Auswahl der wissenschaftlichen Literatur zum Thema „Cxcr1-2“
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Zeitschriftenartikel zum Thema "Cxcr1-2"
Zhang, Jing, Shouguo Huang, Lini Quan, Qiu Meng, Haiyan Wang, Jie Wang und Jin Chen. „Determination of Potential Therapeutic Targets and Prognostic Markers of Ovarian Cancer by Bioinformatics Analysis“. BioMed Research International 2021 (19.03.2021): 1–13. http://dx.doi.org/10.1155/2021/8883800.
Der volle Inhalt der QuelleDoroshenko, Tatyana, Yuri Chaly, Valery Savitskiy, Olga Maslakova, Anna Portyanko, Irina Gorudko und Nikolai N. Voitenok. „Phagocytosing neutrophils down-regulate the expression of chemokine receptors CXCR1 and CXCR2“. Blood 100, Nr. 7 (01.10.2002): 2668–71. http://dx.doi.org/10.1182/blood.100.7.2668.
Der volle Inhalt der QuelleKonrad, F. M., und J. Reutershan. „CXCR2 in Acute Lung Injury“. Mediators of Inflammation 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/740987.
Der volle Inhalt der QuelleFeniger-Barish, Rotem, Dan Belkin, Alon Zaslaver, Shira Gal, Mally Dori, Maya Ran und 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, Nr. 5 (01.03.2000): 1551–59. http://dx.doi.org/10.1182/blood.v95.5.1551.005a36_1551_1559.
Der volle Inhalt der QuelleSmithson, 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, Nr. 12 (Dezember 2005): 1358–63. http://dx.doi.org/10.1128/cdli.12.12.1358-1363.2005.
Der volle Inhalt der QuelleMolczyk, Caitlin, und Rakesh K. Singh. „CXCR1: A Cancer Stem Cell Marker and Therapeutic Target in Solid Tumors“. Biomedicines 11, Nr. 2 (16.02.2023): 576. http://dx.doi.org/10.3390/biomedicines11020576.
Der volle Inhalt der QuelleNgo, 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, Nr. 11 (01.11.2006): 2418. http://dx.doi.org/10.1182/blood.v108.11.2418.2418.
Der volle Inhalt der QuelleKhandaker, Masud H., Luoling Xu, Rahbar Rahimpour, Gordon Mitchell, Mark E. DeVries, J. Geoffrey Pickering, Sharwan K. Singhal, Ross D. Feldman und 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, Nr. 4 (15.08.1998): 1930–38. http://dx.doi.org/10.4049/jimmunol.161.4.1930.
Der volle Inhalt der QuelleVacchini, Alessandro, Anneleen Mortier, Paul Proost, Massimo Locati, Mieke Metzemaekers und 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, Nr. 12 (27.11.2018): 3768. http://dx.doi.org/10.3390/ijms19123768.
Der volle Inhalt der QuelleBurton, Victoria J., Alan M. Holmes, Loredana I. Ciuclan, Alexander Robinson, Jan S. Roger, Gabor Jarai, Andrew C. Pearce und 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, Nr. 17 (27.10.2011): 4750–58. http://dx.doi.org/10.1182/blood-2011-05-347393.
Der volle Inhalt der QuelleDissertationen zum Thema "Cxcr1-2"
Sitaru, Sebastian [Verfasser], und 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.
Der volle Inhalt der QuelleMateo, 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.
Der volle Inhalt der QuelleCancer 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
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.
Der volle Inhalt der QuelleMedulloblastoma (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
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.
Der volle Inhalt der QuelleIn 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
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.
Der volle Inhalt der QuellePrimary 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
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/.
Der volle Inhalt der QuelleLiebick, Marcel [Verfasser], Martin [Akademischer Betreuer] Oppermann, Susanne [Akademischer Betreuer] Lutz und 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.
Der volle Inhalt der QuelleFrange, Pierre. „Caractérisation virologique des virus VIH-1 isolés en primo-infection en France“. Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T022.
Der volle Inhalt der QuelleHigh 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
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.
Der volle Inhalt der QuelleHIV 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
Drwal, Veronika [Verfasser], und 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.
Der volle Inhalt der QuelleBücher zum Thema "Cxcr1-2"
Livingston, Schuyler, Benjamin Young, Martin Markowitz, Poonam Mathur und Bruce L. Gilliam. HIV Virology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0017.
Der volle Inhalt der QuelleBuchteile zum Thema "Cxcr1-2"
Mir, Manzoor Ahmad, Masrat Bashir und 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.
Der volle Inhalt der QuelleRettig, Michael P., Pablo Ramirez, Bruno Nervi und 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.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Cxcr1-2"
Choi, Yong Won, Hyun-Young Cha, Tae Jun Park, Mi Sun Ahn, Hyun Woo Lee, Seong Hyun Jeong, Seok Yun Kang, Joon Seong Park und 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.
Der volle Inhalt der QuelleBurton, 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.
Der volle Inhalt der QuelleWu, Sheng, Michelle L. Varney, Seema Singh und 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.
Der volle Inhalt der QuelleSharma, Ira, Avninder Singh, Fouzia Siraj und 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.
Der volle Inhalt der QuelleSingh, JK, G. Farnie, RB Clarke und 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.
Der volle Inhalt der QuelleCarbone, Carmine, Anna Tamburrino, Geny Piro, Marco Zanotto, Maria Mihaela Mina, Silvia Zanini, Federico Boschi, Aldo Scarpa, Giampaolo Tortora und Davide Melisi. „Abstract 3605: Combined inhibition of IL-1, CXCR1/2, and TGFβ signaling pathways modulates in vivo acquired resistance to anti-VEGF treatment“. In 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.
Der volle Inhalt der QuelleMillrud, Camilla, Elin Gyllenbäck, Petter Skoog, Annika Sanfridson und 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“. In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0145.
Der volle Inhalt der QuelleSchott, 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.
Der volle Inhalt der QuelleSchott, 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.
Der volle Inhalt der QuelleSingh, Seema, Michelle L. Varney und 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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