Relevant bibliographies by topics / CD133+

Academic literature on the topic 'CD133+'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "CD133+"

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Rey, Imelda, Agung Putra, Dharma Lindarto, and Fauzi Yusuf. "Relationship between CD 163 Tumor-Associated Macrophages and Colorectal-Cancer Stem Cell Markers." Open Access Macedonian Journal of Medical Sciences 9, B (October 19, 2021): 1381–86. http://dx.doi.org/10.3889/oamjms.2021.7188.

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BACKGROUND: Colorectal-cancer stem cells (CR-CSCs) represent a specific subpopulation of colorectal cancer (CRC) cells, which are characterized by the expression of CD133 and CD166. Tumor-associated macrophages (TAMs), found near CSCs may represent polarized macrophages, which are characterized by CD163 expression. In most tumors, TAMs may promote aggressive tumor development, leading to poor prognoses. AIM: The aim of this study was to determine whether any association exists between CD163 expression in TAMs and CD133 and CD166 expression in CR-CSCs. METHODS: This study used a cross-sectional design that was conducted at the General Hospital and affiliates in Medan, from September 2018 to July 2019. CRC tissues were collected from colonoscopy biopsies and surgical resections performed on CRC patients, who fulfilled all necessary inclusion and exclusion criteria and provided informed consent. Subjects were divided into high- and low-CD163-level groups. We analyzed the expression levels of CD163, CD133, and CD166 using immunohistochemical (IHC) assays. RESULTS: A total of 118 CRC patients were enrolled in this study, of whom 58.5% were male. No significant differences in hemoglobin, leukocyte, or platelet levels were observed between high- and low-level CD163 expression. We didn’t find any significant association of CD163 TAM with CRC histological grade and TNM stagings. Significant associations were found between the CD 163 expression level and the CD133 expression level (p < 0.001) and between the CD 163 expression level and the CD166 expression level (p< 0.001). Increased TAM levels of CD163 was associated with 2.770-fold and 2.616-fold increased risks of elevated CD133 and CD166 levels, respectively. CONCLUSION: An association was found between the expression levels of CD163 in TAMs and the expression levels of CD133 and CD166 in CR-CSCs.
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S. Kirshenbaum, Arnold, Yuzhi Yin, J. Bruce Sundstrom, Geethani Bandara, and Dean D. Metcalfe. "Description and Characterization of a Novel Human Mast Cell Line for Scientific Study." International Journal of Molecular Sciences 20, no. 22 (November 6, 2019): 5520. http://dx.doi.org/10.3390/ijms20225520.

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Background: Laboratory of allergic diseases 2 (LAD2) human mast cells were developed over 15 years ago and have been distributed worldwide for studying mast cell proliferation, receptor expression, mediator release/inhibition, and signaling. LAD2 cells were derived from CD34+ cells following marrow aspiration of a patient with aggressive mastocytosis with no identified mutations in KIT. Another aspiration gave rise to a second cell line which has recently been re-established (LADR). We queried whether LADR had unique properties for the preclinical study of human mast cell biology. Methods: LADR and LAD2 cells were cultured under identical conditions. Experiments examined proliferation, beta-hexosaminidase (β-hex) release, surface receptor and granular protease expression, infectivity with HIV, and gene expression. Results: LADR cells were larger and more granulated as seen with Wright–Giemsa staining and flow cytometry, with cell numbers doubling in 4 weeks, in contrast to LAD2 cells, which doubled every 2 weeks. Both LADR and LAD2 cells released granular contents following aggregation of FcεRI. LADR cells showed log-fold increases in FcεRI/CD117 and expressed CD13, CD33, CD34, CD63, CD117, CD123, CD133, CD184, CD193, and CD195, while LAD2 cells expressed CD33, CD34, CD63, CD117, CD133, CD193 but not CD13, CD123, CD184, or CD195. LADR tryptase expression was one-log-fold increased. LADR cell and LAD2 cell chymase expression were similar. Both cell lines could be infected with T-tropic, M-tropic, and dual tropic HIV. Following monomeric human IgE stimulation, LADR cells showed greater surface receptor and mRNA expression for CD184 and CD195. Expression arrays revealed differences in gene upregulation, especially for the suppressor of cytokine signaling (SOCS) family of genes with their role in JAK2/STAT3 signaling and cellular myelocytomatosis oncogene (c-MYC) in cell growth and regulation. Conclusions: LADR cells are thus unique in that they exhibit a slower proliferation rate, are more advanced in development, have increased FcεRI/CD117 and tryptase expression, have a different profile of gene expression, and show earlier infectivity with HIV-BAL, LAV, and TYBE when compared to LAD2 cells. This new cell line is thus a valuable addition to the few FcεRI+ human mast cell lines previously described and available for scientific inquiry.
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Florian, Stefan, Karoline Sonneck, Alexander W. Hauswirth, Maria-Theresa Krauth, Wolfgang R. Sperr, and Peter Valent. "Phenotyping of Neoplastic (CD34+/CD38−/CD123+) Stem Cells in Myeloid Malignancies Reveals Expression of Multiple Molecular Targets." Blood 106, no. 11 (November 16, 2005): 1381. http://dx.doi.org/10.1182/blood.v106.11.1381.1381.

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Abstract Recent data suggest that myeloid neoplasms are organized hierarchically in terms of self renewal and maturation of early progenitor cells, similar to normal myelopoiesis. In acute myeloid leukemia (AML), the NOD/SCID mouse-repopulating leukemic stem cells usually co-express CD123 with CD34, but lack CD38. So far, however, little is known about expression of other markers and targets on these progenitors. In the present study, expression of target antigens on CD34+/CD38− cells was analyzed by multicolor flow cytometry in patients with AML (n=18), myelodysplastic syndromes (MDS, n=6), chronic myeloid leukemia (CML, n=8), systemic mastocytosis (SM, n=9), and normal bone marrow (n=5). The IL-3Ra chain (CD123) was found to be expressed on CD34+/CD38− cells in a majority of all patients in all disease-categories. Independent of the type of disease, the vast majority of these stem cells also co-expressed aminopeptidase-N (CD13) and the target receptor CD44 in all patients. CD34+/CD38− progenitor cells expressed variable amounts of the Mylotarg® receptor CD33, KIT (CD117), HLA-DR, and AC133 (CD133). With regard to AC133, two distinct subpopulations of progenitor cells were detected in many cases, namely a CD133+ and a clearly CD133- cell-fraction. In patients with AML, the levels of CD33 varied from patient to patient with a broad range of reactivity, whereas in most patients with MDS, CML, and SM, CD33 was found to be consistently expressed on most progenitors. In most patients, neoplastic stem cells did not express substantial amounts of the GM-CSF receptor alpha chain (CD116), Thy-1 (CD90), E-NPP3 (CD203c), MDR-1 (CD243), or PAR-2. In the normal bone marrow, CD34+/CD38− cells co-expressed CD13, CD44 and CD45, but did not express CD33, CD116, or CD123. In conclusion, neoplastic stem cells in various myeloid neoplasms appear to express a similar phenotype including target receptors such as CD13, CD33, and CD44. These antigens may thus be attractive targets of therapy in AML. However, since many of these targets are not expressed on all stem cells in all patients, the elimination of the entire clone may require combinations of targeted antibodies or use of additional drugs. In other cases (CD13, CD44, CD45), the target antigen is also expressed on normal stem cells, so that targeted therapy is likely to be an ablative maneuver and thus would require a combined stem cell transplantation approach.
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Kanazawa, Tokunori, Kentaro Ohara, Kazunari Yoshida, and Hikaru Sasaki. "PATH-59. HISTOPATHOLOGICAL INVESTIGATION OF THE 1p/19q-CODELETED GLIOMAS RESECTED FOLLOWING ALKYLATING AGENTS CHEMOTHERAPY." Neuro-Oncology 21, Supplement_6 (November 2019): vi156. http://dx.doi.org/10.1093/neuonc/noz175.654.

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Abstract BACKGROUND Little is known about histopathological changes after chemotherapy in lower-grade gliomas (LrGGs). METHODS We investigated 15 1p/19q-codeleted gliomas resected following tumor volume decrease after alkylating agents chemotherapy in comparison with their pre-chemotherapy specimens. Histopathological changes by chemotherapy were evaluated by hematoxilyn-eosin staining and immunohistochemistry for Ki-67/MIB-1, CD68 as pan macrophage/monocyte marker, CD163 as presumed marker of M2 polarity, and nestin and CD133 as markers of glioma stem cells (GSCs). RESULTS Histologically, there were several presumed chemotherapy-related changes in the post-chemotherapy specimens, with the most frequent findings being sparse glial background and abundant foamy cell infiltration. The Ki-67/MIB-1 indices significantly decreased, and CD68+ cells significantly increased after chemotherapy. The increasing rate of CD68+ cells in the post-/pre-chemotherapy specimens was prone to be associated with patients’ progression-free survival (PFS) and overall survival (OS), but not tumor response. The number of CD163+ cells and the ratio of nestin+ cells and CD133+ cells significantly increased after chemotherapy. The number of CD163+ cells, the ratio of nestin+ cells and CD133+ cells, and M2 (CD163+)/M1+M2 (CD68+) ratio in the post-chemotherapy specimens were negatively correlated with patients’ PFS and OS. There was no difference between chemotherapy regimens (temozolomide versus nitrosourea-based) in the number of CD163+ cells and the ratio of nestin+ and CD133+ cells. CONCLUSIONS GSCs in conjunction with M2 macrophages constitute the mechanism of resistance to and recurrence after alkylating agents chemotherapy in LrGGs.
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Sebert, Marie, Elodie Lainey, Sylvain Thepot, Maximilien Tailler, Lionel Ades, Claude Gardin, Pierre Fenaux, Guido Kroemer, and Simone Boehrer. "Erlotinib Inhibits ABC Transporters of AML Progenitors with Stem Cell Features and Increases Chemosensitivity to Current AML Drugs." Blood 116, no. 21 (November 19, 2010): 2163. http://dx.doi.org/10.1182/blood.v116.21.2163.2163.

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Abstract Abstract 2163 Background: Treatment failure in AML is attributed to the persistence of AML progenitors able, among others, to efflux chemotherapeutic drugs via ABC-transporters. Increased efflux capacity is considered a stem cell feature, and therapeutic inhibition may increase chemosensitivity and help eradicate this progenitor population. Nevertheless, clinical studies assessing a potential benefit of ABC-inhibitors in AML treatment showed no significant survival advantage, possibly because AML cells express different ABC-transporters and classical inhibitors target only a restricted type of efflux channels. We assessed the efficacy of the TKI erlotinib (Erlo) to antagonize drug efflux via most important AML-associated efflux channels, ie P-gp, MRP and BCRP. Methods: Overall drug efflux via ABC-transporters (substrate: mitoxantrone-MTZ), and specific efflux via P-gp (substrates: DioC23 and rhodamine-123), MRP (substrates: calcein and CDCFDA) and BCRP (substrate: Hoechst 33342) were quantified by FACS at 1h and 6h following incubation with 10mM Erlo. Biochemical inhibitors of the respective ABC-transporters (CSA, verapamil, MK-571, KO143) served as controls. Surface expression of P-gp, MRP and BCRP was quantified by FACS. To assess chemosensitivity, 10mM Erlo was combined to AraC (100nM), doxorubicine (Dox, 100nM), or VP-16 (1mM) and apoptosis over-time (24, 48, 72h) quantified by DioC3(6)/PI staining. Assays were carried out in myeloid cell lines (KG-1, MOLM-13, HL-60) and ex vivo AML cells (n=3). Immaturity of AML cells was determined in 2 samples by comparing CD34+ versus CD34- cells, and in one pt by co-staining for CD34, CD38, CD123 and CD133. Results: We found that I) Erlo inhibited efflux via P-gp and MRP as demonstrated by increased intracellular retention of DioC23/Rho-123, and calcein/CDCFDA, respectively; II) this degree of inhibition was higher in KG-1 cells than in MOLM-13 or HL-60 cells; III) inhibition of drug efflux was observed already at 1h of incubation, increased over time (6h); IV) Erlo increased intracellular retention of MTZ faster (at 1h with a further increase at 6h) and at least to the same extent than a combination of all three biochemical efflux inhibitors, showing that Erlo's capacity to hinder drug efflux is not restricted to a single ABC-transporter: V) surface expression of P-gp, MRP and BCRP was strongest on KG-1 cells and not altered upon 1h and 6h of Erlo incubation VI) Erlo increased Dox- and VP16-induced apoptosis (48h KG-1: Erlo alone 20%, Dox alone 10%, VP-16 alone 20%, Erlo+Dox: 40%, VP-16+Erlo: 70%), while having no impact on AraC-induced apoptosis; VI) this pattern of chemosensitization was observed in all myeloid cell lines, but once more most pronounced in KG-1 cells. To test the hypothesis that Erlo has comparable effects in pt-derived AML cells ex vivo, we showed by concomitant cell surface staining that I) immature AML subpopulations had a higher efflux capacity (notably via P-gp) than their more mature counterparts (i.e. in one pt with chemoresistant AML: DioC23/Rho-123 fluorescence twice as high in the CD34-/CD38+, CD123+, CD133- than in the CD34+/CD38dim, CD123-, CD133+ subpopulation); II) cell surface expression of P-gp is twice as high in this more immature population (CD34+/CD38dim, CD123-, CD133+) than in CD34-/CD38+, CD123+, CD133+ cells; III) Erlo antagonizes drug efflux via P-gp and MRP at 1h (increasing further at 6h) of incubation; IV) this effect is most pronounced in the immature progenitor cells (1h: decrease of DioC23/Rho-123 efflux in CD34-/CD38+, CD123+, CD133- cells by about 50% and in the more immature CD34-/CD38+, CD123-, CD133+ cells by about 70%); V) Erlo diminishes cell surface expression of P-gp (48h), most effectively in the progenitor populations (by 30% in the CD34-/CD38+, CD123+, CD133- cells versus 50% in CD34-/CD38+, CD123+, CD133- cells); VI) Erlo is able to retain MTZ in both CD34- and CD34+ AML-subpopulations; VII) these effects are accompanied by an increased sensitivity towards Dox and VP-16; VIII) Erlo-induced chemosensitization is higher in the CD34+ than in CD34- AML cells. Conclusions: We here provide novel evidence that erlotinib is able to overcome the stem cell features of increased expression and functionality of ABC-transporters thereby antagonizing the intrinsic chemoresistance of (immature) AML cells. Those results suggest a potential clinical interest of combining erlotinib to chemotherapy in AML Disclosures: Fenaux: CELGENE, JANSSEN CILAG, AMGEN, ROCHE, GSK, NOVARTIS, MERCK, CEPHALON: Consultancy.
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Chen, Ling, Stephanie Jean-Noel, Kevin Hall, Ying Shi, and Griffin P. Rodgers. "In Vitro Hematopoietic Lineage Interconversion from Human Bone Marrow Stem and Progenitor Cells." Blood 104, no. 11 (November 16, 2004): 4160. http://dx.doi.org/10.1182/blood.v104.11.4160.4160.

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Abstract The cell surface antigen, CD133, marks a fraction of hematopoietic stem and progenitor cells and has been successfully used to study their differential biology. To evaluate the differentiating capacity of stem/progenitor cells, we cultivated purified normal human bone marrow CD133 selected cells for 2 weeks with erythropoietin (EPO) or granulocyte colony-stimulating factor (G-CSF) to induce erythroid or myeloid differentiation, respectively. After the second week of cultivation, we reversed the seeding environment of the two populations by placing EPO treated cells into a G-CSF environment and G-CSF treated cells into an EPO environment for an additional 2-week culture. The cells produced in the culture were phenotypically defined by morphology and flow cytometry, and genotypically by RNA and proteomic analyses. Three-color flow cytometry was used for identifying CD133+ progenitors, CD36+ erythroid and CD13+ myeloid cells, as shown in Table 1. The morphology of the cultured cells, assessed by Wright-Giemsa staining, is consistent with the conversion of cellular specific markers. Rapid analysis of gene expression demonstrated co-expression of 76% of 266 genes analyzed among the erythroid and myeloid lineages. Furthermore, proteomic analysis exhibited the sharing of 33% of 9518 expressed protein spots assayed in the two populations after the first 2-week culture, and 32% after 2 weeks of the switch culture. Our data clearly demonstrate that the committed erythroid and myeloid precursors are able to change their fate and can switch into the opposite cell type by a conversion pathway under a specifically defined condition. We termed this switch as interconversion, considering conversion of hematopoietic cells to non-hematopoietic cells. Furthermore, the observations presented in this study show that cytokines used can improve the conversion. We are developing a mathematical model describing the kinetics of hematopoietic stem/progenitor cell transitions into specific lineages, along with the conversion of committed cells based on multiple potential energy wells corresponding to different cell states and cytokines. Table 1. Expression of cell surface markers after 4-week culture D0 1 week 2 weeks 4 weeks CD expression (%) E G E G E2w →G2w → G2w E2w Data are presented as a mean of at least 2 experiments. E: EPO; G: G-CSF; E2w or G2w: EPO or G-CSF treatment for two weeks. CD133+ 96.19 15.74 13.6 0.24 0.36 0.01 0.63 CD36+ 0 60.37 27.39 96.37 25.87 45.41 68.54 CD13+ 0.43 35.41 57.29 24.41 92.1 85.87 37.76 CD133+ / CD36+ 0.44 22.24 15.97 0.12 0.18 1.55 7.65 CD133+ / CD13+ 1.24 19.43 13.36 0.36 1.09 13.31 14.92 CD36+ / CD13+ 0.09 41.25 17.80 23.69 54.1 46.60 79.41
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Chen, Haiming, Mingjie Li, Eric Sanchez, Cathy S. Wang, Ariana M. Berenson, Jennifer Li, Jeffrey A. Steinberg, et al. "Characterization of Cancer Stem Cells in Multiple Myeloma." Blood 112, no. 11 (November 16, 2008): 495. http://dx.doi.org/10.1182/blood.v112.11.495.495.

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Abstract Cancer stem cells persist in tumors as a distinct population and cause relapse and metastasis by giving rise to new tumors. Development of specific therapies targeted at cancer stem cells gives hope for improvement in the survival and quality life of cancer patients. Multiple myeloma (MM) is a cancer characterized by clonal expansion of terminally differentiated B cells. In order to characterize whether cancer stem cells can be identified in these patients, fresh bone marrow biopsies with 90% MM cells from MM patients were implanted into the superficial gluteal muscle of C.B-17 severe combined immunodeficient (SCID) mice. The tumors were excised from donor mice two months following implantation, and digested with proteinase-E to produce a single cell suspension. These cells were analyzed using flow cytometry to identify specific cellular phenotypes within the tumor population. Approximately 13% of the tumor cells were CD138+ cells, 1–2% CD20+ cells and 2–3% CD133+ cells. To examine gene expression within these populations, we isolated the tumor cells using immunomagnetic bead selection. Cells (1X108) were incubated with 200ml of anti-CD138 microbeads and either anti-CD133 or CD20 microbeads. The cell suspension was applied to the magnetic column and unbound cells were passed through the column by washing followed by centrifugation, and finally resuspended. Total RNA was purified from the cells and gene expression of each population was examined using RT-PCR analysis of specific previously identified stem cell-related transcription factors. β-catenin plays a critical role in stem cell development; and, furthermore, the Wnt-β-catenin signaling pathway is important for maintaining the balance of proliferation versus differentiation in the stem cell population. The gene expression of KLT-4, Oct-4, SOX2, and C-myc has recently been shown to convert nonterminally differentiated B cells into a pluripotent stem cell state. In our studies, we found that the CD20+/CD138− and CD133+/CD138− subpopulations both expressed high levels of β-catenin, KLT-4, Oct-4, SOX2, and C-myc. These small populations of tumor cells are likely to represent MM cancer stem cells as they express genes consistently identified in cancer stem cells identified in other types of cancers. We unexpectedly found that CD138+ cells also expressed β-catenin, KLT-4, Oct-4, SOX2, and C-myc. This population of cells might be a “premature” tumor cell in MM at a middle stage of tumor cell differentiation which ultimately differentiates into a mature MM cell. Only CD20−/CD138− cells showed no expression of β-catenin, KLT-4 and SOX2 and markedly reduced Oct-4 gene expression whereas the amount of C-myc gene expression was similar to the levels in the other tumor cell subtypes. Only CD133−/CD138− cells lost β-catenin and showed a reduction in Oct-4 gene expression but still expressed the KLT-4, SOX2, and C-myc genes. To further examine these cancer stem cell and mature tumor cell populations in terms of growth in vivo, we have injected subcutaneously CD20+/CD138−, CD133+/CD138−, CD20−/CD138−, and CD133−/CD138− tumor cell subpopulations back into SCID mice. We will assess growth of cells from these subtypes in vivo as determined by changes in tumor volume and Ig protein levels. We also will determine the sensitivity of these subtypes in vivo to treatment with a variety of agents with anti-MM activity including bortezomib, lenalidomide, melphalan, and Doxil. These studies have uncovered specific subpopulations within the tumor clone of MM and identified differences in expression of genes known to be involved in stem cell function. Further work should lead to specific treatments that can effectively treat these different subpopulations within the tumor clone in MM.
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Greco, N. J., V. J. Pompili, H. M. Lazarus, D. Adler, T. Lasser, R. Fox, L. Solchaga, et al. "Correlative Cellular Analyses in a Phase I Trial (Safety and Efficacy of Autologous Intracoronary Stem Cell Injections in Total Coronary Artery Occlusions (SEACOAST)) of Autologous Bone Marrow-Derived CD133 Cells." Blood 108, no. 11 (November 16, 2006): 1689. http://dx.doi.org/10.1182/blood.v108.11.1689.1689.

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Abstract Correlative laboratory studies were developed in a phase I trial to evaluate the safety of intracoronary injection of escalating doses of bone marrow (BM) CD133+ cells in patients with chronic coronary ischemia. Concurrent with patient cellular therapy, CD133+ cells were phenotyped and tested functionally with endothelial cell colony formation and in vitro and in vivo transmigration. BM (194 ± 11 ml) was isolated from patients meeting study inclusion criteria. CD133+ cells (20 ± 13 x 106, 84 ± 7% purity and 76 ± 7% viability (7AAD)) were isolated using the CliniMACS device (Miltenyi). Contaminating cells following the CliniMACS selection were: < 5% of CD3, CD3neg/CD56, CD19 (immature/mature), CD14, and CD71 cells with 5% CD61, 8% CD13+ SSChigh. BM, PB (peripheral blood), cord blood (CB)-derived endothelial progenitor cells (EPC) were assessed by a culture assay (StemCell Technologies) scoring early outgrowth CFU-EC. SEACOAST patients yielded significantly less colonies compared to controls of matched PB and BM (donors 28–48 yrs) and CB: normal donor (ND) PB, 65; ND BM, 40; CB, 43; SEACOAST patient PB, 2, SEACOAST patient BM, 1. Transmigration assays were used to evaluate the functionality of selected CD133+ cells to chemotactic agents stromal derived factor-1 (SDF-1) and vascular endothelial growth factor (VEGF). Selected CD133+ cells were recovered, resuspended in DMEM/1% HSA media and after a 37°C incubation for 16–20 hrs, 5 x 104 CD133+ cells were added to transwells (5 mm) for 3 hours. Transmigrated cells were quantitated by flow cytometry using anti-CD45, anti-CD133 antibodies, and Fluorosphere beads. Surface expression on ND BM CD133+ cells of CXCR4 and VEGF-R2 was 0–16.4% and 1.2–4.3%, respectively. Transmigration was effected by 200 ng/ml (range of 16–62%) but not to 10 ng/ml VEGF. For CD133+ cells devoid of the expression of CXCR4, SDF-1-induced transmigration was absent. Expression of CXCR4 and VEGF-R2 on clinical trial patient-selected CD133+ cells was 0–5% and 0–2%, respectively, and transmigration was 5–19% to 200 ng/ml SDF-1 but not to 10 ng/ml VEGF. Patient selected CD133+ cells or PB mononuclear cells (PBMC), ND CD133+ cells, or a vehicle control were injected via a left intraventricular route into NOD/SCID mice with a femoral artery ligation immediately after injury. Doppler flow measurements were obtained weekly for 6 weeks comparing the perfusion ratio of ischemic/healthy limbs. At 28 days, perfusion ratios were statistically higher in study groups receiving ND CD133+ cells (0.51 ± 0.06) compared to controls (0.37 ± 0.03, p=0.025). Mice receiving patient CD133+ cells (0.46 ± 0.04) or PBMC (0.37 ± 0.08) did not show statistically significant improvement over control animals (p= 0.07, p= 0.94, respectively). BM was harvested to assess human engraftment by cytometric analysis. Mice injected with 0.5 x 106 patient BM CD133+ cells showed <0.2% huCD45+ cells compared to 1.6 ± 0.4% ND BM huCD45+. Beyond the demonstrated safety of the delivery of CD133+ cells (>70% purity and >70% viability) to chronic ischemic patients via an intracoronary route, important correlative in vitro and in vivo assays has demonstrated the diminished potency of BM-derived CD133+ cells as compared to CB and ND PB and BM-derived cells.
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Anbarlou, Azadeh, Amir Atashi, Masoud Soleimani, Mahshid AkhavanRahnama, Mahbobeh Bohloli, and Majid Mossahebi-Mohammadi. "Differential characteristics of CD133+ and CD133− Jurkat cells." In Vitro Cellular & Developmental Biology - Animal 51, no. 6 (January 29, 2015): 556–61. http://dx.doi.org/10.1007/s11626-015-9869-z.

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FERRANDINA, G., G. BONANNO, L. PIERELLI, A. PERILLO, A. PROCOLI, A. MARIOTTI, M. CORALLO, et al. "Expression of CD133-1 and CD133-2 in ovarian cancer." International Journal of Gynecologic Cancer 18, no. 3 (May 2008): 506–14. http://dx.doi.org/10.1111/j.1525-1438.2007.01056.x.

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Cancer stem cells have been isolated from several solid tumors including prostate, colon, liver, breast, and ovarian cancer. Stem cells isolated from nervous system and prostate express CD133 antigen, which is widely used to isolate hematopoietic stem and progenitor cells. The aims of this study were to investigate the expression of the CD133-1 and CD133-2 epitopes in primary ovarian tumors and to biologically characterize CD133+ovarian cancer cells, also according to clinicopathologic parameters. Tissue specimens were obtained at primary surgery from 41 ovarian carcinomas; eight normal ovaries and five benign ovarian tumors were also collected. Flow cytometry with monoclonal antibodies against CD133-1 and CD133-2 epitopes was employed. FACS (fluorescence activated cell sorting) analysis enabled the selection of CD133+cells, whose epithelial origin was confirmed by immunofluorescence analysis with monoclonal anti-cytokeratin 7. CD133+cells gave rise to a 4.7 ± 0.9-fold larger number of colonies than that documented in CD133−population (P< 0.001). Moreover, CD133+cells showed an enhanced proliferative potential compared to CD133−cells. The percentages of CD133-1- and CD133-2-expressing cells were significantly lower in normal ovaries/benign tumors with respect to those in ovarian carcinoma. Both the percentages of CD133-1- and CD133-2-expressing cells were significantly lower in omental metastases than in primary ovarian cancer (P= 0.009 and 0.007 for CD133-1- and CD133-2-expressing cells, respectively). There seems not to be any difference in the distribution of the percentage of CD133-1- and CD133-2-expressing cells according to clinicopathologic parameters and response to primary chemotherapy. CD133-1 and CD133-2 may be useful in order to select and enrich the population of CD133+ovarian tumor cells, which are characterized by a higher clonogenic efficiency and proliferative potential.
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Dissertations / Theses on the topic "CD133+"

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Ahmed, Tarek Mohamed Abdel Moneim Mohamed Elsaba. "Role of CD133 in colorectal cancer." Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/28630/.

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CD133 is a pentaspan transmembrane glycoprotein of ~120 kDa, which was initially used to identify haematopoietic stem cells and, later on, used for the isolation and study of cancer stem cells in many different types of solid tumour including colorectal cancer. Although CD133 expressing cells are thought to represent cancer stem cells, little is known about the exact role of CD133 and the molecular mechanisms underlying control of CD133 expression. This project sought to investigate these questions in colorectal cancer. Initially the expression of CD133 was tested by immunohistochemistry in a two tissue microarray (TMA) sets consisting of (a) 449 cases of primary colorectal cancer, and (b) 45 cases of primary and matched liver metastases. High CD133 expression was marginally associated with shorter overall survival (OS) (p=0.05, Log-rank test) but no difference in expression was found between primary tumours and corresponding metastases. Next, the functional activity of CD133 was evaluated in colorectal cancer (CRC) cell lines by knockdown in cell lines with high CD133 expression. In order to identify appropriate cell lines, the expression of CD133 was tested by quantitative RT -PCR in a series of 29 CRC cell lines and 10 samples of normal mucosa and, in selected cell lines, validated by testing for protein expression by flow cytometry. CD133 mRNA was expressed in 24/29 colorectal cancer cell lines with a heterogenous level of expression. 10 cell lines were chosen on the basis of CD133 mRNA expression level to assess the protein level. CD133 mRNA and protein expression were generally correlated (rs = 0.831, p= 0.003, spearman rank correlation coefficient test) although, interestingly, CD133 mRNA level was higher in normal samples compared with that in cancer cell lines and was significantly higher in cell lines derived from metastatic sites than those derived from site of primary tumour (p=0.009; Mann-whitney test). In addition, it was noted that many cell lines had a stable biphasic phenotype containing CD133+ and CD133- cell populations. This allowed functional analysis of CD133 by sorting the two populations. HT29 was identified as a high expresser of CD133 (95%) and was used for gene-knockdown studies, SW480 had a biphasic population consisting of 42% CD133+ cells and 58% CD133- cells and each population was isolated by cell sorting before functional analysis. Functional assays included proliferation, migration, colony formation and staurosporine induced apoptosis assays. These showed that CD133 expressing cells had greater cell motility (p= 0.04, and p = 0.03, unpaired t-test, for knocked down cells and sorted populations respectively) , enhanced colony forming abilities (p=0.0001, and p=0.003, unpaired t-test for 2D and 3D colony formation respectively using sorted populations only), and increased resistance to staurosporine induced apoptosis (p=0.01, and p=0.008, unpaired t-test, for knocked down and sorted populations respectively) than CD133 negative counterparts. In addition, sorted monophasic populations reverted to a biphasic state in both CD133+/- populations from SW480. Further studies demonstrated that CD133-induced cell motility was independent of E-cadherin, β-catenin, and suggestive of not being regulated by Cten or Wnt, but further work is warranted to verify these results. In addition, regulation of CD133 was partly dependent on STAT3 signalling and on CD133 promoter methylation. Levels of mRNA of some stem cell related genes such as KLF-4, Musashi-1, OCT4, Nanog, and Lgr5 were higher in CD 133 + compared to CD 133 negative cells (p=0.008, p=0.004, p=0.006, p=0.001, and p=0.11; unpaired t-test, respectively) In conclusion, in CRC, CD133 was found to be a significant prognostic factor which enhances cell motility and is associated with features of "stemness". It is a target of ST AT3 signalling and partly regulated by promoter methylation. More in depth studies are warranted to discover the downstream and upstream targets of CD133 before translating these preclinical and laboratory investigations into clinical management of colorectal cancer.
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Marçola, Marina. "Perfil circadiano da expressão de microRNAs em células progenitoras CD133+." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-19052015-092113/.

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Culturas de células primárias diferem de acordo com as condições ambientais nas quais se encontra o doador. Recentemente demonstramos que o ciclo claro/escuro impõe um programa molecular hereditário em cultura celular. Com o intuito de investigar os mecanismos moleculares da memória celular, no presente trabalho isolamos células progenitoras CD133+ de explante de músculo cremaster e investigamos se a expressão de microRNAs (miRNAs), resulta em fenótipos diferentes de acordo com o ciclo claro/escuro. O sequenciamento global de miRNAs utilizando a plataforma SOLiD 4 e analisado pelos programas EdgeR, TargetScan e Metacore resultou na identificação de 541 miRNAs maduros, os quais apresentam dois perfis de expressão distintos de acordo com a hora de obtenção das culturas. miR-1249 e miR-129-2-3p são mais expressos em células obtidas durante o dia e favorecem a manutenção da pluri/multipotência celular. Já células obtidas à noite expressam maior conteúdo dos miR-182, miR-96-5p, miR-223-3p, miR-146a-3p e miR-146a-5p resultando na inibição da resposta inflamatória e no favorecimento da maturação celular quando comparadas às células obtidas de dia. A análise funcional da inibição da resposta inflamatória em células obtidas à noite foi confirmada por PCR array que revelou na menor expressão de genes relacionados à via de sinalização TLR/NF-κB, incluindo Traf6, um alvo do miR-146a. Além disso, a translocação nuclear de NF-κB é reduzida à noite e é inversamente proporcional ao nível de melatonina plasmática. Demonstramos ainda que a melatonina in vitro favorece o estado de pluripotência celular por aumentar a expressão de CD133, miR-1249 e miR-129-2-3p. No entanto, esse efeito depende do contexto celular visto que a expressão de receptores de melatonina também varia de acordo com a hora de obtenção da cultura. Em conjunto, nossos dados sugerem que o ciclo claro/escuro interfere no perfil de expressão de miRNAs e impõe uma variação no fenótipo de células progenitoras CD133+
The phenotype of primary cells in culture varies according to the donor environmental condition. We have recently shown that the light/dark cycle impose a molecular program that is hereditable in culture. In order to evaluate the molecular mechanisms of cellular memory, here we isolated CD133+ progenitor cells from cremaster muscle explants and investigated whether the expression of microRNAs (miRNAs), could result in different phenotypes according the phase of ligh/dark cycle when cells were obtained. The global miRNA sequencing using SOLiD4 Platform, and analyzed by EdgeR, TargetScan and MetaCore, revealed the expression of a total of 541 mature miRNAs, and two distinct miRNAs signatures according to the hour when cells were obtained. miR-1249 and miR-129-2-3p are more expressed during daytime and favor the maintenance of cellular pluri/multipotency. Nighttime cells express higher amounts of miR-182, miR96-5p, miR-223-3p, miR-146a-3p and miR-146a-5p that inhibit the inflammatory response and favor the cellular maturation when compared to daytime cells. The functional analysis of the inflammatory response inhibition during nighttime was confirmed by PCR array and revealed lower expression level of genes related to TLR/NF-κB pathway, including Traf6, a putative target mRNA of miR-146a. Additionally, the nuclear translocation of NF-κB is reduced in nighttime cells and it is inversely correlated to the nocturnal the plasma level of melatonin. We also showed that melatonin in vitro favors the cellular pluri/multipotency, increasing CD133, miR-1249 and miR-129-2-3p expression. However, this effect depends on cellular context, as the expression of melatonin receptors also shows a daily variation. Altogether, our data suggest that the light/dark cycle interferes on miRNAs expression profile and imposes a rhythmic phenotype variation in CD133+ cells
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Damianoff, Karin. "CD133 positive "Cancer Stem Cells" in Gliomen verschiedener Malignitätsgrade." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-126442.

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Zhai, Xiao Qun. "Biology of adult human normal and leukaemia CD133+ stem cells." Thesis, University of Central Lancashire, 2010. http://clok.uclan.ac.uk/21488/.

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Recently, CD133 has been used extensively as a marker for identification of stem cells from human normal and malignant tissues. Human normal CD 133+ stem cells are capable of multilineage in vitro and in vivo differentiation providing a novel source of stem cells for regenerative therapy, whereas, malignant CD133+ stem cells are a potential therapeutic target for anti-cancer treatment. This PhD thesis investigated the neural differentiation of human adult bone marrow and foetal liver CD133+ stem cells; explored the presence of CD133 and embryonic stem cell marker Oct-4 positive stem cells in adult human normal and malignant tissues, including normal brain tissues, normal and malignant bone marrow stem cells; and evaluated the anti-acute myeloid leukaemia (AML) effect of 5 novel synthetic ajoene compounds using drug-resistant AML cell line for overcoming drug resistance in elderly AML patients. A novel serum-free culture system for inducing neural differentiation of human adult bone marrow and foetal liver CD 133+ stem cells in vitro was demonstrated. Following only two weeks' culture of selected bone marrow CD 133+ cells in serum-free medium supplemented by 50% human astrocyte conditioned medium and other cytokines, 25.5% of bone marrow CD 133+ stem cells differentiated into neural (17.8%) and glial (7.7%) cells. After three weeks' culture of selected foetal liver CD133+ cells in serum-free medium supplemented by several cytokines without astrocyte conditioned medium, only 10.8% of these stem cells differentiated into neural and glial cells. These neural differentiated cells expressed mature neural and glial markers including NF-h, NF-m, NSF and GFAP, and exhibited mature neural morphologies. The astrocyte conditioned medium was the essential ingredient in all effective serum-free culture conditions suggesting it may contain other more potent neural/glial inducing factors. The serumfree culture system is clinically relevant and provides a vehicle for generating neural cells from adult human bone marrow CD 133+ stem cells for the treatment of patients with neurodegenerative diseases. CD 1 33-isoform 2 (CD 133-2) and embryonic stem cell marker Oct-4 expression was revealed in three adult human normal and malignant tissues and cells, including normal brain (substantia nigra and striatum), normal and malignant CD34+ marrow stem cells. There was no expression of CD133-isoform I (CD133-1) in these tissues. The very small population of CD133-2 and Oct-4 positive stem cells in adult human normal substantia nigra and striatum may represent the embryonic remnants and provide a potential source of adult neural stem cells that may be induced to undergo neural diffeentiation for the treatment of neurodegenerative conditions, such as Parkinson's disease. The substantial expression of Oct-4 in adult human normal and drug-resistant myeloid leukaemia KG1a marrow stem cells demonstrates that, alongside CD133, Oct-4 is a novel cancer stem cell marker suggesting the CD 133-2 and Oct-4 positive KGIa cells are the most likely targets in disease development and are novel therapeutic targets for effective treatment of AML. Novel synthetic ajoene compounds were shown to significantly inhibit growth, induce apoptosis plus necrosis, and reduce Bcl-2 expression in human drug-resistant CD34+ AML KG 1 a cells, both alone and in combination with low dose (1 jxM) cytarabine. E/Zbenzyl was the most potent growth inhibition compound,. whereas, Z-ajoene was the most cytotoxic compound. Low dose cytarabine-induced cytotoxicity was significantly enhanced by the five novel compounds in the following order: Z-ajoene > E-ajoene > Ephthalimide> E/Z-benzyl > Z-pthalimide. The combination of Z-ajoene and low dose cytarabine provides a promising combination therapy for elderly AML patients to overcome drug resistance. This PhD thesis provides the basis for appropriate identification and clinical application of stem cells from adult human normal tissues (brain and bone marrow) and foetal liver for autologous transplantation for the treatment of neurodegenerative diseases, such as Parkinson's disease, and also the identification of cancer stem cells in human AML marrow stem cells indicating novel therapeutic targets for anti-cancer treatment. Moreover, it demonstrates significant anti-cancer effect of 5 novel synthetic ajoene compounds in drug-resistant AML cells highlighting their potential for overcoming drug resistance in elderly patients with AML.
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Lechner, Axel. "Die Rolle des Tumorstammzellmarkers CD133 in der Initiierung von Tumoren." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-173238.

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Adikibi, Tonye T. "Investigation into the functional role of the stem cell marker CD133." Thesis, Kingston University, 2011. http://eprints.kingston.ac.uk/22964/.

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CD133 is a pentaspan membrane protein found on pseudopodia, microvilli and other plasma protrusions irrespective of cell type in both humans and mice. CD 133 has been classified as a marker of primitive haemopoietic and neural stem cells. At the molecular level it interacts with cholesterol and is located within lipid micro domains known as lipid rafts. Using cellular and molecular techniques we investigated the functional role CD 133 plays in stem cell biology. Prior to commencing the functional experiments, we determined that MUTZ-2, Caco-2 and primary CD34+ cells provided the best characteristics to investigate CD133 function. We established growth conditions, patterns and CD 133 expression for all 3 cell types and concluded that Caco-2 was the preferential cell line based on CD133 expression and cell stability. A number of approaches were used to knock down CD133 usmg a variety of RNAi oligonucleotides. Plasmid vectors were used in an attempt to produce a permanent CD 133 knockout Caco-2 cell line. However, after successfully inserting the plasmid, the cell line failed to proliferate. Ultimately, a 73% CD 133 phenotypic knockdown was achieved using RNAi technology from Santa Cruz, with 50% CD133 re-expression within 5 days, confirmation by both PCR and flow cytometry. Knockdown of CD 133 in Caco-2 cells. resulted in no change in proliferation or adhesive properties to plastic, however a slight increase in cell cycle activity was observed. Gene profiling of CD 133 knocked down Caco-2 and control cells was carried out using microarray technology. This was also applied to cells incubated with monoclonal antibodies against epitopes of CD133, as these are often used as a means of cell isolation for CD133 functional studies. A variety of genes were up and down regulated in both groups when compared to the control cells. CD 133 knockdown caused an up-regulation of genes associated with cell migration, motility, cell cycle, Wnt and tyrosine kinase pathway inhibitors and lipid transport across the membrane and down-regulated cell adhesion genes and apoptotic related genes. Caco-2 cells incubated with monoclonal antibodies against CD 133 showed up regulation in genes associated with cell cycle, migration and DNA replication and down regulation of genes associated with regulation of cell proliferation and apoptosis. This result is significant due to the extensive use ofCD133 antibodies in functional CD133 and CD133+ cell population studies. Confocal studies showed partial co-localisation between the lipid rafts and CD133, removal of the lipid rafts using the drug Beta Methyl Cyclodextrine caused loss of CD 133. However, lipid raft expression remained relatively constant on CD133 knockdown cells. Examining the distribution of CD 133 on Caco-2 cells adhered to fibronectin compared to glass via confocal analysis, showed there is no direct involvement of CD133 with anchorage type cell adhesion. However, considering the confocal analysis showing the association of CD 133 within lipid rafts and the results of microarray, this would imply a more indirect role of CD 133 within the processes of cell adhesion. This study has revealed that that CD133 plays a suppressive role in stem cell biology and play a regulatory role in maintaining quiescence, keeping the early stem and progenitor cells in a non proliferating, non motile state. A number of studies in recent years have attempted to determine the function of CD133 which still remains relatively elusive. However, this study has contributed to a greater understanding of CD133 function and identified key areas for further investigation.
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Bandopadhyay, Gogori. "Funtional analysis of the role of CD133 in high grade glioma progression." Thesis, University of Nottingham, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537635.

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Donovan, Laura K. "CD133, the holy grail of neuro-oncology, or a promiscuous red herring?" Thesis, University of Portsmouth, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516153.

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Every organ in the adult mammalian body harbours a rare population of stem cells. Most tumours arise from the transformation of a single stem cell into a cancer stem cell that has the innate capacity to perpetuate through self-renewal, and to generate mature neoplastic cells of a particular tissue through differentiation in vivo. C0133, a 120kOa transmembrane spanning glycoprotein, was the first in a class of novel pentaspan membrane proteins to be identified in both humans and mice, and was originally characterised as a possible marker of cancer stem cells in the haematopoietic system. Since its first discovery, C0133, independently or in combination with other stem cells markers, has been identified in a variety of human tumours including prostate tumours, breast cancers, colon carcinomas, lung cancers, and brain tumours. However, the belief that C0133 may act as a universal marker of cancer stem cells has been met with a high degree of controversy in the neuro-oncology research community as the precise biological role of C0133 has yet to be established. In vivo, glioblastoma multiforme contains poorly vascularised areas associated with decreasing oxygen tension (hypoxia), recently correlated with poor patient prognosis. In this study, a direct link between decreasing oxygen tension and C0133 expression was established. Furthermore, the in vitro hypoxic micro-environment appeared to facilitate a role in the biological behaviour of the glioma, as well as upregulating the CD133 phenotype. Distinct biological differences were also obvious between the CD133+ve and CD133"ve cell fractions; the CD133 protein appeared to not facilitate a role in cellular adhesion; the C0133"ve cell fraction displayed an increased invasive propensity in comparison to the C0133+ve cells; the II CD133+ve cells did not evoke cellular invasion, instead this cell fraction may be inversely linked to this biological process. Whether the CD133 protein precisely defines cancer stem cells within neoplastic glia remains to be clarified. However, this study has made significant progress towards identifying the functional role of CD133.
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Ott, Sabrina [Verfasser], and Olivier [Akademischer Betreuer] Gires. "Untersuchungen zur Genregulation durch den Tumormarker CD133 / Sabrina Ott ; Betreuer: Olivier Gires." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1127527894/34.

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Luna, Ealber Carvalho Macedo. "ExpressÃo imuno-histoquÃmica de cd133 em displasias epiteliais orais e carcinomas epidermoides orais." Universidade Federal do CearÃ, 2015. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=14830.

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FundaÃÃo Cearense de Apoio ao Desenvolvimento Cientifico e TecnolÃgico
IntroduÃÃo: CÃlulas-tronco cancerÃgenas constituem uma subpopulaÃÃo de cÃlulas neoplÃsicas que apresentam propriedades fenotÃpicas de diferenciaÃÃo, renovaÃÃo celular e proliferaÃÃo semelhantes Ãs cÃlulas-tronco normais, sendo responsÃveis pela manutenÃÃo tumoral. Objetivo: investigar a imunoexpressÃo de CD133, marcador de cÃlulas-tronco cancerÃgenas, em displasias epiteliais orais e em carcinomas epidermoides orais. Material e MÃtodo: a amostra se constituiu de 15 casos de CEO e 15 casos de DEO, sendo realizada a imuno-histoquÃmica pela tÃcnica da estreptoavidina-biotina, utilizando o anticorpo anti-CD133 (GTX60471, GeneTexÂ, San Antonio, TX, USA), com diluiÃÃo de 1:650 e recuperaÃÃo antigÃnica com citrato PH 6. A anÃlise quantitativa foi realizada por meio da contagem percentual de cÃlulas com imunomarcaÃÃo positiva em cinco campos, no aumento de 400X, utilizando o programa Image J. Os resultados foram obtidos e comparados entre grupos por meio dos testes t de Student e ANOVA multifatorial seguido do pÃs-teste de Bonferroni, tomando como base os nÃveis de significÃncia de 5%. Resultados: a avaliaÃÃo imuno-histoquÃmica evidenciou marcaÃÃo positiva em todos os casos da amostra (100% dos casos). No grupo de DEO, observou-se que 77,6Â16.0 das cÃlulas epiteliais exibiam imunoexpressÃo positiva para CD133 e, no grupo de CEO, verificou-se que 82.6Â7.2 das cÃlulas epiteliais exibiam imunoexpressÃo positiva para CD133; contudo, nÃo houve diferenÃa estatisticamente significativa entre os grupos estudados (p=0.283). Ademais, observou-se que, com relaÃÃo a sexo, localizaÃÃo anatÃmica e grau de displasia, a marcaÃÃo positiva ocorreu da seguinte forma: sexo masculino (DEO: 76.4Â10.9 e CEO: 82.9Â6.3) (p=0.526) e feminino (DEO: 78.0Â17.9 e CEO: 82.1Â8.9) (p=0.588); lÃngua (DEO: 69.6Â23.2 e CEO: 83.5Â9.3) (p=0.217), mucosa jugal (DEO: 84.8Â14.7 e CEO: 79.0Â5.7) (p=0.618) e palato (DEO: 74.5Â6.7 e CEO: 86.8Â10.3); DEO leve (78.0Â18.4), DEO moderada (72.7Â11.4) e DEO severa (80.1Â1.8) (p=0.899). Todavia, nÃo houve diferenÃa estatisticamente significativa entre os grupos estudados. ConclusÃo: sugere-se que a presenÃa dessa subpopulaÃÃo celular pode nÃo ser imprescindÃvel para a determinaÃÃo do fenÃtipo maligno
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Books on the topic "CD133+"

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Corbeil, Denis, ed. Prominin-1 (CD133): New Insights on Stem & Cancer Stem Cell Biology. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5894-4.

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Chen, Lieping, ed. CD137 Pathway: Immunology and Diseases. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/0-387-32829-7.

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name, No. Ectopeptidases: CD13/aminopeptidase N and CD26/dipeptidylpeptidase IV in medicine and biology. New York, NY: Kluwer Academic/Plenum, 2003.

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Marchina, Wanda. Untersuchung von CD34[superscript pos] und CD133[superscript pos] Vorläuferzellen in Bezug auf ihr Wachstum in Kurz- und Langzeitkulturen. 2008.

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Chen, Lieping. CD137 Pathway: Immunology and Diseases. Springer, 2006.

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Chen, Lieping. CD137 Pathway: Immunology and Diseases. Springer London, Limited, 2007.

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Chen, Lieping. CD137 Pathway: Immunology and Diseases. Springer, 2014.

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Langner, Jürgen, and Siegfried Ansorge. Ectopeptidases: CD13/Aminopeptidase N and CD26/Dipeptidylpeptidase IV in Medicine and Biology. Springer London, Limited, 2012.

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(Editor), Jürgen Langner, and Siegfried Ansorge (Editor), eds. Ectopeptidases: CD13/Aminopeptidase N and CD26/Dipeptidylpeptidase IV in Medicine and Biology. Springer, 2002.

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Langner, Jürgen, and Siegfried Ansorge. Ectopeptidases: CD13/Aminopeptidase N and CD26/Dipeptidylpeptidase IV in Medicine and Biology. Springer, 2012.

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Book chapters on the topic "CD133+"

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Matsuoka, Tasuku, and Masakazu Yashiro. "CD133 as Biomarker in Breast Cancer." In Biomarkers in Cancer, 429–45. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7681-4_24.

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Matsuoka, Tasuku, and Masakazu Yashiro. "CD133 as Biomarker in Breast Cancer." In Biomarkers in Cancer, 1–14. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-7744-6_24-1.

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Fargeas, Christine A. "Prominin-2 and Other Relatives of CD133." In Advances in Experimental Medicine and Biology, 25–40. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5894-4_2.

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Herold-Mende, Christel, and Benito Campos. "Glioma Patients: Role of CD133 Stem Cell Antigen." In Stem Cells and Cancer Stem Cells, Volume 1, 69–76. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1709-1_8.

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Chan, Anthony W. H., and Ka-Fai To. "CD133 and EpCAM as Biomarkers in Liver Diseases." In Biomarkers in Disease: Methods, Discoveries and Applications, 349–72. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7675-3_12.

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Chan, Anthony W. H., and Ka-Fai To. "CD133 and EpCAM as Biomarkers in Liver Diseases." In Biomarkers in Disease: Methods, Discoveries and Applications, 1–24. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7742-2_12-1.

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Khan, Zarine, Leroy Shervington, and Amal Shervington. "Is CD133 the Appropriate Stem Cell Marker for Glioma?" In Stem Cells and Cancer Stem Cells, Volume 1, 107–12. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1709-1_13.

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Tabu, Kouichi, Tetsuya Taga, and Shinya Tanaka. "Tumor Stem Cells: CD133 Gene Regulation and Tumor Stemness." In Stem Cells and Cancer Stem Cells, Volume 2, 145–53. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2016-9_16.

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Corbeil, Denis, Jana Karbanová, Christine A. Fargeas, and József Jászai. "Prominin-1 (CD133): Molecular and Cellular Features Across Species." In Advances in Experimental Medicine and Biology, 3–24. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5894-4_1.

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Handgretinger, Rupert, and Selim Kuçi. "CD133-Positive Hematopoietic Stem Cells: From Biology to Medicine." In Advances in Experimental Medicine and Biology, 99–111. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5894-4_7.

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Conference papers on the topic "CD133+"

1

Hongo, Kumiko, Junichirou Tanaka, Nelson H. Tuno, Takeshi Nishikawa, Yasutaka Shuno, Kazuhito Sasaki, Manabu Kaneko, et al. "Abstract 3367: CD133- colorectal cancer cells have higher chemo-resistance ability than CD133+cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3367.

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AbdusSamad, Maryam, Anirudh Gaur, Hengbo Zhou, John L. Zapas, Cynthia M. Simbulan-Rosenthal, Edward C. McCarron, and Dean S. Rosenthal. "Abstract 4224: CD133 knockdown sensitizes melanoma to kinase inhibitors." 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.am2015-4224.

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Bandopadhyay, Gagori, Anna M. Grabowska, Beth Coyle, and Susan A. Watson. "Abstract 4306: Functional role of CD133 in glioblastoma multiforme." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4306.

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Vacas-Oleas, A., J. de la Rosa, R. Garcia-Lopez, B. Vera-Cano, G. Gallo-Oller, M. Alfaro, M. H. Shahi, et al. "Abstract 257:In vitrotumorigenicity and stemness characterization of the U87MG glioblastoma cell line: Monolayer cultures, neurospheres, and CD133+ and CD133- sorted fractions." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-257.

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Ching, Yick Pang, and Wing Lim Chan. "Abstract 3386: The oncogenic role of CD133 in hepatocellular carcinoma." 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.am2018-3386.

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Dai, Z., B. Liu, D. Yi, X. Zhang, and Y. Zhao. "CD133+ Vascular Progenitor Cells Contribute to the Pathogenesis of PAH." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3630.

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Sasai, Ken, Miho Nodagashira, and Shinya Tanaka. "Abstract C1: GLI1 induces CD133 expression in xenografts derived from transformed astrocytes but not in cultured cells: Extrinsic control of CD133 expression in gliomas." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-c1.

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Zhou, Hengbo, Maryam Abdussamad, Amani Alomari, Anirudh Gaur, Cynthia S. Rosenthal, John L. Zapas, and Dean S. Rosenthal. "Abstract 3891: CD133 is associated with resistance of melanoma to multikinase inhibition." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3891.

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Sato, Mizuho, Yoshiaki Miura, and Masato Yamamoto. "Abstract 3541: Therapeutic effect of CD133-targeted oncolytic adenovirus in colon cancer." 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.am2015-3541.

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Tsunekuni, Kenta, Masamitsu Konno, Jun Koseki, Ayumu Asai, Kazuaki Matsuoka, Teiji Takechi, Yuichiro Doki, Masaki Mori, and Hideshi Ishii. "Abstract 2963: CD44+/CD133+colorectal cancer stem cells are sensitive to trifluridine." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2963.

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