind CXCR2. They have the same downstream pathways but potentially separate roles in the tumor microenvironment. CXCR1 is becoming more well known for its role as a cancer stem cell identifier and therapeutic target. This review elucidates the role of the CXCR1 axis as a CSC marker in several solid tumors and discusses the utility of CXCR1 as a therapeutic target.
7

Ngo, Hai, Evdoxia Hatjiharissi, Xavier Leleu, Judith Runnels, Anne-Sophie Moreau, Xiaoying Jia, Garrett O’Sullivan, et al. "The CXCR4/SDF-1 Axis Regulates Migration and Adhesion in Waldenstrom Macroglobulinemia." Blood 108, no. 11 (November 1, 2006): 2418. http://dx.doi.org/10.1182/blood.v108.11.2418.2418.

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Abstract Background: Waldenstrom Macroglobulinemia (WM) is characterized by widespread involvement of the bone marrow (BM), and lymphadenopathy in 20% of the patients, implying continuous trafficking of WM cells into and out of the BM and lymph nodes. The normal process of B-cell homing is regulated by cytokines, chemokines, and adhesion molecules. One of the most extensively studied chemokines in migration is stromal derived factor SDF-1 and its receptor CXCR4. Here we study the role of chemokine receptors, and the SDF-1/CXCR4 axis on migration and adhesion in WM. Methods: Flow cytometry for CXC and CC chemokine receptors (CXCR1, CXCR2, CXCR3, CXCR4, CXCR5, CCR2, CCR4, CCR5, CCR6 and CCR7), and adhesion molecules (VLA-4 and LFA-1) on WM cell lines (BCWM.1 and WM-WSU) and patient samples was performed. Migration was determined using the transwell migration assay (Costar, NY). Cells were placed in the upper chambers of the migration assay with 1% FCS medium in the presence of serial concentrations of SDF-1 in the lower chambers. After 4 hours of incubation, cells that migrated to the lower chambers were counted. Similarly, adhesion was determined using an adhesion assay (EMD Biosciences, San Diego, CA) with 96-well plated coated with fibronectin. Immunoblotting for proteins downstream of CXCR4 was performed. The CXCR4 inhibitor AMD3100 (10–100uM, Sigma, MO) and Gi protein inhibitor pertussis toxin PTX (10–200ng/ml, Sigma, MO) were used to inhibit CXCR4 signaling. Results: The following chemokine receptors were expressed on patient CD19+WM cells with over 30% expression: CXCR1 (mean 60%), CXCR2 (mean 47%), CXCR4 (mean 47%), CXCR5 (mean 69%), CCR4 (mean 54%) and CCR6 (mean 61%). Similar expression was observed on WM cell lines. We next determined the effect of SDF-1 on migration and signaling pathways in WM. SDF-1 (10–100nM) induced migration in a bell-shaped curve with 30nM inducing maximum migration (110% compared to control). SDF-1 30nM induced a rapid activation of signaling pathways downstream of CXCR4 including pERK1/2, pAKT, and pPKC at 1 min, with maximum activation at 5min. The CXCR4 inhibitor AMD3100 inhibited migration of BCWM.1 in the presence of 30nM SDF-1, with AMD3100 10uM inhibiting migration at 59% of control, and 20 to 50uM leading to a plateau in inhibition of migration at 54% of control. AMD3100 inhibited pERK and pPKC activation, downstream of CXCR4 in a dose-dependent fashion. Similar results were observed using PTX, with inhibition of migration of WM cells at 50% compared to control. To determine the role of SDF-1 on adhesion, we first demonstrated that WM cells from patients and cell lines expressed high levels of surface VLA-4 expression (mean 95% surface expression). WM cells had an increase in adhesion to fibronectin (VLA-4 ligand) compared to BSA control. AMD3100 10uM inhibited adhesion to fibronectin (63 % of control), indicating that the SDF-1/CXCR4 axis regulates adhesion. Conclusion: CXCR4 is highly expressed on WM cells and regulates migration and adhesion, indicating a potential role in regulating WM trafficking into the BM and lymph nodes. These studies provide the preclinical framework to study CXCR4 inhibitors in the regulation of homing and adhesion in WM.
8

Khandaker, Masud H., Luoling Xu, Rahbar Rahimpour, Gordon Mitchell, Mark E. DeVries, J. Geoffrey Pickering, Sharwan K. Singhal, Ross D. Feldman, and David J. Kelvin. "CXCR1 and CXCR2 Are Rapidly Down-Modulated by Bacterial Endotoxin Through a Unique Agonist-Independent, Tyrosine Kinase-Dependent Mechanism." Journal of Immunology 161, no. 4 (August 15, 1998): 1930–38. http://dx.doi.org/10.4049/jimmunol.161.4.1930.

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Abstract The expression of the seven-transmembrane domain chemokine receptors CXCR1 and CXCR2 modulates neutrophil responsiveness to the chemoattractant IL-8 and a number of closely related CXC chemokines. In the present study, we investigated the mechanism by which bacterial LPS induces the down-modulation of IL-8 responsiveness and CXCR1 and CXCR2 expression on human neutrophils. Treating neutrophils with LPS reduced IL-8R expression to 55 ± 5% of the control within 30 min and to 23 ± 2% within 1 h of stimulation. Furthermore, this down-modulation could not be attributed to increased concentrations of IL-8, TNF-α, or IL-1β, since ELISA studies indicated that LPS-stimulated neutrophils did not release detectable amounts of these proteins before 2 h poststimulation. The tyrosine kinase (TK) inhibitors genistein and herbimycin A attenuated the LPS-mediated down-modulation of CXCR1 and CXCR2, indicating that the activation of a TK is required for LPS to mediate its effect. The effect of LPS on receptor expression paralleled the hyperphosphorylation of the protein TK p72syk. Although IL-8 induced a comparable down-modulation of CXCR1 and CXCR2, TK inhibitors did not attenuate this effect. These studies provide the first evidence of an agonist-independent, TK-dependent pathway of chemokine receptor regulation by endotoxin.
9

Vacchini, Alessandro, Anneleen Mortier, Paul Proost, Massimo Locati, Mieke Metzemaekers, and Elena Borroni. "Differential Effects of Posttranslational Modifications of CXCL8/Interleukin-8 on CXCR1 and CXCR2 Internalization and Signaling Properties." International Journal of Molecular Sciences 19, no. 12 (November 27, 2018): 3768. http://dx.doi.org/10.3390/ijms19123768.

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CXCL8 or interleukin (IL)-8 directs neutrophil migration and activation through interaction with CXCR1 and CXCR2 that belong to the family of G protein-coupled receptors (GPCRs). Naturally occurring posttranslational modifications of the NH2-terminal region of CXCL8 affect its biological activities, but the underlying molecular mechanisms are only partially understood. Here, we studied the implications of site-specific citrullination and truncation for the signaling potency of CXCL8. Native CXCL8(1-77), citrullinated [Cit5]CXCL8(1-77) and the major natural isoform CXCL8(6-77) were chemically synthesized and tested in internalization assays using human neutrophils. Citrullinated and truncated isoforms showed a moderately enhanced capacity to induce internalization of CXCR1 and CXCR2. Moreover, CXCL8-mediated activation of Gαi-dependent signaling through CXCR1 and CXCR2 was increased upon modification to [Cit5]CXCL8(1-77) or CXCL8(6-77). All CXCL8 variants promoted recruitment of β-arrestins 1 and 2 to CXCR1 and CXCR2. Compared to CXCL8(1-77), CXCL8(6-77) showed an enhanced potency to recruit β-arrestin 2 to both receptors, while for [Cit5]CXCL8(1-77) only the capacity to induce β-arrestin 2 recruitment to CXCR2 was increased. Both modifications had no biasing effect, i.e., did not alter the preference of CXCL8 to activate either Gαi-protein or β-arrestin-dependent signaling through its receptors. Our results support the concept that specific chemokine activities are fine-tuned by posttranslational modifications.
10

Burton, Victoria J., Alan M. Holmes, Loredana I. Ciuclan, Alexander Robinson, Jan S. Roger, Gabor Jarai, Andrew C. Pearce, and David C. Budd. "Attenuation of leukocyte recruitment via CXCR1/2 inhibition stops the progression of PAH in mice with genetic ablation of endothelial BMPR-II." Blood 118, no. 17 (October 27, 2011): 4750–58. http://dx.doi.org/10.1182/blood-2011-05-347393.

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Abstract Previous studies from our group have demonstrated that bone morphogenetic protein receptor-II (BMPR-II), expressed on pulmonary artery endothelial cells, imparts profound anti-inflammatory effects by regulating the release of proinflammatory cytokines and promoting barrier function by suppressing the transmigration of leukocytes into the pulmonary vessel wall. Here we demonstrate that, in mice with endothelial-specific loss of BMPR-II expression (L1Cre(+);Bmpr2f/f), reduction in barrier function and the resultant pulmonary hypertension observed in vivo are the result of increased leukocyte recruitment through increased CXCR1/2 signaling. Loss of endothelial expressed BMPR-II leads to elevated plasma levels of a wide range of soluble mediators important in regulating leukocyte migration and extravasation, including the CXCR1/2 ligand, KC. Treatment of L1Cre(+);Bmpr2f/f mice with the CXCR1/2 antagonist SCH527123 inhibits leukocyte transmigration into lung and subsequently reverses the pulmonary hypertension. Our data have uncovered a previously unrecognized regulatory function of BMPR-II, which acts to regulate the expression of CXCR2 on endothelial cells, suggesting that increased CXCR2 signaling may also be a feature of the human pathology and that CXCR1/2 pathway antagonists may represent a novel therapeutic approach for treating pulmonary hypertension because of defects in BMPR-II expression.
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Статті в журналах Дисертації

Дисертації з теми "Cxcr1-2":

1

Sitaru, Sebastian [Verfasser], and Markus [Akademischer Betreuer] Sperandio. "CXCR1/2 inhibition in neutrophil recruitment / Sebastian Sitaru ; Betreuer: Markus Sperandio." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1236502159/34.

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2

Mateo, Lou. "Synthèse et évaluation de nouveaux antagonistes des récepteurs CXCR1-2 pour cibler conjointement l’angiogenèse et l’inflammation dans les pathologies cancéreuses." Thesis, Université Côte d'Azur, 2021. http://www.theses.fr/2021COAZ4006.

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L’angiogenèse et l’inflammation sont deux acteurs primordiaux dans le développement et la progression de nombreux cancers. Une meilleure connaissance des mécanismes cellulaires a permis l’essor des thérapies ciblées anti-angiogéniques. L’intérêt de ces thérapies ciblées anti-angiogéniques, est limité du fait de l’apparition de résistances. En parallèle de la voie du VEGF, il existe un second axe pro-angiogénique et pro-inflammatoire : la voie des CXCL-ELR+/CXCR, qui est particulièrement sollicitée dans le cancer et notamment dans le cancer du rein métastatique. Le but de cette thèse a été de développer de petites molécules originales capables d’inhiber l’interaction ligands/récepteurs (CXCL/CXCR1-2) afin d’avoir une action duale : à la fois anti-inflammatoire et anti-angiogénique. Le motif 2-aminobenzothiazinone a été choisi pour la préparation de trois familles d’inhibiteurs. Des stratégies de synthèse divergentes permettent d’obtenir les composés des deux premières familles, bien que les conditions opératoires aient nécessité une adaptation en fonction de la réactivité de chaque substrat. La dernière famille de molécules, est accessible selon une stratégie de synthèse linéaire qui comporte cependant des limitations lors de la dernière étape de cyclisation. Les évaluations biologiques des molécules obtenues ont mis en évidence un composé prometteur possédant une IC50 de 0.6 μM sur la lignée 786-O et inhibant la chimiotaxie des cellules exprimant les récepteurs CXCR1-2. Des études supplémentaires vont être effectuée pour confirmer ces résultats préliminaires encourageants afin d’envisager par la suite une campagne in vivo sur des poissons-zèbres, avec ce composé afin d’étudier sa capacité à entraver l’angiogenèse
Cancer is one of the main causes of death in the world. Angiogenesis and inflammation represent two essential hallmarks in the development and progression of tumors and are essential for the survival of the cancer cells. Better knowledge of cellular mechanisms has enabled the development of targeted anti-angiogenic therapies. However, the emergence of resistance constitutes the main limitation of these current anti-angiogenics targeted therapies, as you may know the anti-VEGF therapies. But in parallel to the VEGF pathway, another crucial pro-angiogenic and pro-inflammatory axis in cancers is required: the CXCL-ELR+/CXCR pathway, particularly in metastatic kidney cancer. The aim of this work was to develop original small organic molecules able to inhibit the ligand/receptor interaction (CXCL-ELR+ / CXCR1-2) in order to have both anti-inflammatory and anti-angiogenic activities. The 2-aminobenzothiazinone pattern was chosen for the preparation of 3 new classes of inhibitors. Divergent synthesis strategies were used to obtain the members of families 1 & 2, although the conditions have been adapted according to the reactivity of each substrate. The last family of molecules was prepared according to a linear synthesis. However, this latter strategy displayed some limitations during the cyclisation step. Thereafter, biological evaluations revealed a promising compound exhibiting an IC50 of 0.6 μM on the 786-O cell line compared with our reference molecule (IC50 = 2 μM). Other result highlighted that this compound also exerted an inhibition of the chemotaxis of cells expressing CXCR1-2 receptors. Further studies on zebrafish are planned with this compound in order to study its ability to interfere with the angiogenesis phenomenon in vivo
3

Penco-Campillo, Manon. "Le VEGFC et les récepteurs CXCR1/2 : des cibles pertinentes pour le traitement des médulloblastomes pédiatriques." Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6025.

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Le médulloblastome (MB) est la tumeur pédiatrique cérébrale la plus fréquente et la plus agressive. Malgré un traitement multimodal agressif, entraînant des effets secondaires importants, 30% des patients développent une résistance et rechutent suite à l'apparition de métastases dans les 5 ans. Les récidives ne peuvent être contrôlées par des traitements conventionnels (radio et chimiothérapie) ou ciblés (anti-angiogénique, anti-inflammatoire, anti-point de contrôle immunitaire). L'objectif de ma thèse est donc de découvrir de nouvelles cibles et stratégies thérapeutiques pertinentes pour ces patients au diagnostic ou après une rechute.Les MB sont des tumeurs très vascularisées. Le phénomène de résistance est, en partie, lié au développement de vaisseaux sanguins (angiogenèse) et lymphatiques (lymphangiogenèse) dans la tumeur, qui constituent les principales voies de dissémination métastatique. Le facteur de croissance des vaisseaux lymphatiques, le VEGFC, et ses récepteurs/co-récepteurs sont les acteurs majeurs de la lymphangiogenèse. Dans la première partie de ma thèse, j'ai montré que le VEGFC est inversement corrélé à la croissance et l'agressivité cellulaire du MB. En effet, le VEGFC diminue de manière autocrine la prolifération et la migration des cellules MB, ainsi que leur capacité à former des pseudo-vaisseaux in vitro. Les cellules résistantes à la radiothérapie présentent des niveaux élevés de VEGFC et perdent leur capacité à migrer et à former des pseudo-vaisseaux. L'irradiation réduit l'agressivité des cellules de MB par un processus dépendant du VEGFC. Les cellules surexprimant le VEGFC et les cellules résistantes à l'irradiation forment des tumeurs expérimentales plus petites chez la souris Nude. Le VEGC semble être un régulateur négatif de la croissance des MB. Ces résultats ouvrent la voie au développement de thérapies pro-VEGFC dans ces cancers.Dans la seconde partie de ma thèse, j'ai corrélé l'expression de la voie de signalisation pro-angiogénique et pro-inflammatoire ELR+CXCL/CXCR1-2 à une survie plus courte chez des patients atteints de MB. J'ai montré qu'un nouvel inhibiteur pharmacologique (C29) des récepteurs CXCR1-2 inhibe la prolifération, la migration dépendante de CXCL8/CXCR1/2, l'invasion et la formation de pseudo-vaisseaux par des cellules de MB sensibles ou résistantes à la radiothérapie. C29 réduit la croissance de MB expérimentaux dans un modèle de souris organotypique ex vivo et traverse la barrière hémato-encéphalique. Ainsi, le ciblage de CXCR1-2 représente une stratégie prometteuse pour le traitement des MB pédiatriques, en première ligne ou à la suite de rechutes.Mots-clés : médulloblastome pédiatrique, VEGFC/VEGFR, CXCR1-2, cytokines ELR+CXCL, thérapie ciblée, lymphangiogenèse, angiogenèse
Medulloblastoma (MB) is the most common and aggressive pediatric brain tumor. Despite aggressive multimodal treatment, resulting in significant side effects, 30% of patients develop resistance and relapse following the appearance of metastases within 5 years. Recurrences cannot be controlled by conventional (radio- and chemotherapy) or targeted (anti-angiogenic, anti-inflammatory, anti-immune checkpoint) treatments. The objective of my thesis is therefore to discover new targets and relevant therapeutic strategies for these patients at diagnosis or after a relapse.MBs are highly vascularized tumors. The phenomenon of resistance is, in part, linked to the development of blood (angiogenesis) and lymphatic (lymphangiogenesis) vessels in the tumor, which constitute the main routes of metastatic dissemination. The lymphatic growth factor, VEGFC, and its receptors/co-receptors are the major players in lymphangiogenesis. In the first part of my thesis, I showed that VEGFC is inversely correlated to MB cell growth and aggressiveness. Indeed, VEGFC decreases the proliferation and migration of MB cells, as well as their ability to form pseudo-vessels in vitro, by an autocrine signalization. Cells resistant to radiotherapy show elevated levels of VEGFC and lose their ability to migrate and form pseudo-vessels. Irradiation reduces the aggressiveness of MB cells by a VEGFC-dependent process. VEGFC-overexpressing cells and radiation-resistant cells form smaller experimental tumors in nude mice. Thus, VEGC appears to be a negative regulator of MB growth. These results pave the way for the development of pro-VEGFC therapies in these cancers.In the second part of my thesis, I correlated the expression of the ELR+CXCL/CXCR1-2 pro-angiogenic and pro-inflammatory signaling pathway to shorter survival in patients with MB. I showed that a novel pharmacological inhibitor (C29) of CXCR1-2 receptors inhibits proliferation, CXCL8/CXCR1-2-dependent migration, invasion and pseudo-vessel formation by susceptible or resistant MB cells to radiotherapy. C29 reduces the growth of experimental MBs in an ex vivo organotypic mouse model and crosses the blood-brain barrier. Thus, targeting CXCR1-2 represents a promising strategy for the treatment of pediatric MB, at first line or at relapse.Key words: pediatric medulloblastoma, VEGFC/VEGFR, CXCR1-2, ELR+CXCL cytokines, targeted therapy, lymphangiogenesis, angiogenesis
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Fabre, Marie. "Conception, synthèse et optimisation de nouveaux antagonistes des récepteurs CXCR1/2 pour le traitement de la DMLA exsudative." Thesis, Université Côte d'Azur, 2021. http://www.theses.fr/2021COAZ4044.

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Dans les pays occidentaux, la dégénérescence maculaire liée à l’âge (DMLA) exsudative est l’une des principales causes de cécité chez les personnes âgées. Cette maladie est caractérisée par une vascularisation anormale de la choroïde et une forte inflammation intraoculaire. Actuellement, seuls les traitements symptomatiques anti-VEGF existent, à base d’anticorps monoclonaux humanisés et des glycoprotéines de fusion recombinantes ciblant les facteurs pro-angiogéniques. À l’heure actuelle, uniquement 30 % des patients présentent une réponse durable aux traitements.Le blocage de la voie de signalisation des cytokines ERL+ CXCL a été proposé comme une alternative prometteuse pour cibler simultanément la vascularisation de la choroïde et l’inflammation. En effet, cette sous-famille de cytokines est impliquée à la fois dans le processus inflammatoire et dans le stade précoce du signal pro-angiogénique.Deux composés de la famille des diarylurées, MCK133 et MCK140, ont permis d’établir une preuve de concept d’efficacité in vitro et in vivo. À partir de ces composés, nous allons concevoir et développer de nouvelles familles de composés inspirées du même pharmacophore, portant un noyau triazole, pour améliorer les activités, les propriétés physico-chimiques et pharmacologiques.Quatre séries de composés dérivées du pharmacophore ont été envisagées : deux avec un noyau imidazole et deux portants un noyau triazole. Les voies d’accès synthétiques à chacune de ces familles ont été étudiées. Une famille de triazole a été particulièrement explorée, et 63 analogues ont été synthétisés pour déterminer les relations structure-activité, en faisant varier des positions clés de la molécule. Tous les composés synthétisés ont été évalués sur plusieurs modèles in vitro d’angiogenèse, d’inflammation, de migration et de prolifération cellulaire pour apprécier leur potentiel à lutter contre la DMLA exsudative. Un composé Lead prometteur a été identifié. Les perspectives de cette thèse sont l’évaluation de ce composé sur plusieurs modèles in vivo de DMLA exsudative.Finalement, la dernière partie de ce manuscrit présente deux projets annexes : (i) une étude du transfert des biamidines vers les biguanides et (ii) l’étude de la stabilité du NRPa-308
In western countries, exudative age-related macular degeneration (AMD) is one of the leading causes of blindness in the elderly. This disease is characterized by an abnormal vascularization of the choroid and a strong intraocular inflammation. Currently, only anti-VEGF symptomatic treatments exist, which rely on humanized monoclonal antibodies (mAbs) and recombinant fusion glycoprotein targeting pro-angiogenic factors. Moreover, only 30% of the patients present a durable response to this treatment.The blockage of the ERL+ CXCL cytokines signaling pathway has been proposed as a promising alternative to target simultaneously choroid vascularization and inflammation. Indeed, this sub-family of cytokines is specifically involved both in inflammation and in the early stage of the pro-angiogenic signal.Two compounds of diarylurea family, MCK133 and MCK140, have established a proof of concept in vitro and in vivo. Therefore, a new series of compounds has been designed that features the same pharmacophore bearing a triazole core, to enhance the activity, the physicochemical and pharmacological properties.Four series based on the pharmacophore were considered: two with an imidazole core and two with a triazole core. Synthetic pathways to each of these families have been studied. A triazole family has been particularly explored, and 63 analogs have been synthesized to determine the structure-activity relationships, by varying key positions of the molecule. All synthesized compounds were evaluated on several in vitro models of angiogenesis, inflammation, migration, and cell proliferation to assess their potential against exudative AMD. A promising lead compound has been identified. The perspectives of this thesis are the evaluation of this compound on several in vivo models of exudative AMD.Finally, the last part of this manuscript presents two annexe projects: (i) the study of the biamidines transfer to biguanides and (ii) the stability study of NRPa-308
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Abdelouahab, Hadjer. "Etude des mécanismes impliqués dans l'hématopoièse extra-médullaire dans les myélofibroses primaires et secondaires." Paris 7, 2014. http://www.theses.fr/2014PA077212.

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Les myélofibroses (MF) primaires et secondaires sont des néoplasmes myéloprolifératifs (NMP) rares et complexes. Elles se caractérisent par une fibrose médullaire et une mobilisation constitutive des cellules souches et des progéniteurs hématopoïétiques (CSPH) associée à une hématopoïèse extra-médullaire (HEM) dans le foie et la rate. Les MF se caractérisent également par un statut mutationnel complexe. JAK2V617F et MPLW515 sont les principales mutations sur les molécules de signalisation. Elles entraînent une activation constitutive des voies de signalisation. Au cours de ce travail, nous avons étudié le rôle du couple CXCL12/CXCR4 dans la mobilisation constitutive des CSPH et dans la progression de l'HEM dans les MF. Nos résultats montrent que les cellules CD34+ de patients MF se caractérisent par une forte réponse chimiotactique à CXCL12. Cette forte migration ne corrèle pas avec une forte expression de CXCR4, mais semble corréler avec une activation des voies de signalisation. Nos résultats montrent également que les voies de signalisation de l'axe CXCL12/CXCR4 et des cytokines sont synergiques dans le chimiotactisme cellulaire. Nous avons également démontré que le traitement des patients MF avec des inhibiteurs de JAK2 mobilisait les cellules CD34+ dans le sang périphérique. Enfin, l'inhibition de CXCR4 réduit la migration des cellules CD34+ MF en réponse à CXCL12 et induit une diminution de l'HEM dans deux modèles murins de MF. L'ensemble de ces résultats suggère que la mobilisation constitutive des CSPH et l'HEM dans les MF sont dépendantes de la signalisation de CXCL12/CXCR4
Primary and secondary myelofibrosis (MF) are rare and complex myeloproliferative neoplasms (MPN). They are characterized by medullary fibrosis and constitutive mobilization of stem cells and hematopoietic progenitors (HSPC), associated with extramedullary hematopoiesis in the liver and spleen. MF are also characterized by a complex mutational profile with JAK2V617F and MPLW515 being the main mutations in signaling molecules, leading to constitutive activation of signaling pathways. During this work, we have studied the role of CXCL12/CXCR4 in the constitutive HSPC mobilization and in the progression of the EMH in MF. Our results have shown that CD34+ MF patient cells are characterized by a strong chemotactic response to CXCL12 in vitro. This strong migration did not correlate with a high CXCR4 membrane expression, but seems correlated with activation of signaling pathways. Our results further demonstrated that the signaling pathways of CXCL12/CXCR4 and cytokines/cytokine receptors were synergistic in the chemotactic responses of cells to CXCL12. Furthermore, treatment MF patients with JAK2 inhibitors mobilizes CD34+ cells in peripheral blood. Finally, CXCR4 inhibition reduced the migration of MF CD34 cells in response to CXCL12 and induced a decrease in EMH in two mouse models of MF. Altogether, these resulb suggest that the constitutive HSPC mobilization and EMH in MF depend on CXCL12/CXCR4 signaling
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Shi, Yu. "Coreceptor usage and sensitivity to neutralization of HIV-1 and HIV-2 /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-093-1/.

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Liebick, Marcel [Verfasser], Martin [Akademischer Betreuer] Oppermann, Susanne [Akademischer Betreuer] Lutz та Dieter [Akademischer Betreuer] Kube. "Chemokine receptors CXCR4 and CCR5: Cell surface expression, signaling and modulation by β-arrestin 2 / Marcel Liebick. Gutachter: Susanne Lutz ; Dieter Kube. Betreuer: Martin Oppermann". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2015. http://d-nb.info/1067626565/34.

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Frange, Pierre. "Caractérisation virologique des virus VIH-1 isolés en primo-infection en France." Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T022.

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L’épidémiologie moléculaire des virus VIH-1 en France est caractérisée par une augmentation constante de la diversité virologique et de la fréquence des virus de sous-types non-B chez les patients en primo-infection. Entre 1997 et 2007, 28.4% des 591 patients suivis étaient infectés par des virus de sous-types non-B. De plus, 49 patients (8.3%) étaient infectés par des souches de sous-types différents sur les gènes pol et env, témoignant d’évènements de recombinaisons entre ces gènes. Ces virus recombinants étaient isolés à la fois chez des patients originaires d’Afrique sub-saharienne (28.3%) et des sujets caucasiens (6.3%). Ces résultats témoignent des échanges de souches virales entre les populations d'origine africaine et caucasienne, contribuant encore à augmenter la diversité virologique dans ces deux populations. Parmi 131 virus de sous-types non-B, 12.2% étaient classés comme ayant un tropisme CXCR4 par méthode génotypique, mais seulement 0.8% par méthode phénotypique, indiquant d’une part la faible proportion de virus non-B de tropisme CXCR4 en primo-infection en France, et d’autre part le manque de spécificité des méthodes génotypiques de détermination du tropisme pour ces sous-types, rendant nécessaire la mise au point d’autres algorithmes spécifiques pour ces virus.L’analyse de 987 virus isolés dans la cohorte entre 1999 et 2010 a mis en évidence que 12.7% d’entre eux étaient regroupés en "clusters" de transmission. Les patients en primo-infection contribuent donc de façon significative à la propagation de l’épidémie de VIH en France, particulièrement les hommes homo/bi-sexuels, avec une fréquence augmentant au cours de la période récente (2006-2010).La comparaison des quasi-espèces virales circulant concomitamment chez 8 patients en primo-infection (« receveurs ») et leurs 8 partenaires sexuels respectifs (« donneurs ») a révélé dans tous les cas la transmission d’un virus unique, présent de façon minoritaire parmi les sous-populations virales du donneur. La transmission virale muqueuse implique donc une sélection génétique drastique
High genetic diversity is a major characteristics of HIV-1. In France, although subtype B strains are still predominant, the proportion of non-B viruses isolated in patients at the time of primary HIV-1 (PHI) infection increases over time. Between 1997 and 2007, 28.4% of patients were infected with non-B subtypes strains. Forty-nine viruses showed different phylogenies between the pol and env genes, indicating that recombinations have occurred in 8.3% of cases. These recombinants were isolated both in patients from Sub-Saharan Africa (28.3%) and in white subjects (6.3%).The phenotypic analysis of viral tropism of 131 non-B strains showed a very low (0.8%) proportion of CXCR4-tropic strains (X4 strains) at the time of PHI. Compared to phenotypic tests, genotypic predictions can overestimate (12.2% versus 0.8%) the proportion of X4 strains in non-B subtypes.The phylogenetic analysis of 987 strains isolated in 1999-2010 showed that 12.7% of PHI cosegregated into 56 transmission chains. PHIs are a significant source of onward transmission, especially in men having sex with men, with increasing frequency during the recent years (10.2% in 1999-2006 versus 15.2% in 2006-2010, p=0.02).The comparison of the viral quasispecies isolated in plasma and PBMC samples from 8 patients at the time of PHI ("recipients") and their transmitting partners ("donors") suggested that a severe genetic bottleneck occurrs during HIV-1 heterosexual and homosexual transmission. Indeed, we observed in all cases the transmission of a single variant, which was derived from an infrequent variant population within the blood of the donor. The proportion of X4 quasispecies in donors were higher in case of X4 versus CCR5-tropic viral transmission, suggesting that X4 transmission may be associated with a threshold of X4 circulating quasispecies in donors
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Fortier, Yasmina. "Étude de la dynamique des lymphocytes TFH et B au niveau de la rate et des ganglions mésentériques et impact d'un traitement anti-apoptotique sur la dynamique de ces populations et de la réponse humorale chez le macaque rhésus infecté par le VIS." Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCB034.

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L'infection par le VIH est une pathologie caractérisée par la dissémination du virus dans l'ensemble de l'organisme et une destruction progressive des lymphocytes T CD4+ (LT CD4+) résultant en une immunité altérée. L'épuisement et l'apoptose des cellules T mémoires induites par le virus amènent à l'apparition d'un SIDA. Il a été montré que les centres germinatifs (GCs), structures anatomiques spécialisées au sein des follicules B des organes lymphoïdes secondaires, représentent des lieux privilégiés de la persistance virale. Parmi les organes lymphoïdes, la rate et les ganglions mésentériques seraient des sanctuaires viraux du fait de leur rôle dans la réponse immunitaire. La rate est le principal organe de la réponse B, et les ganglions mésentériques sont essentiels dans l'établissement de la réponse immune mucosale. Les GCs sont principalement constitués de lymphocytes B mais également de lymphocytes T folliculaires (TFH), sous-population de LT CD4+ effecteurs mémoires jouant un rôle essentiel dans le développement de la réponse B, en particulier dans la maturation des anticorps de haute affinité. Des études dont celles du laboratoire ont montré que l'altération de la réponse B observée au cours de l'infection VIH serait due à une perte et à un défaut de différentiation des lymphocytes TFH. Plus récemment, il a été observé que les GCs sont également constitués de lymphocytes T mémoires CD8+ folliculaires (LT CD8+ folliculaires), exprimant le récepteur de chimiokine CXCR5. De récents travaux suggèrent un rôle de ces cellules dans le contrôle de l'infection par le VIH. Le but de ma thèse a été d'étudier la dynamique des lymphocytes TFH au sein de ces deux organes que sont la rate et les ganglions mésentériques, et de déterminer dans quelle mesure l'administration d'un inhibiteur d'apoptose permet de restaurer des fonctions effectrices telle que la production d'anticorps. Ces travaux ont été réalisés chez le macaque rhésus infecté par la souche SIVmac251. Mes résultats montrent que l'infection persistante des ganglions mésentériques est associée à une perte et une altération des follicules B ainsi qu'à une déplétion et une altération des lymphocytes TFH. Ils montrent également une altération de l'expression de la chimiokine CXCL13, ligand de CXCR5, qui serait à même de créer un environnement défavorable à la différenciation des cellules B. Ils montrent aussi que l'administration d'un inhibiteur d'apoptose au cours de la phase de primo-infection chez les singes infectés induit une diminution de l'apoptose des LT CD4+ comme attendu, une diminution des cytokines inflammatoires, et une réponse B systémique spécifique plus importante chez les singes traités. Ceci pourrait contribuer à un meilleur contrôle de la réplication virale. Enfin, mes travaux démontrent qu'au niveau de la rate, on observe une augmentation du nombre de LT CD8+ qui infiltre les follicules B et que ceux-ci n'expriment pas majoritairement la protéine CXCR5 chez les singes infectés en particulier progresseurs. De même, on observe une augmentation de la chimiokine MIP1b, susceptible de jouer un rôle dans le recrutement de LT CD8+ conventionnels chez les singes infectés, et une augmentation de l'expression des marqueurs de cytotoxicité chez les singes non-progresseurs comparativement aux singes progresseurs. Enfin, ces travaux semblent indiquer que les LT CD8+ folliculaires des individus progresseurs ne contrôlent pas l'infection par le VIS. En conclusion, l'infection par le VIS induirait la formation d'un réservoir viral au niveau des follicules B et des GCs induisant une réponse B altérée, associée à une altération des follicules B, à un défaut des lymphocytes TFH, ainsi qu'à un enrichissement en LT CD8+ folliculaires potentiellement défectifs. Ensemble, mes travaux portant sur l'étude des lymphocytes T folliculaires ont mis en exergue et confirmé l'importance de ces cellules T dans les relations hôtes-pathogènes
HIV infection is characterized by a viral spread in the host body and a progressive destruction of CD4+ T cells, leading to a defect in the immune system. The memory T cells apoptosis and exhaustion induced by the virus leads the outcome of an AIDS. It was showed that germinal centers (GCs), specialized anatomical structures present in the B follicles of the secondary lymphoid organs, represent privileged viral reservoir. Among secondary lymphoid organs, spleen and mesenteric lymph nodes would be viral sanctuaries because of their role in the generation of the immune response. Spleen is the main organ of the B cell response, and mesenteric lymph nodes are essentials in the establishment of the mucosal immune response. GCs are mainly composed by B cells but also by TFH cells, a sub-population of effector memory CD4+ T cells, crucial for the generation of the B cell response, especially for the maturation of the highly efficient antibodies. Previous works from our laboratory showed that the defect of the B cell response during HIV infection is due to a loss and a defect of the TFH cells. Recently, it was showed that GCs are also composed of follicular memory CD8+ T cells, expressing the chemokine receptor CXCR5. Recent works suggested that those cells are implicated in the control of HIV infection. Thus, the aim of my thesis was to study the dynamic of follicular T cells in these two organs, spleen and mesenteric lymph nodes, and to set how well the administration of a pan-caspase inhibitor during acute phase of SIV infection help to restore effective functions as the antibody production. Those works were done in rhesus monkeys infected with the strain SIVmav251. My results show that the persistent infection of mesenteric lymph node is associated with a loss and a defect of B follicles and with a defect of TFH cells. They also show a defect in the expression of the CXCL13 chemokine, ligand of the CXCR5 receptor, potentially capable of creating a bad environment for B cell differentiation. My results show also that the administration of a pan-caspase inhibitor during the acute phase of infection leads to a decrease in the CD4+ T cells apoptosis as expected, a decrease in the inflammatory cytokines expression and in a better specific systemic B cell response in treated monkeys. These could help in the control of the viral replication. Finally, my results show that in the spleen, there's an increase of the follicular CD8+ T cells filtering the B follicles, which mainly doesn't express the CXCR5 receptor in infected monkeys, especially the progressor ones. They also show that there's an increase in the expression of the MIP1b chemokine, possibly responsible of the recruitment of conventional CD8+ T cells in the infected monkeys, and an increase in the expression of cytotoxic markers in the non-progressors monkeys compared to the progressors ones. Thus, these work seems to show that follicular CD8+ T cells of progressor monkeys fail to control SIV infection. Thus, SIV infection induce an altered B cell response, associated to a defect of B follicles, a defect of TFH cells, and an increase in follicular CD8+ T cells potentially inefficient. Altogether, my works focused on the study of follicular T cells show and confirm the strength the importance of these T cells in the host-pathogen relationship
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Drwal, Veronika [Verfasser], and Thomas [Akademischer Betreuer] Wex. "Die Bedeutung der Expression der G-Protein-gekoppelten-Rezeptoren BRS 3, CCKA, CXCR 4, GHRH, GRPR, NK 1, NMBR, NT 2, PAC 1, VPAC 1 und VPAC 2 bei kolorektalen Tumoren in Abhängigkeit von Tumorstadium und Differenzierungsgrad / Veronika Drwal. Betreuer: Thomas Wex." Magdeburg : Universitätsbibliothek, 2012. http://d-nb.info/1054135525/34.

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Книги з теми "Cxcr1-2":

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Livingston, Schuyler, Benjamin Young, Martin Markowitz, Poonam Mathur, and Bruce L. Gilliam. HIV Virology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0017.

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HIV is a member of the lentivirus subfamily of retroviruses. Two distinct groups of viruses are pathogenic in humans: HIV-1 and HIV-2. Both are transmitted sexually and known to cause immunodeficiency disease. HIV enters the cell through use of the CD4 receptor and chemokine co-receptors, primarily CCR5 and CXCR4. The viral genome is transcribed from RNA to DNA by reverse transcriptase and integrated into the host genome by integrase. The HIV genome encodes 15 proteins, comprising three categories: structural, regulatory, and accessory. After budding from the host cell, the virus matures into its infectious form through cleavage of viral precursor proteins by protease.

Частини книг з теми "Cxcr1-2":

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Mir, Manzoor Ahmad, Masrat Bashir, and Ishfaq. "Role of the CXCL8–CXCR1/2 Axis in Cancer and Inflammatory Diseases." In Cytokine and Chemokine Networks in Cancer, 291–329. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-4657-0_11.

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Rettig, Michael P., Pablo Ramirez, Bruno Nervi, and John F. DiPersio. "Chapter 2 CXCR4 and Mobilization of Hematopoietic Precursors." In Methods in Enzymology, 57–90. Elsevier, 2009. http://dx.doi.org/10.1016/s0076-6879(09)05203-3.

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Тези доповідей конференцій з теми "Cxcr1-2":

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Choi, Yong Won, Hyun-Young Cha, Tae Jun Park, Mi Sun Ahn, Hyun Woo Lee, Seong Hyun Jeong, Seok Yun Kang, Joon Seong Park, and Jin-Hyuk Choi. "Abstract 469: Therapy-induced senescence associated secretory phenotype enhances breast cancer cell invasion and stemness via CXCR1/2-CXCR1/2 ligands axis." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-469.

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Burton, Victoria J., Nicholas Duggan, Betty Shamji, David Rowlands, Neil Press, Zarin Brown, Daniel Sutton, et al. "Inhibition Of The Chemokine Receptor CXCR1/2 Attenuates Experimental Severe Pulmonary Arterial Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5091.

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Wu, Sheng, Michelle L. Varney, Seema Singh, and Rakesh K. Singh. "Abstract 733: A therapeutic opportunity in melanoma: Targeting CXCR1/2-dependent signaling attenuates therapy resistance." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-733.

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Sharma, Ira, Avninder Singh, Fouzia Siraj, and Sunita Saxena. "Abstract B058: Role of IL8-CXCR1/2 axis in glioblastoma cell proliferation, invasion, and vascular mimicry." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-b058.

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Singh, JK, G. Farnie, RB Clarke, and NJ Bundred. "P3-17-04: CXCR1/2 Regulates Human Breast Cancer Stem Cell Activity Via EGFR/HER2−Dependent and -Independent Pathway." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p3-17-04.

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Carbone, Carmine, Anna Tamburrino, Geny Piro, Marco Zanotto, Maria Mihaela Mina, Silvia Zanini, Federico Boschi, Aldo Scarpa, Giampaolo Tortora та Davide Melisi. "Abstract 3605: Combined inhibition of IL-1, CXCR1/2, and TGFβ signaling pathways modulates in vivo acquired resistance to anti-VEGF treatment". У Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3605.

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Millrud, Camilla, Elin Gyllenbäck, Petter Skoog, Annika Sanfridson та David Liberg. "145 Nadunolimab inhibits IL-1α/β-induced CXCR1/2 ligand expression and reduces serum levels of CXCL1 and CXCL5 in NSCLC and PDAC patients". У SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0145.

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Schott, Anne F., Max S. Wicha, Raymond P. Perez, Giraldo Kato, Tiffany Avery, Massimo Cristofanilli, James M. Reuben, et al. "Abstract C22: A phase Ib study of the CXCR1/2 inhibitor Reparixin in combination with weekly paclitaxel in metastatic HER2 negative breast cancer - final analysis." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-c22.

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Schott, Anne F., Max S. Wicha, Raymond P. Perez, Giraldo Kato, Tiffany Avery, Massimo Cristofanilli, James M. Reuben, et al. "Abstract P6-03-01: A phase Ib study of the CXCR1/2 inhibitor reparixin in combination with weekly paclitaxel in metastatic HER2 negative breast cancer – First analysis." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p6-03-01.

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Singh, Seema, Michelle L. Varney, and Rakesh K. Singh. "Abstract 3486: CXCR1 and CXCR2 silencing alters endothelial cell proliferation, migration and capillary tube formation." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3486.

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