Relevant bibliographies by topics / CD155

Academic literature on the topic 'CD155'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "CD155"

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Zhang, Hongpan, Zhihao Yang, Guobo Du, Lu Cao, and BangXian Tan. "CD155-Prognostic and Immunotherapeutic Implications Based on Multiple Analyses of Databases Across 33 Human Cancers." Technology in Cancer Research & Treatment 20 (January 1, 2021): 153303382098008. http://dx.doi.org/10.1177/1533033820980088.

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Growing evidence has suggested that CD155 participates in the regulation of many biological processes ranging cell growth, invasion, and migration from regulation of immune responses in most malignances. However, the impact of prognostic value and CD115-related immune response on the survival in multiple cancers remains incompletely clear. In our study, we assessed the prognostic significance and immune-associated mechanism of CD155 based on data from multiple databases and methods, including UCSC Xena, Oncomine, PrognoScan. We identified that CD155 was commonly upregulated in most human cancers, and High expression of CD155 was closely correlated with unfavorable clinical outcomes in 10/33 of human cancers, while CD155 at low level was responsible for better survival in KICH and PAAD. More intriguingly, CD155 expression had a significant interaction with immune function in several tumors by analyzing Tumor mutational burden and microsatellite in stability, immune score and stromal score. The correlation between immune infiltration and CD155 expression also indicated that CD155 expression positively correlated with CD4+ T cells in Head and Neck squamous cell carcinoma, Lung adenocarcinoma and Colon adenocarcinoma, while had inversely interaction with CD8+ T in Kidney renal clear cell carcinoma and Head and Neck squamous cell carcinoma as well as Tregs in Skin Cutaneous Melanoma, Head and Neck squamous cell carcinoma and Bladder Urothelial Carcinoma. These findings indicate CD155 correlates with cancer immunotherapy function. In conclusions, our observations revealed CD155 might function as immune-associated system in the development of human cancers, and acted as a promising prognostic and therapeutic target against human cancers.
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Yoshikawa, Katsuhiro, Mitsuaki Ishida, Hirotsugu Yanai, Koji Tsuta, Mitsugu Sekimoto, and Tomoharu Sugie. "Immunohistochemical analysis of CD155 expression in triple-negative breast cancer patients." PLOS ONE 16, no. 6 (June 11, 2021): e0253176. http://dx.doi.org/10.1371/journal.pone.0253176.

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Introduction CD155 is an immune checkpoint protein. Its overexpression is an indicator of poor prognosis in some types of cancer. However, the significance of CD155 expression in patients with triple-negative breast cancer, and the relationship between CD155 and programmed death-ligand 1 (PD-L1) expression, have not yet been analyzed in detail. Methods Using immunohistochemical staining and tissue microarrays, we analyzed the expression profiles of CD155 and PD-L1 in 61 patients with triple-negative breast cancer. Relapse-free survival and overall survival rates were compared according to CD155 expression. The correlation between CD155 expression and clinicopathological factors, including PD-L1 expression (using SP142 and 73–10 assays), was also examined. Results CD155 expression was noted in 25 patients (41.0%) in this cohort. CD155 expression did not correlate with pathological stage, histological grade, Ki-67 labeling index, or stromal tumor-infiltrating lymphocytes. Only PD-L1 expression in tumor cells by SP142 assay significantly correlated with CD155 expression (p = 0.035); however, PD-L1 expression in tumor cells by 73–10 assay did not show a correlation (p = 0.115). Using the 73–10 assay, 59% of patients showed CD155 and/or PD-L1 expression in tumor cells. Moreover, using the SP142 assay, 63.3% of patients showed CD155 and/or PD-L1 expression in immune cells. CD155 expression did not correlate with either relapse-free survival or overall survival (p = 0.485 and 0.843, respectively). Conclusions CD155 may be a novel target for antitumor immunotherapy. The results of this study indicate that CD155 may expand the pool of candidates with triple-negative breast cancer who could benefit from antitumor immunotherapy.
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Zhu, Xudong, Rongpu Liang, Tianyun Lan, Dongbing Ding, Shengxin Huang, Jun Shao, Zongheng Zheng, et al. "Tumor-associated macrophage-specific CD155 contributes to M2-phenotype transition, immunosuppression, and tumor progression in colorectal cancer." Journal for ImmunoTherapy of Cancer 10, no. 9 (September 2022): e004219. http://dx.doi.org/10.1136/jitc-2021-004219.

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BackgroundOnco-immunogenic molecule CD155 is overexpressed in various tumor microenvironments (TME) including in colorectal cancer (CRC). Tumor-associated macrophages (TAMs) are the most abundant immune cells in CRC TME and play a vital role in CRC progression and metastasis. Most studies have focused on investigating the role of CRC cell-specific CD155 on CRC progression, while the contribution of TAMs-specific CD155 is still unknown. Here, we sought to investigate the expression pattern of CD155 in CRC TAMs and its role in tumor immunity and progression.MethodsCD155 expression patterns in CRC TAMs and macrophages in paratumor or adjacent normal tissue were analyzed in 50 patients with CRC using flow cytometry and in 141 patients with CRC using immunohistochemistry. The correlation of CD155 expression level in TAMs with M1 and M2 phenotypic transition was analyzed. The role of macrophage-specific CD155 in CRC progression and tumor immune response was investigated in vitro and in vivo. We further analyzed the effect of CRC cells on the regulation of CD155 expression in macrophages.ResultsCRC TAMs from clinical samples showed robustly higher expression of CD155 than macrophages from paratumor and adjacent normal tissues. The CD155 expression level was higher in TAMs of CRC at III/IV stages compared with the I/II stages and was negatively associated with the survival of patients with CRC. CD155+ TAMs showed an M2 phenotype and higher expression of interleukin (IL)-10 and transforming growth factor (TGF)-β. CD155+ macrophages promoted CRC cell migration, invasion, and tumor growth supporting the findings from the clinical tissue analysis. This effect was mainly regulated by TGF-β-induced STAT3 activation-mediated release of matrix metalloproteinases (MMP)2 and MMP9 in CRC cells. CD155–⁄– bone marrow transplantation in wild-type mice, as well as CD155– macrophages treatment, promoted the antitumor immune response in the mice ectopic CRC model. Additionally, CRC cells released IL-4 to trigger CD155 expression in macrophages indicating the regulatory role of CRC cells in the development of CD155+ TAMs.ConclusionsThese findings indicated that CD155+ TAMs are responsible for the M2-phenotype transition, immunosuppression, and tumor progression in CRC. The specific localization of CD155+ TAMs in CRC tissue could turn into a potential therapeutic target for CRC treatment.
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Murakami, Daisuke, Kenji Matsuda, Hiromitsu Iwamoto, Yasuyuki Mitani, Yuki Mizumoto, Yuki Nakamura, Ibu Matsuzaki, et al. "Prognostic value of CD155/TIGIT expression in patients with colorectal cancer." PLOS ONE 17, no. 3 (March 24, 2022): e0265908. http://dx.doi.org/10.1371/journal.pone.0265908.

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Introduction The interaction of CD155 with its ligand, the T cell immunoreceptor with Ig and ITIM domains (TIGIT), is being studied owing to its potential to act as a target in the treatment of various solid tumors. However, the relationship between CD155 and TIGIT in colorectal cancer (CRC) prognosis is not known. We hypothesized that the TIGIT–CD155 pathway suppresses the attack of T cells on tumors, thereby affecting CRC prognosis. Methods We examined the expression of CD155 and TIGIT using immunohistochemical staining in 100 consecutive patients with CRC who underwent complete resection of ≤Stage III tumors at Wakayama Medical University Hospital between January and December 2013. We assessed the correlation between CD155 and TIGIT expressions and prognosis as well as the clinicopathological background of CD155 and TIGIT. Results Patients with high CD155 and TIGIT expressions showed worse prognosis than those with other levels of expression (p = 0.026). In multivariate analysis that also included the existing prognostic markers, high CD155 and TIGIT expressions were identified as independent poor prognostic factors. Conclusions The interaction between CD155 and TIGIT possibly plays an important role in the immunological mechanism of CRC. Therefore, it may be possible to effectively predict the postoperative prognosis of CRC by evaluating the combined expression of CD155 and TIGIT. The study findings suggest that CD155 and TIGIT can predict clinical outcomes, thereby contributing to the personalized care of CRC.
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Yan, Zhang. "Increased expression of CD155 and CD112 on monocytes in septic patients (INC6P.327)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 192.29. http://dx.doi.org/10.4049/jimmunol.194.supp.192.29.

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Abstract The poliovirus receptor CD155 and its family member CD112 (PRR-2 (poliovirus receptor-related family 2), also called nectin-2) are ligands for human and mouse CD226. Human CD112 and CD155 are broadly distributed on epithelial and endothelial cells in many tissues, and overexpressed on certain tumors. Several reports have shown that the interaction between CD155 and CD226 are important for the elimination of target cells by NK and cytotoxic T cells, however, it remains elusive how CD155 and CD112 are regulated in sepsis. In our study, we showed that the expression of CD155 and CD112 on monocytes was significantly upregulated in septic patients which all had a significant reduction in expression of HLA-DR on monocytes, an immunosuppression marker of sepsis, indicating the existence of negative correlation between CD155/122 and HLA-DR. Next studies were undergoing on the mechanisms underlying regulation of the expression of CD155 and CD112 in sepsis and whether signals by CD155/CD112 negatively regulated the expression of HLA-DR.
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Tang, Xiyang, Jie Yang, Anping Shi, Yanlu Xiong, Miaomiao Wen, Zhonglin Luo, Huanhuan Tian, et al. "CD155 Cooperates with PD-1/PD-L1 to Promote Proliferation of Esophageal Squamous Cancer Cells via PI3K/Akt and MAPK Signaling Pathways." Cancers 14, no. 22 (November 15, 2022): 5610. http://dx.doi.org/10.3390/cancers14225610.

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Background: Esophageal cancer is still a leading cause of death among all tumors in males, with unsatisfactory responses to novel immunotherapies such as anti-PD-1 agents. Herein, we explored the role of CD155 in esophageal squamous cell cancer (ESCA) and its underlying molecular mechanisms. Methods: Publicly available datasets were used for differential gene expression and immune infiltration analyses, and their correlation with patient survival. A total of 322 ESCA and 161 paracancer samples were collected and evaluated by performing immunohistochemistry and the H score was obtained by performing semiquantitative analysis. In vitro transfection of ESCA cell lines with lentivirus vectors targeting CD155 was performed to knockdown the protein. These cells were analyzed by conducting RNA sequencing, and the effects of CD155 knockdown on cell cycle and apoptosis were verified with flow cytometry and Western blotting. In addition, in vivo experiments using these engineered cell lines were performed to determine the role of CD155 in tumor formation. A small interfering RNA-mediated knockdown of Nectin3 was used to determine whether it phenocopied the profile of CD155 knockdown. Results: CD155 is highly expressed in ESCA tissues and is positively associated with PD1, PDL1, CD4, IL2RA, and S100A9 expression. Furthermore, CD155 knockdown inhibited ESCA cells’ proliferation by impairing the cell cycle and inducing cell apoptosis. Bioinformatics analysis of the gene expression profile of these engineered cells showed that CD155 mainly contributed to the regulation of PI3K/Akt and MAPK signals. The downregulation of Nectin3 expression phenocopied the profile of CD155 knockdown. Discussion: CD155 may cooperate with PD-1/PD-L1 to support ESCA proliferation in ways other than regulating its underlying immune mechanisms. Indeed, CD155 downregulation can impair ESCA cell pro-cancerous behavior via the inhibition of the PI3K/Akt and MAPK signaling pathways. Moreover, Nectin3 may be a ligand of CD155 and participate in the regulation of ESCA cells’ proliferation. Hence, the inhibition of CD155 may enhance the therapeutic effect of anti-PD-1 immunotherapies in ESCA.
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Li, Yu-Chen, Quan Zhou, Qing-Kun Song, Rui-Bin Wang, Shuzhen Lyu, Xiudong Guan, Yan-Jie Zhao, and Jiang-Ping Wu. "Overexpression of an Immune Checkpoint (CD155) in Breast Cancer Associated with Prognostic Significance and Exhausted Tumor-Infiltrating Lymphocytes: A Cohort Study." Journal of Immunology Research 2020 (January 13, 2020): 1–9. http://dx.doi.org/10.1155/2020/3948928.

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Purpose. The immune checkpoint inhibitor is approved for breast cancer treatment, but the low expression of PD-L1 limits the immunotherapy. CD155 is another immune checkpoint protein in cancers and interacts with ligands to regulate immune microenvironment. This study is aimed at investigating the expression of CD155 and the association with prognosis and pathological features of breast cancer. Methods. 126 patients were recruited this cohort study consecutively, and CD155 expression on tumor cells was detected by immunohistochemistry. The Kaplan-Meier survival curve and Cox hazard regression model were used to estimate the association. Results. 38.1% patients had an overexpression of CD155, and the proportion of tumor cells with CD155 overexpression was 17%, 39%, 37%, and 62% among Luminal A, Luminal B, HER2-positive, and triple negative breast cancer cases, respectively (p<0.05). Patients with CD155 overexpression had the Ki-67 index significantly higher than that of patients with low expression (42% vs. 26%). Though the number of tumor-infiltrating lymphocytes was higher among patients with CD155 overexpression (144/HPF vs. 95/HPF), the number of PD-1+ lymphocytes was significantly higher (52/HPF vs. 25/HPF, p<0.05). Patients of CD155 overexpression had the disease-free and overall survival decreased by 13 months and 9 months, respectively (p<0.05). CD155 overexpression was associated with an increased relapse (HR=13.93, 95% CI 2.82, 68.91) and death risk for breast cancer patients (HR=5.47,1.42,20.99). Conclusions. Overexpression of CD155 was correlated with more proliferative cancer cells and a dysfunctional immune microenvironment. CD155 overexpression introduced a worse relapse-free and overall survival and might be a potential immunotherapy target for breast cancer.
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He, Yongning, Steffen Mueller, Paul R. Chipman, Carol M. Bator, Xiaozhong Peng, Valorie D. Bowman, Suchetana Mukhopadhyay, Eckard Wimmer, Richard J. Kuhn, and Michael G. Rossmann. "Complexes of Poliovirus Serotypes with Their Common Cellular Receptor, CD155." Journal of Virology 77, no. 8 (April 15, 2003): 4827–35. http://dx.doi.org/10.1128/jvi.77.8.4827-4835.2003.

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ABSTRACT Structures of all three poliovirus (PV) serotypes (PV1, PV2, and PV3) complexed with their cellular receptor, PV receptor (PVR or CD155), were determined by cryoelectron microscopy. Both glycosylated and fully deglycosylated CD155 exhibited similar binding sites and orientations in the viral canyon for all three PV serotypes, showing that all three serotypes use a common mechanism for cell entry. Difference maps between the glycosylated and deglycosylated CD155 complexes determined the sites of the carbohydrate moieties that, in turn, helped to verify the position of the receptor relative to the viral surface. The proximity of the CD155 carbohydrate site at Asn105 to the viral surface in the receptor-virus complex suggests that it might interfere with receptor docking, an observation consistent with the properties of mutant CD155. The footprints of CD155 on PV surfaces indicate that the south rim of the canyon dominates the virus-receptor interactions and may correspond to the initial CD155 binding state of the receptor-mediated viral uncoating. In contrast, the interaction of CD155 with the north rim of the canyon, especially the region immediately outside the viral hydrophobic pocket that normally binds a cellular “pocket factor,” may be critical for the release of the pocket factor, decreasing the virus stability and hence initiating uncoating. The large area of the CD155 footprint on the PV surface, in comparison with other picornavirus-receptor interactions, could be a potential limitation on the viability of PV escape mutants from antibody neutralization. Many of these are likely to have lost their ability to bind CD155, resulting in there being only three PV serotypes.
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Chandramohan, Vidyalakshmi, Jeffrey D. Bryant, Hailan Piao, Stephen T. Keir, Eric S. Lipp, Michaela Lefaivre, Kathryn Perkinson, Darell D. Bigner, Matthias Gromeier, and Roger E. McLendon. "Validation of an Immunohistochemistry Assay for Detection of CD155, the Poliovirus Receptor, in Malignant Gliomas." Archives of Pathology & Laboratory Medicine 141, no. 12 (December 1, 2017): 1697–704. http://dx.doi.org/10.5858/arpa.2016-0580-oa.

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Context.— The oncolytic polio-rhinovirus recombinant (PVSRIPO) has demonstrated promise in currently ongoing phase I/II clinical trials against recurrent glioblastoma and was granted breakthrough therapy designation by the Food and Drug Administration/Center for Biologics Evaluation and Research. A reliable clinical assay to document expression of the poliovirus receptor, CD155, in routinely available patient tumor samples is needed for continued clinical development of PVSRIPO oncolytic immunotherapy in primary brain tumors and beyond. Objectives.— To validate a novel anti-CD155 antibody for immunohistochemistry and develop a robust, reliable, and specific protocol for detecting CD155 expression in glioblastoma formalin-fixed, paraffin-embedded (FFPE) tissue samples. To characterize the expression of CD155 in human glioblastoma cells as well as to evaluate the influence of CD155 expression levels on tumor cell susceptibility to PVSRIPO infection and killing. Design.— Immunohistochemical staining on glioblastoma FFPE tissue sections and immunoblot of corresponding frozen tissues were performed. Positive controls were confirmed sites of poliovirus propagation, spinal cord anterior horn, and tonsils; negative controls were vascular smooth muscle in patient samples and FFPE sections from a confirmed CD155-negative Burkitt lymphoma line (Raji). Results.— We succeeded in developing a reliable assay to specifically detect CD155 by immunohistochemistry in glioblastoma FFPE sections. Our data suggest widespread, virtually universal expression of CD155 in glioblastoma cells at levels commensurate with susceptibility to PVSRIPO infection and killing. Conclusions.— Anti-CD155 antibody D3G7H achieves monospecific detection of CD155 in immunoblots of tumor homogenates and immunohistochemistry of tumor FFPE sections. Our assay has utility in defining appropriate use of PVSRIPO in oncolytic immunotherapy against malignant glioma and other cancer histotypes.
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Cho, Monica, Madison Phillips, Longzhen Song, Amy Erbe-Gurel, and Christian M. Capitini. "CD155 axis modulation promotes natural killer cell-mediated graft-versus-tumor effects against osteosarcoma." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 62.06. http://dx.doi.org/10.4049/jimmunol.208.supp.62.06.

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Abstract Patients with relapsed/refractory osteosarcoma (OSA) have a poor prognosis with few treatment options. Immunotherapy with allogeneic natural killer (NK) cells after allogeneic bone marrow transplant (BMT) is an attractive approach to employ a graft-versus-tumor (GVT) effect against OSA. However, NK cells have had limited success against solid tumors in vivo. CD155 is overexpressed on OSA and interacts with DNAM-1, an activating ligand, and TIGIT, an inhibitory ligand, on NK cells. The impact of blocking CD155 after allogeneic BMT is unknown. IL-15-expanded C57BL/6 (B6, H-2b) and BALB/c (H-2d) murine NK cells were co-cultured with K7M2 murine OSA (H-2d) after CD155 and CD155 ligand blockade, and analyzed by flow cytometry and cytotoxicity assays. BALB/c mice were also transplanted with T cell depleted allogeneic B6 or syngeneic BALB/c bone marrow, challenged with K7M2 and treated with IL-15-expanded NK cells and CD155 blockade. Allogeneic NK cells showed increased degranulation, interferon-gamma production and cytotoxicity against K7M2 OSA in vitro compared to syngeneic NK cells. NK cell activation and cytotoxicity were further enhanced by CD155 and TIGIT blockade, but decreased with DNAM-1 blockade. In vivo, allogeneic NK cell infusion and anti-CD155 treatment decreased tumor growth and increased survival compared to syngeneic NK cell treatment, without induction of graft-versus-host-disease. CD155 blockade augments NK cell activation, cytotoxicity and GVT effects against OSA without toxicity, suggesting TIGIT is the dominant CD155 checkpoint during allogeneic BMT. CD155 blockade with allogeneic NK cell therapy after BMT may be an effective combination immunotherapy platform for treating relapsed/refractory OSA. Supported by NIH grants (T32 CA009135, R01 CA215461)
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Dissertations / Theses on the topic "CD155"

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Martel, André Bernard. "Targeting CD155 on Myeloid Derived Suppressor Cells to Prevent Postoperative Immunosuppression in Cancer Patients." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41151.

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Surgery, although required to treat most solid cancers, can increase tumour seeding and metastases. We have previously shown that surgery-induced myeloid derived suppressor cells (Sx-MDSCs) play an important role in this process by directly suppressing NK cells. The Sx- MDSCs increase significantly immediately after surgery but the exact mechanism by which Sx-MDSCs suppress NK cells is still unknown. In this work, we have discovered that CD155 poliovirus receptor is significantly and specifically upregulated on Sx-MDSCs following surgical stress but is minimally expressed on other immune cells. We also demonstrate that blocking CD155 in vivo leads to an improved NK cell phenotype, measured by DNAM-1 and NKG2D, and increased NK cytotoxicity. Additionally, ex vivo CD155 blockade significantly decreases the suppressive effect of Sx-MDSCs in cancer patients. Expansion of CD155 on Sx- MDSCs could be responsible for the profound postoperative NK cell suppression, which makes it a very appealing perioperative target for immunotherapy.
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Maier, Michael Klaus. "Studien zur Funktion von murinem CD155 bei der Migration von Leukozyten und der Entstehung einer humoralen Immunantwort." kostenfrei, 2007. http://d-nb.info/988269511/34.

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Baury, Béatrice. "CD155, un membre de la superfamille des immunoglobulines : homologies avec le gène Tage4 du rat, expression des formes membranaires et solubles." Nantes, 2002. http://www.theses.fr/2002NANT21VS.

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Notre projet a été axé autour de deux membres de la superfamille des immunoglobulines, le gène Tage4 de rat, dont la principale caractéristique est sa surexpression dans les tumeurs coliques chez le rat et la souris et le gène CD155 humain codant pour le récepteur du virus de la poliomyélite (PV). Nous avons déterminé l'organisation structurale du gène Tage4 en mettant notamment au point une technique de marche sur l'ADN pour isoler la région promotrice. Nos résultats ont souligné l'existence de nombreuses homologies structurales entre les gènes Tage4 et CD155. De plus, le produit du gène Tage4 permet l'entrée des virus utilisant le CD155 comme récepteur, à l'exception du PV. Ces homologies structurales et fonctionnelles suggèrent que le gène Tage4 est probablement l'orthologue du gène CD155. En outre, nous avons mis en évidence une surexpression du CD155 dans les carcinomes colorectaux. A l'instar de l'antigène carcinoembryonnaire (ACE), la surexpression du CD155 est un événement précoce dans la carcinogenèse colique. . .
Our project focused on two members of the immunoglobulin superfamily, the rat Tage4 gene, which is overexpressed in rat and mice colon tumors, and the human CD155 gene coding for the poliovirus (PV) receptor. We have determined the structural organisation of the Tage4 gene by designing a DNA walking method to isolate the promoter region. Our results have underlined the existence of numerous homologies between Tage4 and CD155. Moreover, the product of the Tage4 gene can mediate entry into cells of the viruses, except PV, that use CD155 as a receptor. These structural and functional homologies suggest that the Tage4 gene is probably orthologous to the gene for CD155. Besides, we have shown by RT-PCR and immunohistochemistry that CD155 is overexpressed in colorectal carcinoma. As the carcinoembryonic antigen (CEA), the CD155 overexpression is an early event in colon carcinogenesis. However, unlike the CEA, the CD155 expression is not regulated by the interferon gamma nor by the nuclear receptor PPAR gamma (Peroxisome Proliferator-Activated Receptor). We have demonstrated the existence of CD155 secreted isoforms by immunoprecipitation in serum, in cerebrospinal fluid and in culture medium of polarised epithelial cell. .
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Jassam, Samah Ali. "Role of CD15 and CD15s in the cellular mechanisms of cancer cell metastasis from lung to the brain." Thesis, University of Portsmouth, 2016. https://researchportal.port.ac.uk/portal/en/theses/role-of-cd15-and-cd15s-in-the-cellular-mechanisms-of-cancer-cell-metastasis-from-lung-to-the-brain(de581581-027d-4106-9c23-9daa534d684f).html.

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Non-small cell lung cancer is one of the most common primary tumours to metastasise to the brain in adults. The underlining molecular mechanisms of brain metastasis are still not fully understood. Interactions between brain endothelial cells and cancer cells play key roles in brain metastasis. CD15 and CD15s are cell-cell adhesion molecules which interact with E-selectin which is expressed on endothelial cells and known to be involved in the leukocyte homing process as well as being implicated in metastasis with many non-CNS neoplasms. The aim of this project was to investigate the role of CD15 and CD15s in cancer cell adhesion to brain endothelial cells and transendothelial migration of lung cancer cells during brain metastasis. Expression of CD15, CD15s and CD62E was characterised in human primary and brain metastatic lung cancer cells using immunocytochemistry, flow cytometry, Western blot and immunohistochemistry in human tissue sections. Effects of CD15 and CD15s expression on NSCLC metastatic to brain were assessed using genetic manipulation (overexpression and knockdown) followed by functional assays. Both CD15 and CD15s were overexpressed and knockdowned and cell-cell adhesion was then examined using qualitative and quantitative adhesion assays, under both static and flow physiological conditions. Transendothelial migration potential was also assessed using a voltometer, Electric Cell-Substrate Impedance sensing system and cell-monitoring system CellZscope™. Findings showed that CD15 and CD15s were prominently expressed on metastatic lung cancer cells (SEBTA-001, SEBTA-005 and NCI-H1299) and weakly expressed on both primary lung cancer cells (COR-L105 and A549) and brain endothelium (hCMEC/D3). The highest expression of CD62E was observed on brain endothelium stimulated with TNF-α (25pg/ml) (p < 0.001). CD15, CD15s and CD62E expression was detected in human metastatic tissues. The absence of CD62E and immunoblocking and knockdown of CD15 and CD15s significantly reduced the adhesion of cancer cells under both static and shear stress conditions (p<0.0001). Overexpression of CD15 and CD15s significantly increased their adhesion on an endothelial monolayer (p < 0.001). Metastatic cancer cells were able to transmigrate through a brain endothelial monolayer compared to primary and glioblastoma multiforme (GBM) cells. Knockdown of CD15 and CD15s decreased the transendothelial migration potential of cancer cells while even primary lung cancer cells and GBM cells transmigrated following overexpression of CD15 and CD15s. These results confirmed the correlation between CD15 and CD15s in adhesion as well as transendothelial migration of cancer cells during cerebral metastasis.
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Zevian, Shannin Christine. "Structure-function analysis of Tetraspanin CD151." Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/3022.

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The basement membrane protein laminin-332 (laminin-5) mediates both stable cell adhesion and rapid cell migration, and thus has the potential to either restrain or promote tumor cell metastasis. The major cellular receptors for laminin-332 are integrin α3β1, which mediates rapid tumor cell migration, and integrin α6β4, which often mediates stable cell attachment. Tetraspanin protein CD151 interacts directly with both α3β1 and α6β4 integrins and with other tetraspanins, thereby promoting α3β1 and α6β4 association with tetraspanin-enriched microdomains on the cell surface. To explore the possibility of selectively modulating tumor cell responses to laminin-332, we re-expressed a series of CD151 mutants in epidermoid carcinoma cells with near total, RNAi- mediated silencing of endogenous CD151. CD151's interactions with its integrin partners or its interactions with other tetraspanins were selectively disrupted by specific mutations in the CD151 large extracellular loop (EC2 domain) or in intracellular CD151 palmitoylation sites, respectively. CD151- integrin association and CD151-tetraspanin association were both important for α3β1 integrin- dependent initial adhesion and rapid migration on laminin-332. Remarkably, however, only CD151-integrin association was required for stable, α6β4 integrin-dependent cell attachment on laminin-332. In gap-filling assays, where CD151-silenced cells moved more rapidly than WT cells, again, only CD151-integrin association was required to restrict movement into the gap, suggesting that both α3β1 and α6β4 integrin must be able to associate with CD151 in order restrict group motility. In addition, we found that a QRD amino acid motif in the CD151 EC2 domain that had been thought to be crucial for CD151-integrin interaction is not essential for CD151-integrin association or for CD151's ability to promote several different integrin functions. These new data suggest potential strategies for selectively modulating migratory cell responses to laminin-332, while leaving stable cell attachment on laminin-332 intact.
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Romanets, Olga. "Study of the role of measles virus receptor CD150 in viral immunopathogenesis and characterization of novel CD150 isoform." Phd thesis, Ecole normale supérieure de lyon - ENS LYON, 2012. http://tel.archives-ouvertes.fr/tel-00923189.

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Measles virus (MV) causes an acute childhood disease, associated in certain cases with the infection of the central nervous system (CNS). MV induces a profound immunosuppression, resulting in high infant mortality. The major cellular receptor for MV is CD150, which binds MV hemagglutinin (MV-H). As dendritic cell (DC) dysfunction is considered to be essential for the MV immunopathogenesis, we analyzed consequences of MV-H interaction with DCs. We developed an experimental model allowing us to analyze the direct CD150-MV-H interaction in the absence of infectious context. This interaction caused the downregulation of surface expression of CD80, CD83, CD86 and HLA-DR molecules and inhibition of IL-12 production in DCs. DCs also failed to activate T cell proliferation. The CD150-MV-H interaction in DCs and B cells decreased the phosphorylation of JNK1/2, but not ERK1/2 kinases, after subsequent CD150 ligation with anti-CD150 antibodies. Moreover, MV-H by itself induced Akt phosphorylation via CD150 in DCs and B cells. Engagement of CD150 by MV-H in mice transgenic for human CD150 decreased the inflammatory reaction, contact hypersensitivity response, confirming the immunosuppressive effect of CD150-MV-H interaction in vivo. Furthermore, our studies revealed the CD150 expression in CNS tumors and identified the novel CD150 isoform, containing an additional 83bp exon expressed in lymphoid cells, DCs and CNS tumors. Although its isoforms remain intracellular in tumor cells, CD150 may represent a new marker for human brain tumors. Novel mechanism of CD150-induced immunosuppression and new CD150 isoform identified in these studies shed new light on its immunoregulatory role and CD150 isoform diversity and open perspectives for their clinical applications.
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Moyano, Rodríguez Yolanda 1992. "Mitosis exit regulation by Cdc5 and PP2A-Cdc55." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668051.

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In this thesis we studied the role of PP2ACdc55 in the cytokinesis regulation and the contribution of Cdc5 kinase in the mitosis exit using budding yeast as model. Previously, it was suggested a putative PP2ACdc55 role in cytokinesis based on the elongated phenotype in absence of Cdc55. However, the PP2ACdc55 function during cytokinesis and its direct targets were not identified. In this thesis, we demonstrated that PP2ACdc55 regulates the IPC’s phosphorylation and their residence time at the bud neck. In addition, we showed that PP2ACdc55 coordinates actomyosin ring (AMR) contraction with septa formation. As a second objective, we analyzed the Net1 residues to be phosphorylated by Cdc5 kinase contributing to the Cdc14 release from the nucleolus and mitotic exit progression.
En esta tesis hemos investigado el papel de la fosfatasa PP2ACdc55 en la regulación de la citocinesis y la contribución de la quinasa Cdc5 en la salida de mitosis en la levadura de gemación. Previamente, se había sugerido un posible papel de la PP2ACdc55 en citocinesis basándose en el fenotipo elongado en ausencia de Cdc55. Sin embargo, la función de la PP2ACdc55 durante la citocinesis y sus sustratos no han sido estudiados. En esta tesis, hemos demostrado que la PP2ACdc55 regula la desfosforilación de las proteínas de IPC que regulan la citocinesis; así como, su tiempo de localización en el cuello. Además, hemos observado como la PP2ACdc55 realiza un papel en la coordinación de la contracción del anillo de actomiosina y la formación del septo. En cuanto a Cdc5, analizamos los posibles residuos de Net1 fosforilados por Cdc5 que contribuyen a la liberación de Cdc14 en la salida de mitosis.
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Maurik, Andre van. "The role of CD40-CD154 interactions in allograft transplantation." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249302.

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Dewitte, Antoine. "Plaquettes sanguines et insuffisance rénale aiguë : rôle du couple CD154/CD40 dans la constitution des lésions tubulaires." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0906.

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L’insuffisance rénale aiguë (IRA) est une pathologie fréquente en réanimation. Elle est associée à une mortalité et une morbidité importante. Le sepsis en est la cause la plus fréquente. La compréhension de la physiopathologie du sepsis et de ses complications a beaucoup progressé ces dernières années mais ne s’est pas encore traduite par des avancées thérapeutiques significatives en pratique clinique. Le paradigme d’une altération de la perfusion sanguine comme paramètre clé de la constitution des lésions rénales a ainsi été remis en question, plusieurs travaux révélant que le débit sanguin rénal n’est pas toujours altéré en cas de sepsis, et qu’une IRA peut se développer en cas de débit sanguin rénal préservé, voire augmenté. Le sepsis est caractérisé par de profondes perturbations de la réponse immunitaire et une réaction inflammatoire disproportionnée. A l’origine de l’atteinte rénale, l’inflammation et les altérations de la microcirculation sont maintenant considérés comme des mécanismes physiopathologiques fondamentaux. Au-delà de leur rôle dans l’hémostase, la contribution des plaquettes sanguines à la réponse inflammatoire, au maintien de l’intégrité tissulaire et à la défense contre les infections a considérablement élargi le spectre de leurs compétences et en a fait des acteurs physiopathologiques potentiels dans le sepsis. Les plaquettes sanguines exercent la plupart de ces fonctions grâce à l’expression de nombreux médiateurs membranaires ou solubles. Parmi eux, le CD154 tient une place particulière : les plaquettes sont une source essentielle de CD154 dans l’organisme et il joue un rôle central dans la réponse inflammatoire. Nous proposons dans ce travail un aperçu de ces avancées physiopathologiques récentes et nous discutons de la contribution des plaquettes et du CD154 dans les atteintes microcirculatoires et les défaillances multi-viscérales dans le sepsis. Nous nous sommes intéressés au rôle pro-inflammatoire du CD154 en conditions d’hypoxie au niveau de l’épithélium tubulaire rénal. Des données récentes soulignent en effet l’importance de l’hypoxie dans la réaction inflammatoire. Le contrôle de la production d’interleukine (IL)-6, une cytokine centrale de la réponse inflammatoire, par le CD154 a été étudié dans un modèle de culture de cellules épithéliales tubulaires (CET) rénales. Un modèle murin d’IRA par ischémie/reperfusion rénale a également été mis au point et appliqué à des souris déficientes en CD154 et CD40. Nos travaux révèlent que le CD154 induit fortement la sécrétion d’IL-6 par les CET en conditions d’hypoxie et que les souris déficientes en CD154 régénèrent plus rapidement leur épithélium tubulaire après ischémie/reperfusion rénale. Ces résultats pourraient ouvrir la voie à de potentielles pistes thérapeutiques pour la prise en charge des IRA d’origine septique
Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with increased morbidity and mortality. Sepsis is the most common cause of AKI. The understanding of sepsis pathophysiology and its complications has progressed significantly in recent years but has not yet been translated into significant therapeutic advances in clinical practice. The traditional paradigm that sepsis-induced AKI is linked to renal hypoperfusion has been challenged by recent evidences showing that renal blood flow is not universally impaired during sepsis,and that AKI can develop in the presence of normal or even increased renal bloodflow. Sepsis is characterized by profound alterations of the immune response and adisproportionate inflammatory response. Inflammation and microcirculatorydysfunction are now considered as fundamental pathophysiological mechanisms atthe origin of renal injuries. Beyond haemostasis, the contribution of platelets ininflammation, tissue integrity and defence against infections has considerablywidened the spectrum of their role and made them potential physiopathologicalactors in sepsis. Platelets fulfil most of these functions through the expression ofmembrane-bound or soluble mediators. Among them, CD154 holds a peculiarposition, as platelets represent a major source of CD154 and as CD154 is a centralregulator of inflammation. Here, we provide an overview of these recentpathophysiological advances and discuss the platelets and CD154 contribution tomicrocirculatory alterations in multi-organ dysfunction in sepsis. We investigated thepro-inflammatory role of CD154 under hypoxic conditions in the renal tubularepithelium as recent data highlight the importance of hypoxia in the inflammatoryreaction. We studied the control of interleukin (IL)-6 production, a key cytokineinvolved in inflammation, by CD154 in oxygen deprivation conditions using a kidneytubular epithelial (TEC) cell line model. We also studied a murine model of kidneyinjury after ischemia/reperfusion, a model that was applied in CD154 and CD40deficient mice. We found that CD154 is a potent inducer of IL-6 secretion by TEC inhypoxia and that CD154-deficient mice regenerate earlier the tubular epithelium afterischemia/reperfusion injury. These findings may provide potential avenues for septicAKI management and therapy
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Higa, Ryoko. "CD105 maintains the thermogenic program of beige adipocytes by regulating Smad2 signaling." Kyoto University, 2018. http://hdl.handle.net/2433/235056.

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Books on the topic "CD155"

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Churchill, Jeremy. Honda CB/CD125 T & CM125 C twins owners workshop manual. Haynes, 1990.

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Books, Bchimak. Buchhaltung: Einfaches Einnahmen- und Ausgaben Kassenbuch Für Kleinunternehmen, Einfaches Buchhaltungsbuch Für Selbstständige, Freiberufler und Als Haushaltsbuch Für Die Buchhaltung, über 3300 Einträge Auf 120 Seiten). Cd55. Independently Published, 2021.

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Chronic Care for Neglected Infectious Diseases: Leprosy/Hansen's Disease, Lymphatic Filariasis, Trachoma, and Chagas Disease. Pan American Health Organization, 2021. http://dx.doi.org/10.37774/9789275122501.

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In 2016, PAHO's Directing Council, through Resolution CD55.R9, approved the “Plan of Action for Elimination of Neglected Infectious Diseases (NID) and Post-Elimination Actions, 2016-2022.” This Resolution urges Member States to implement a set of interventions to reduce the burden of disease by NID in the Americas by 2022, including “…support promotion of treatment, rehabilitation, and related support services through an approach focused on integrated morbidity management and disability prevention for individuals and families afflicted by those neglected infectious diseases that cause disability and generate stigma.” NIDs can have devastating chronic sequelae for patients, such as disability, visible change or loss in body structure, loss of tissue, and impairment of proper tissue and organ function, among others. All of these can in turn lead to unjustified discrimination, stigmatization, mental health problems, and partial or total incapacity to work, perpetuating the vicious cycle of neglected diseases as both a consequence and a cause of poverty. Patients with chronic conditions caused by NIDs require proper health care in order to prevent further damage and improve their living and social conditions. This should be provided at the primary health care level, as patients suffering from NIDs are often unable to travel to or afford to pay for specialized care services. Care for patients suffering from chronic morbidity caused by NID should be integrated into care for other chronic conditions caused by non-communicable diseases. This manual provides a framework for morbidity management and disability prevention of patients affected by NIDs and gives specific guidance for the proper care of patients suffering from chronic conditions caused by lymphatic filariasis, leprosy, trachoma, and Chagas disease. It is intended to be used mainly by health care workers at the primary health care level, but health workers at more complex and specialized levels may also find it useful.
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Book chapters on the topic "CD155"

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Malla, R. R., Seema Kumari, V. Gayatri Devi, Anil Badana, and G. Murali Mohan. "CD151." In Encyclopedia of Signaling Molecules, 842–46. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101599.

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Malla, R. R., Seema Kumari, V. Gayatri Devi, Anil Badana, and G. Murali Mohan. "CD151." In Encyclopedia of Signaling Molecules, 1–5. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101599-1.

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Nicholson-Weller, A. "Decay Accelerating Factor (CD55)." In Membrane Defenses Against Attack by Complement and Perforins, 7–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77014-2_2.

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Calderhead, D. M., Y. Kosaka, E. M. Manning, and R. J. Noelle. "CD40-CD154 Interactions in B-Cell Signaling." In Signal Transduction and the Coordination of B Lymphocyte Development and Function II, 73–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59641-4_4.

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Tokunaga, Osamu, Rahmawati Minhajat, and Daisuke Mori. "Tumor Angiogenesis in Cancers: Expression of CD105 Marker." In Methods of Cancer Diagnosis, Therapy, and Prognosis, 41–50. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3186-0_3.

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Seon, Ben K., and Shant Kumar. "CD105 Antibody for Targeting of Tumor Vascular Endothelial Cells." In The New Angiotherapy, 499–515. Totowa, NJ: Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-126-8_26.

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Law, Che-Leung, and Iqbal S. Grewal. "Therapeutic Interventions Targeting CD40L (CD154) and CD40: The Opportunities and Challenges." In Advances in Experimental Medicine and Biology, 8–36. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-89520-8_2.

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Ishihara, K., and T. Hirano. "BST-1/CD157 Regulates the Humoral Immune Responses in vivo." In Human CD38 and Related Molecules, 235–55. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000058772.

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Malla, Rama Rao. "CD151: A Lateral Organizer and Modulator of Tumor Microenvironment in Gastrointestinal Cancers." In Novel therapeutic approaches for gastrointestinal malignancies, 83–99. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5471-1_6.

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Juhl, H., F. Helmig, H. Kalthoff, and B. Kremer. "Limitation der Antikörpertherapie gastrointestinaler Karzinome durch die Komplementresistenzfaktoren CD55 und CD59." In Chirurgisches Forum ’96 fur experimentelle und klinische Forschung, 455–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80138-9_92.

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Conference papers on the topic "CD155"

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Sayitoglu, Ece C., Michael Chrobok, Anna-Maria Georgoudaki, Benjamin J. Josey, Michelle Hartman, Esha Vallabhaneni, Rajeev Herekar, et al. "Abstract A55: Natural killer cells genetically modified to overexpress DNAM-1 exert enhanced antitumor responses against CD112/CD155+ sarcomas and other malignancies." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a55.

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Briukhovetska, D., J. Jobst, S. Endres, and S. Kobold. "P09.03 Activation of IL-22 signaling correlates with higher CD155 expression and stratifies poor outcomes of early-stage lung and breast cancer patients." In iTOC9 – 9th Immunotherapy of Cancer Conference, September 22–24, 2022 – Munich, Germany. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-itoc9.59.

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Song, Qingkun, and Shuzhen Lv. "Abstract P1-09-05: Overexpression of CD155 in breast cancer microenvironment, associated with higher counts of tumor-infiltrating lymphocytes and increased risk of relapse and death." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p1-09-05.

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Cao, Liang, Fatima Karzai, Andrea Apolo, Ravi Madan, Yunkai Yu, James Gulley, William Figg, and William Dahut. "Abstract 2048: Pharmacodynamic biomarker studies of TRC105 anti-endoglin (CD105) antibody revealed anti-angiogenic activity associated with CD105 depletion." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2048.

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Fritchie, Karen, Steven Attia, Scott Okuno, Carola Arndt, and Steven Robinson. "Abstract B237: CD105: A therapeutic target for sarcomas." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b237.

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Cron, RQ, A. Genin, and M. Brunner. "OP0139 Regulation of cd154 in systemic lupus erythematosus." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.72.

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Detchokul, Sujitra, Michael W. Parker, Elizabeth D. Williams, Olivia M. Herdiman, Melissa Davis, Kelvin Kee, Damien M. Bolton, and Albert G. Frauman. "Abstract 469: CD151 and cell motility in prostate cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-469.

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Salibi, Rami, Robert M. Kottmann, Everett Porter, Richard Phipps, and Patricia J. Sime. "CD40 Ligand (CD154) Is Elevated In Fibrotic Lung Diseases." 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.a2658.

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Michaelson, J. E., F. Zhang, X. Zhang, and H. Huang. "Traction force in tetraspanin CD151 deficient human dermal microvascular endothelial cells." In 2010 36th Annual Northeast Bioengineering Conference. IEEE, 2010. http://dx.doi.org/10.1109/nebc.2010.5458143.

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Jin, Hongyan, John T. Hoff, Xinyu Deng, Ronny I. Drapkin, and Xiuwei H. Yang. "Abstract 4613: A role of integrin-associated CD151 in human ovarian cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4613.

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Reports on the topic "CD155"

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Zhang, Dan, Jingting Liu, Mengxia zheng, Chunyan Meng, and Jianhua Liao. Prognostic and Clinicopathological significance of CD155 Expression in Cancer Patients: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0087.

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Review question / Objective: The present study aimed to comprehensively explore the relationship between CD155 expression and clinical characteristics and prognosis of cancer patients. The study was based on comprehensive search of relevant literature. In particular, the study attempted to define the role of CD155 in various cancer types. Eligibility criteria: The pre-established inclusion criteria were as follows: (1) all subjects were cancer patients who received standard treatment; (2) The expression of CD155 in the cancer patients was well-examined, and all patients were assigned into two groups based on the expression; (3) survival analysis was performed based on these two groups, and provided sufficient data to estimate the risk ratio (HR) and 95% confidence interval (CI) for overall survival (OS); and (4) scientific and reasonable research. Case reports, reviews, abstracts, letters, bioinformatic analysis, TCGA analysis, and articles that did not meet the inclusion criteria were excluded from analyses.
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Yang, Xiuwei. Critical Roles of CD151-alpha6beta1 and CD151-alpha6beta4 Integrin Complexes in Human Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada517279.

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Yang, Xiuwei. CD151 Synergy With ErbB Receptors During Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada501759.

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Hemler, Martin E. Targeting of CD151 in Breast Cancer and in Breast Cancer Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada477433.

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Dimitrova, Violeta S., Vanyo I. Mitev, and Antonia R. Isaeva. The α and β Subunits of CK2 Are Individually and Phenotypespecifically Involved in Autocrine and BMP4‑Triggered Regulation of Proliferation of STRO‑1+, STRO‑1-, CD105+ and CD105- Cells within Human Apical Papilla. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, December 2020. http://dx.doi.org/10.7546/crabs.2020.12.07.

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Granata, Joseph, Hugo Sanchez, Phillip Loeschinger, and Jodi Evans. CD105 Deficiency in Mouse Aorta-Derived Progenitor Cells Promotes an Enhanced Inflammatory Response to Lipopolysaccharide. Journal of Young Investigators, October 2018. http://dx.doi.org/10.22186/jyi.35.4.61-66.

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