Thematische Bibliographien / Motility of leukemia cells

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  1. Zeitschriftenartikel
  2. Dissertationen
  3. Bücher
  4. Buchteile
  5. Konferenzberichte
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Auswahl der wissenschaftlichen Literatur zum Thema „Motility of leukemia cells“

Autor: Grafiati
Veröffentlicht am 28. Juni 2021
Zuletzt aktualisiert am 1. Februar 2022

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Zeitschriftenartikel zum Thema "Motility of leukemia cells"

1

Raje, Manoj, und Karvita B. Ahluwalia. „Motility of leukemic lymphocytes“. Proceedings, annual meeting, Electron Microscopy Society of America 48, Nr. 3 (12.08.1990): 368–69. http://dx.doi.org/10.1017/s0424820100159382.

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In Acute Lymphocytic Leukemia motility of lymphocytes is associated with dissemination of malignancy and establishment of metastatic foci. Normal and leukemic lymphocytes in circulation reach solid tissues where due to in adequate perfusion some cells get trapped among tissue spaces. Although normal lymphocytes reenter into circulation leukemic lymphocytes are thought to remain entrapped owing to reduced mobility and form secondary metastasis. Cell surface, transmembrane interactions, cytoskeleton and level of cell differentiation are implicated in lymphocyte mobility. An attempt has been made to correlate ultrastructural information with quantitative data obtained by Laser Doppler Velocimetry (LDV). TEM of normal & leukemic lymphocytes revealed heterogeneity in cell populations ranging from well differentiated (Fig. 1) to poorly differentiated cells (Fig. 2). Unlike other cells, surface extensions in differentiated lymphocytes appear to originate by extrusion of large vesicles in to extra cellular space (Fig. 3). This results in persistent unevenness on lymphocyte surface which occurs due to a phenomenon different from that producing surface extensions in other cells.
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2

Liu, Hsiao-Chuan, Eun Ji Gang, Hye Na Kim, Yongsheng Ruan, Heather Ogana, Zesheng Wan, Halvard Bönig, K. Kirk Shung und Yong-Mi Kim. „Characterizing the Motility of Chemotherapeutics-Treated Acute Lymphoblastic Leukemia Cells by Time-Lapse Imaging“. Cells 9, Nr. 6 (16.06.2020): 1470. http://dx.doi.org/10.3390/cells9061470.

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Drug resistance is an obstacle in the therapy of acute lymphoblastic leukemia (ALL). Whether the physical properties such as the motility of the cells contribute to the survival of ALL cells after drug treatment has recently been of increasing interest, as they could potentially allow the metastasis of solid tumor cells and the migration of leukemia cells. We hypothesized that chemotherapeutic treatment may alter these physical cellular properties. To investigate the motility of chemotherapeutics-treated B-cell ALL (B-ALL) cells, patient-derived B-ALL cells were treated with chemotherapy for 7 days and left for 12 h without chemotherapeutic treatment. Two parameters of motility were studied, velocity and migration distance, using a time-lapse imaging system. The study revealed that compared to non-chemotherapeutically treated B-ALL cells, B-ALL cells that survived chemotherapy treatment after 7 days showed reduced motility. We had previously shown that Tysabri and P5G10, antibodies against the adhesion molecules integrins α4 and α6, respectively, may overcome drug resistance mediated through leukemia cell adhesion to bone marrow stromal cells. Therefore, we tested the effect of integrin α4 or α6 blockade on the motility of chemotherapeutics-treated ALL cells. Only integrin α4 blockade decreased the motility and velocity of two chemotherapeutics-treated ALL cell lines. Interestingly, integrin α6 blockade did not affect the velocity of chemoresistant ALL cells. This study explores the physical properties of the movements of chemoresistant B-ALL cells and highlights a potential link to integrins. Further studies to investigate the underlying mechanism are warranted.
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Okabe-Kado, Junko, Takashi Kasukabe, Yoshio Honma und Yasuhiko Kaneko. „Inverse Correlation of NM23 Expression with Lysophosphatidic Acid Receptor EDG2/lpa1 Expression of Human Leukemia Cells during Myeloid Differentiation Induced by All-Trans Retinoic Acid“. Blood 112, Nr. 11 (16.11.2008): 4490. http://dx.doi.org/10.1182/blood.v112.11.4490.4490.

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Abstract Overexpression of the nm23 gene is found in many hematological malignancies, and predicts poor treatment outcome. Because the amount of intracellular NM23-H1 protein is inversely correlated with differentiation and exogenous over expression of the nm23-H1 in myeloid leukemia cells reduced the sensitivity to induction of myeloid differentiation, nm23-overexpression is considered to function as a differentiation-suppressor. However, the molecular mechanism of this phenomenon is unknown. Recently, lysophosphatidic acid (LPA) receptor EDG2/lpa1 was identified as a gene down-regulated by nm23-H1 and associated with cell motility/metastasis suppressor functions in breast cancer cells. Although the clinical significance of nm23-H1 overexpression in leukemia is completely opposite to that in breast cancer, there might be a common molecular mechanism between the metastasis-suppressing activity and differentiation-inhibiting activity of nm23-H1 overexpression, because many functional characteristics of macrophages/neutrophils are similar to those of motile and metastatic tumor cells. Here, we examined the EDG2/lpa1 expression level and its association with NM23 expression level and myeloid differentiation of leukemia cells. EDG2 and NM23 proteins were expressed at different levels in all leukemia cells tested (HL-60, NB4, THP-1, U937, K562, HEL, BALM-1, BALM-3, MOLT4, Jurkat). During all-trans retinoic acid (ATRA)-induced myeloid differentiation of HL-60 cells, the NM23 expression decreased and EDG2 expression inversely increased. Similar effects of ATRA were observed in myeloid differentiation of NB4 and THP-1 cells. NM23 expression levels and EDG2 expression levels modulated by ATRA treatment were inversely correlated (Spearman’s correlation coefficient, rs = −0.7538, p = 0.0237). However, these correlations were not found in the erythroid differentiation of ATRA-treated HEL and K562 cells. Cell motility is required for myeloid differentiation; therefore, there might be a common mechanism, the inhibition of cell motility thorough EDG2 down-regulation by NM23-H1 overexpression, between differentiation-inhibiting activity in leukemia cells and motility-inhibiting activity in breast cancer cells. The discrepancy in the clinical significance of NM23-H1 overexpression between leukemia and breast cancer might be resolved.
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Resar, Linda, Joelle Hillion, Surajit Dhara, Takita Felder Sumter, Mita Mukherjee, Francescopaolo Di Cello, Amy Belton et al. „The HMGA1a-STAT3 axis: an “Achilles Heel” for Hematopoietic Malignancies Overexpressing HMGA1a?“ Blood 112, Nr. 11 (16.11.2008): 3810. http://dx.doi.org/10.1182/blood.v112.11.3810.3810.

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Abstract Although the high mobility group A1 (HMGA1) oncogene is widely overexpressed in high-risk hematopoietic malignancies and other aggressive cancers, the molecular mechanisms underlying transformation by HMGA1 are only beginning to emerge. The HMGA1 gene encodes the HMGA1a and HMGA1b protein isoforms, which function in regulating gene expression. We showed that HMGA1 induces leukemic transformation in cultured human lymphoid cells. Inhibiting HMGA1 expression blocks the transformed phenotype in cultured human leukemia and lymphoma cells. We also engineered HMGA1a transgenic mice and all mice develop aggressive lymphoid malignancy which closely models human T-cell acute lymphoblastic leukemia. Because HMGA1 participates in transcriptional regulation, we hypothesize that it drives leukemic transformation by dysregulating specific molecular pathways. To discover genes targeted by HMGA1 in leukemic transformation, we performed gene expression profile analysis. The signaltransducer andactivator oftranscription 3 (STAT3) gene was identified as a critical downstream target of HMGA1. STAT3 mRNA and protein are up-regulated in leukemic cells overexpressing HMGA1a and activated STAT3 recapitulates the transforming activity of HMGA1a. HMGA1a binds directly to a conserved region of the STAT3 promoter in vivo and activates transcription of the STAT3 promoter in human leukemia cells. Blocking STAT3 function with a small molecule, platinum compound inhibitor (CPA-7) induces apoptosis in leukemic cells from HMGA1 transgenic mice, but not in control cells. In primary, human leukemia samples, there is a positive correlation between HMGA1a and STAT3 mRNA. Moreover, blocking STAT3 function with a dominant-negative construct in human leukemia or lymphoma cells leads to decreased cellular motility and colony formation. We also showed that treatment with a small molecule, oligonucleotide inhibitor decreases the leukemic burden in the HMGA1a transgenic mice. Our results demonstrate that the HMGA1a-STAT3 axis is a potential “Achilles heel” that could be exploited therapeutically in selected hematopoietic malignancies.
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Schwieger, Maike, Andrea Schüler, Martin Forster, Afra Engelmann, Michael A. Arnold, Ruud Delwel, Peter J. Valk et al. „Homing and invasiveness of MLL/ENL leukemic cells is regulated by MEF2C“. Blood 114, Nr. 12 (17.09.2009): 2476–88. http://dx.doi.org/10.1182/blood-2008-05-158196.

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Abstract Acute myelogenous leukemia is driven by leukemic stem cells (LSCs) generated by mutations that confer (or maintain) self-renewal potential coupled to an aberrant differentiation program. Using retroviral mutagenesis, we identified genes that generate LSCs in collaboration with genetic disruption of the gene encoding interferon response factor 8 (Irf8), which induces a myeloproliferation in vivo. Among the targeted genes, we identified Mef2c, encoding a MCM1-agamous-deficiens-serum response factor transcription factor, and confirmed that overexpression induced a myelomonocytic leukemia in cooperation with Irf8 deficiency. Strikingly, several of the genes identified in our screen have been reported to be up-regulated in the mixed-lineage leukemia (MLL) subtype. High MEF2C expression levels were confirmed in acute myelogenous leukemia patient samples with MLL gene disruptions, prompting an investigation of the causal interplay. Using a conditional mouse strain, we demonstrated that Mef2c deficiency does not impair the establishment or maintenance of LSCs generated in vitro by MLL/ENL fusion proteins; however, its loss led to compromised homing and invasiveness of the tumor cells. Mef2c-dependent targets included several genes encoding matrix metalloproteinases and chemokine ligands and receptors, providing a mechanistic link to increased homing and motility. Thus, MEF2C up-regulation may be responsible for the aggressive nature of this leukemia subtype.
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Hogeman, P. H. G., A. J. P. Veerman, D. R. Huismans, C. H. van Zantwijk und P. D. Bezemer. „Motility of Leukemic Cells in Collagen Gel Related to Immunological Phenotype in Childhood Acute Lymphoblastic Leukemia“. Acta Haematologica 78, Nr. 4 (1987): 229–32. http://dx.doi.org/10.1159/000205883.

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Kornblau, Steven M., Andrew Pierce, Stefan Meyer, Farhad Ravandi, Gautam Borthakur, Kevin R. Coombes, Nianxiang Zhang und Anthony Whetton. „Transglutaminase2 Expression in Acute Myeloid Leukemia: Association with Adhesion Molecule Expression and Leukemic Blast Motility“. Blood 120, Nr. 21 (16.11.2012): 1427. http://dx.doi.org/10.1182/blood.v120.21.1427.1427.

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Abstract Abstract 1427 Background: In prior proteomic analysis on Acute myeloid leukemia (AML) cell lines evaluating the effects of several leukemogenic oncogenes we observed that transglutaminase2 (TG2) was expressed at greater levels as a consequence of oncogenic transformation. TG2 is a multi-domain, multi-functional enzyme with diverse biological functions, including extracellular matrix formation, integrin-mediated signalling, and signal transduction. It's normal roles remain obscure, but it is linked to the pathogenesis of celiac sprue, neurodegenerative diseases, and some cancers. In malignancy it is reported to be an anti-apoptotic mediator of hypoxia inducible factor (HIF) conferring a growth advantage to tumor cells. Expression has been associated with resistance to chemotherapy and apoptosis. We therefore assess the expression of TG2 protein in primary AML patient samples. METHODS: We analyzed 511 AML samples from patients with newly diagnosed AML using a custom made reverse phase proteomic array. This array included 11 normal bone marrow derived CD34+ samples as controls and had 140 paired same day blood and marrow samples and 49 paired diagnosis and relapse samples. The array was probed with antibodies against 203 targets including TG2 (Abcam, ab2386, UK). Supercurve algorithms were used to generate a single value from the five serial dilutions. Loading control and topographical normalization procedures accounted for protein concentration and background staining variations. RESULTS: Expression of TG2 was statistically similar (p= 0.43) in paired blood and marrow samples and in protein prepared from fresh cells or from cryopreserved cells (p= 0.71). Expression was above, equal to or below that of normal CD34+ cells in 12%, 62%, and 27% of patients. Levels were significantly higher at relapse compared to diagnosis in the 49 paired samples (p = 0.003). Levels were higher in FAB M6 and M7 (P =<0.00001 and < 0.008) and lower in patients with inversion16. Higher TG2 expression was strongly inversely correlated with total WBC (r=.035, p < 0.0001) and the absolute blood blast count (r = −.30, p <0.0001). Patients with higher TG2 level had a shorter but not statistically significant overall survival in the entire cohort, and was not prognostic in subsets stratified based on cytogenetics or mutations (FLT3, NPM1, RAS). Likewise, patients with higher TG2 levels had shorter remission durations, but again this was not significant in the entire cohort or in subsets. Expression of TG2 was significantly correlated with 55 of 203 proteins. Notable among these were numerous integrin and adhesion proteins. Hierarchical clustering of these demonstrated that AML is characterized by two large cohorts, one in which TG2 is elevated and is positively correlated with CD49B, Integrinβ3, FAK, Fibronectin and IGFB2, a second in which TG2 is low and negatively correlated with high expression of Osteopontin, CD11 and, CD44 and a 3rd in which only Caveolin1 is expressed. A Cytoscape interaction plot based on online databases of known protein-protein interactions revealed that TG2 has known interactions with Fibronectin, which it binds and post-translationally modifies, and integrinβ3. In combination this suggests that there is canonical interaction between TG2 and integrin and adhesion proteins active in AML. TG2 expression also correlated positively with numerous anti-apotptosis proteins. CONCLUSION: TG2 is expressed in the majority of cases of AML at levels comparable to normal bone marrow CD34+ cells and levels became significantly higher at relapse suggesting that the protein expression signature associated with high TG2 levels may be selected for, or confer a subtle survival advantage to leukemic blasts. In support of this, while the level of TG2 was not statistically significantly prognostic for either overall survival or remission duration, patents with higher levels were somewhat more likely to relapse, and less likely to be alive beyond 3 years. TG2 has previously been linked to drug resistance in cancer and given the negative correlation between TG2 levels and peripheral blasts observed increased TG2 levels may lead to the protection of the leukemic stem cell due to increased adhesion/reduced motility. TG2 may therefore form part of a network of proteins that define poor outcome in AML patients and potentially offer a target to sensitize AML stem cells to drug treatment. Disclosures: Off Label Use: Clofarabine in AML.
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Casalegno-Garduño, R., C. Meier, A. Schmitt, A. Spitschak, I. Hilgendorf, S. Rohde, C. Hirt, M. Freund, B. M. Pützer und M. Schmitt. „Immune Responses to RHAMM in Patients with Acute Myeloid Leukemia after Chemotherapy and Allogeneic Stem Cell Transplantation“. Clinical and Developmental Immunology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/146463.

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Leukemic blasts overexpress immunogenic antigens, so-called leukemia-associated antigens like the receptor for hyaluronan acid-mediated motility (RHAMM). Persistent RHAMM expression and decreasing CD8+T-cell responses to RHAMM in the framework of allogeneic stem cell transplantation or chemotherapy alone might indicate the immune escape of leukemia cells. In the present study, we analyzed the expression of RHAMM in 48 patients suffering from acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). Furthermore, we correlated transcripts with the clinical course of the disease before and after treatment. Real-time quantitative reverse transcriptase polymerase chain reaction was performed from RNA of peripheral blood mononuclear cells. T cell responses against RHAMM were assessed by tetramer staining (flow cytometry) and enzyme-linked immunospot (ELISPOT) assays. Results were correlated with the clinical outcome of patients. The results of the present study showed that almost 60% of the patients were RHAMM positive; specific T-cells recognizing RHAMM could be detected, but they were nonfunctional in terms of interferon gamma or granzyme B release as demonstrated by ELISPOT assays. Immunotherapies like peptide vaccination or adoptive transfer of RHAMM-specific T cells might improve the immune response and the outcome of AML/MDS patients.
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Ikeyama, S., M. Koyama, M. Yamaoko, R. Sasada und M. Miyake. „Suppression of cell motility and metastasis by transfection with human motility-related protein (MRP-1/CD9) DNA.“ Journal of Experimental Medicine 177, Nr. 5 (01.05.1993): 1231–37. http://dx.doi.org/10.1084/jem.177.5.1231.

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Previously we showed that motility-related protein (MRP-1) is an antigen recognized by monoclonal antibody (mAb) M31-15 inhibiting cell motility and that the sequence of MRP-1 coincides with that of CD9. In the present study, plasmid was constructed in which human MRP-1/CD9 cDNA is expressed under the control of the Abelson murine leukemia virus promoter sequence. The expression plasmid for MRP-1/CD9 was introduced into Chinese hamster ovary cells, human lung adenocarcinoma cell line MAC10 (MRP-1 positive), and human myeloma cell line ARH77 (MRP-1 negative). All of the MRP-1/CD9 (over)expressing clones obtained from these transfected cells showed suppressed cell motility (penetration and phagokinetic track assays) depending on the degree of expression of MRP-1/CD9. Overexpression of MRP-1/CD9 by MAC10 cells resulted in the suppression of cell motility (maximally 73%) associated with considerable inhibition of the cell growth (maximally 48%). However, the inhibition of the growth of MAC10 cells by mAb M31-15 was &lt; 17% at an antibody concentration of 1-5 micrograms/ml, which inhibits cell motility by &gt; 90%. These results suggest that MRP-1/CD9 directly regulates cell motility and may also affect cell growth. Effects on metastasis by the expression of MRP-1 CD9 were investigated with mouse melanoma BL6 cells-BALB/c nu/nu mouse system. Metastatic potential of all transformants expressing MRP-1/CD9 was lower than that of parent BL6 cells.
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Tavor, Sigal, Isabelle Petit, Svetlana Porozov, Polina Goichberg, Abraham Avigdor, Sari Sagiv, Arnon Nagler, Elizabeth Naparstek und Tsvee Lapidot. „Motility, proliferation, and egress to the circulation of human AML cells are elastase dependent in NOD/SCID chimeric mice“. Blood 106, Nr. 6 (15.09.2005): 2120–27. http://dx.doi.org/10.1182/blood-2004-12-4969.

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Abstract The role of the proteolytic enzyme elastase in motility and proliferation of leukemic human acute myeloblastic leukemia (AML) cells is currently unknown. We report a correlation between abnormally high levels of elastase in the blood of AML patients and the number of leukemic blast cells in the circulation. In AML cells, we observed expression of cell-surface elastase, which was regulated by the chemokine stromal cell-derived factor-1 (SDF-1). In vitro inhibition of elastase prevented SDF-1-induced cell polarization, podia formation, and reduced migration of human AML cells as well as their adhesion. Elastase inhibition also significantly impaired in vivo homing of most human AML cells to the bone marrow (BM) of nonobese diabetic-severe combined immunodeficient (NOD/SCID)/beta-2 microglobulin knock-out (B2mnull) mice that underwent transplantation. Moreover, in vitro proliferation of AML cells was elastase dependent. In contrast, treatment with elastase inhibitor enhanced the proliferation rate of human cord blood CD34+ cells, including primitive CD34+/CD38- cells, and their in vivo homing. Finally, NOD/SCID mice previously engrafted with human AML cells and treated with elastase inhibitor had significantly reduced egress of leukemic cells into the circulation. Taken together, our data demonstrate that human AML cells constitutively secrete and express SDF-1-dependent cell-surface elastase, which regulates their migration and proliferation. (Blood. 2005;106:2120-2127)
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Dissertationen zum Thema "Motility of leukemia cells"

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Renaudin, Xavier. „Rôle de FANCA dans la régulation de la neddylation de protéines membranaires“. Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112187.

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Le but de cette thèse était d’identifier de nouveaux substrats au complexe FANC Core,déficient dans l’Anémie de Fanconi, une pathologie génétique rare. Cette maladie estcaractérisée par un phénotype hétérogène associant une pancytopénie à des malformationscongénitales et une prédisposition accrues aux leucémies myéloïdes aigues.L’anémie de Fanconi est causée par la mutation biallélique dans un des seize gènesFANC. Les protéines produites par ces gènes participent à une même voie moléculaireimpliquée dans la signalisation des dommages de l’ADN. Huit de ces protéines forment lecomplexe FANC Core, une E3 ubiquitine ligase, dont les seuls substrats à ce jour sontFANCD2 et FANCI.Dans le but d’identifier de nouveaux substrats du complexe FANC Core, j’ai réalisé uneanalyse protéomique après immunoprécipitation des peptides modifiés par l’ubiquitine ou parles ubiquitin-like NEDD8 et ISG15. Cette expérience a été faite dans des cellules déficientespour la voie FANC, mutées sur les gène FANCA ou FANCC et comparée à des cellulescorrigées par l’expression de ces gènes.Cette analyse révèle que FANCD2 et FANCI sont les seules cibles du complexe FANCCore en réponse à des dommages de l’ADN.Néanmoins, je montre l’existence d’autres protéines qui sont modifiées d’une manièreFANCA dépendante. Ces protéines sont pour la grande majorité des protéines membranairesou associées aux membranes cytoplasmiques. Parmi celles-ci, j’ai pu déterminer que lerécepteur aux chimiokines, CXCR5, était modifié d’une manière FANCA dépendante parl’ubiquitin-like NEDD8. Cette modification impacte sur la localisation de la protéine à lamembrane et à des conséquences sur la migration des cellules.J’ai aussi montré que FANCA participe d’une manière similaire à la régulation de lalocalisation membranaire d’autres protéines comme APLP2.Ainsi, il est proposé par ce travail un rôle de la protéine FANCA en dehors du complexeFANC Core et en dehors de la réparation des dommages à l’ADN. Comment la protéineFANCA participe à la régulation du trafic des protéines membranaires reste un point nonrésolu à ce jour
The aim of this thesis was to find new substrates of the E3-ubiquitin ligase activity of theFANC Core complex, mutated in the rare genetic disorder Fanconi Anemia. This disease ischaracterized by bone marrow failure, developmental abnormalities and predisposition tocancer. Eight of the 16 known FANC proteins participate in the FANCcore nuclear complex,which has E3 ubiquitin-ligase activity and monoubiquitinates FANCD2 and FANCI inresponse to replication stress.In this thesis, I used mass spectrometry to compare cellular extracts from FANC Corecomplex deficient FA-A and FA-C cells to their ectopically corrected counterparts after agenotoxic stress.FANCD2 and FANCI appear to be the only true direct targets of the FANCcore complex.However, I also identified other proteins that undergo post-translational modifications throughFANCA- or FANCC-specific direct or indirect mechanisms that are independent of theFANCcore complex. The majority of these potential FANCA or FANCC target proteinslocalize to the cell membrane.Finally, I demonstrated that (a) the chemokine receptor CXCR5 is a neddylated protein; (b)FANCA, surprisingly, appears to modulate CXCR5 neddylation through a currently unknownmechanism; (c) CXCR5 neddylation is involved in the targeting of this receptor to the cellmembrane; and (d) CXCR5 neddylation stimulates cell migration/motility.I also confirmed that the role of FANCA in neddylation is not restrict to CXCR5 but also to,at least, one other protein, APLP2.My work has uncovered a new signaling pathway that is potentially involved in the rarehuman syndrome Fanconi Anemia and in cell motility and has highlighted a potential newfunction for the FANCA protein independant of the FANC Core complex and of a genotoxicstress
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Smrčková, Zuzana. „Motilita leukemických buněk analyzovaná nekoherentním holografickým kvantitativním zobrazováním fáze“. Master's thesis, Vysoké učení technické v Brně. Fakulta strojního inženýrství, 2021. http://www.nusl.cz/ntk/nusl-444984.

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This diploma thesis deals with the issue of motility analysis in leukemia cells. An accurate description of the cell movement and the detection of differences in motility under experimental conditions can be obtained by quantitative analysis of cell motility using time-lapse recording. The first part of this work describes various types of tumor cell migraton. The second part focuses on methods of analysis of cell motility in tissue culture using time-lapse recording, which include image acquisition and processing. Part of this chapter describes a coherence-controlled holographic microscope, which was used in the practical part and for which an insert was designed to ensure the exact and stable position of the individual chambers. The last part is focused on the research of leukemic cell motility, which is concluded by a discussion of the obtained results. The appendix contains a published study included acknowledgement to the author of this diploma thesis for participation in the project.
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Zhang, Lu [Verfasser]. „Immunogenicity of leukemia stem cells in acute myeloid leukemia / Lu Zhang“. Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1020022574/34.

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Bai, Limiao, und 白利苗. „In silico simulation of actin-based motility“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B46429116.

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Suck, Garnet, Yeh Ching Linn und Torsten Tonn. „Natural Killer Cells for Therapy of Leukemia“. Karger, 2016. https://tud.qucosa.de/id/qucosa%3A71644.

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Clinical application of natural killer (NK) cells against leukemia is an area of intense investigation. In human leukocyte antigen-mismatched allogeneic hematopoietic stem cell transplantations (HSCT), alloreactive NK cells exert powerful anti-leukemic activity in preventing relapse in the absence of graft-versus-host disease, particularly in acute myeloid leukemia patients. Adoptive transfer of donor NK cells post-HSCT or in non-transplant scenarios may be superior to the currently widely used unmanipulated donor lymphocyte infusion. This concept could be further improved through transfusion of activated NK cells. Significant progress has been made in good manufacturing practice (GMP)-compliant large-scale production of stimulated effectors. However, inherent limitations remain. These include differing yields and compositions of the end-product due to donor variability and inefficient means for cryopreservation. Moreover, the impact of the various novel activation strategies on NK cell biology and in vivo behavior are barely understood. In contrast, reproduction of the thirdparty NK-92 drug from a cryostored GMP-compliant master cell bank is straightforward and efficient. Safety for the application of this highly cytotoxic cell line was demonstrated in first clinical trials. This novel ‘off-theshelf’ product could become a treatment option for a broad patient population. For specific tumor targeting chimeric-antigen-receptor-engineered NK-92 cells have been designed.
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Birkenmeier, Gerd, Nasr Y. A. Hemdan, Susanne Kurz, Marina Bigl, Philipp Pieroh, Tewodros Debebe, Martin Buchold, Rene Thieme, Gunnar Wichmann und Faramarz Dehghani. „Ethyl pyruvate combats human leukemia cells but spares normal blood cells“. Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-213853.

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Ethyl pyruvate, a known ROS scavenger and anti-inflammatory drug was found to combat leukemia cells. Tumor cell killing was achieved by concerted action of necrosis/apoptosis induction, ATP depletion, and inhibition of glycolytic and para-glycolytic enzymes. Ethyl lactate was less harmful to leukemia cells but was found to arrest cell cycle in the G0/G1 phase. Both, ethyl pyruvate and ethyl lactate were identified as new inhibitors of GSK-3β. Despite the strong effect of ethyl pyruvate on leukemia cells, human cognate blood cells were only marginally affected. The data were compiled by immune blotting, flow cytometry, enzyme activity assay and gene array analysis. Our results inform new mechanisms of ethyl pyruvate-induced cell death, offering thereby a new treatment regime with a high therapeutic window for leukemic tumors.
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Choi, Mi-Yon. „P53 mediated cell motility in H1299 lung cancer cells“. VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/109.

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Studies have shown that gain-of- function mutant p53, AKT, and NFκB promote invasion and metastasis in tumor cells. Signals transduced by AKT and p53 are integrated via negative feedback between the two pathways. Tumor derived p53 was also indicated to induce NFκB gene expression. Due to the close relationship between p53/AKT and p53/NFκB, we hypothesized that AKT and NFκB can enhance motility in cells expressing mutant p53. Effects on cell motility were determined by scratch assays. CXCL5- chemokine is also known to induce cell motility. We hypothesized that enhanced cell motility by AKT and NFκB is mediated, in part, by CXCL5. CXCL5 expression levels in the presence and absence of inhibitors were determined by qRT-PCR. We also hypothesized that gain-of-function mutant p53 contributes to the activation of AKT. The effect of mutant p53 on AKT phosphorylation was investigated with a Ponasterone A- inducible mutant cell line (H1299/R175H) and vector control. These results indicated that AKT and NFκB enhance motility in cells expressing mutant p53 and this enhanced motility is, in part, mediated by CXCL5. However, AKT phosphorylation was independent of mutant p53.
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Peng, Cong. „Novel Therapeutic Targets for Ph+ Chromosome Leukemia and Its Leukemia Stem Cells: A Dissertation“. eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/473.

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The human Philadelphia chromosome (Ph) arises from a translocation between chromosomes 9 and 22 [t(9;22)(q34;q11)]. The resulting chimeric BCR-ABLoncogene encodes a constitutively activated, oncogenic tyrosine kinase that induces chronic myeloid leukemia (CML) and B-cell acute lymphoblastic leukemia (B-ALL). The BCR-ABL tyrosine kinase inhibitor (TKI), imatinib mesylate, induces a complete hematologic and cytogenetic response in the majority of CML patients, but is unable to completely eradicate BCR-ABL–expressing leukemic cells, suggesting that leukemia stem cells are not eliminated. Over time, patients frequently become drug resistant and develop progressive disease despite continued treatment. Two major reasons cause the imatinib resistance. The first one is the BCR-ABL kinase domain mutations which inhibit the interaction of BCR-ABL kinase domain with imatinib; the second one is the residual leukemia stem cells (LSCs) in the patients who are administrated with imatinib. To overcome these two major obstacles in CML treatment, new strategies need further investigation. As detailed in Chapter II, we evaluated the therapeutic effect of Hsp90 inhibition by using a novel water-soluble Hsp90 inhibitor, IPI-504, in our BCR-ABL retroviral transplantation mouse model. We found that BCR-ABL mutants relied more on the HSP90 function than WT BCR-ABL in CML. More interestingly, inhibition of HSP90 in CML leukemia stem cells with IPI-504 significantly decreases the survival and proliferation of CML leukemia stem cells in vitro and in vivo. Consistent with these findings, IPI-504 treatment achieved significant prolonged survival of CML and B-ALL mice. IPI-504 represents a novel therapeutic approach whereby inhibition of Hsp90 in CML patients and Ph+ ALL may significantly advance efforts to develop a cure for these diseases. The rationale underlying the use of IPI-504 for kinase inhibitor–resistant CML has implications for other cancers that display oncogene addiction to kinases that are Hsp90 client proteins. Although we proved that inhibition of Hsp90 could restrain LSCs in vitro and in vivo, it is still unclear how to define specific targets in LSCs and eradicate LSCs. In Chapter III, we took advantage of our CML mouse model and compared the global gene expression signature between normal HSCs and LSCs to identify the downregulation of Pten in CML LSCs. CML develops faster when Pten is deleted in Ptenfl/fl mice. On the other hand, Pten overexpression significantly delays the CML development and impairs leukemia stem cell function. mTOR is a major downstream of Pten-Akt pathway and it is always activated or overepxressed when Pten is mutated or deleted in human cancers. In our study, we found that inhibition of mTOR by rapamycin inhibited proliferation and induced apoptosis of LSCs. Notably, our study also confirmed a recent clinical report that Pten has been downregulated in human CML patient LSCs. In summary, our results proved the tumor suppressor role of Pten in CML mouse model. Although the mechanisms of Pten in leukemia stem cells still need further study, Pten and its downstream, such as Akt and mTOR, should be more attractive in LSCs study.
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Chu, Peter P. „Immune-mediated apoptosis of chronic lymphocytic leukemia cells /“. Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3031939.

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Sawai, Hirofumi. „Role for ceramide in apoptosis of leukemia cells“. Kyoto University, 1997. http://hdl.handle.net/2433/202164.

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Bücher zum Thema "Motility of leukemia cells"

1

Cobaleda, César, und Isidro Sánchez-García, Hrsg. Leukemia Stem Cells. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0810-4.

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Cell movement and cell behaviour. London: Allen & Unwin, 1986.

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Lackie, J. M. Cell movement and cell behaviour. London: Allen & Unwin, 1986.

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Zhang, Haojian, und Shaoguang Li, Hrsg. Leukemia Stem Cells in Hematologic Malignancies. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7342-8.

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Murase, Mosatoshi. Dynamics of cellular motility. Chichester [England]: Wiley, 1992.

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Murase, Masatoshi. Dynamics of cellular motility. Chichester: J. Wiley & Sons, 1992.

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Bray, Dennis. Cell movements: From molecules to motility. 2. Aufl. New York: Garland Pub., 2001.

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1947-, Jones Gareth E., Dunn Graham 1944- und Lackie J. M, Hrsg. Cell behaviour: Control and mechanism of motility. London: Portland on behalf of The Biochemical Society, 1999.

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M, Lackie J., Dunn Graham 1944- und Jones Gareth E. 1947-, Hrsg. Cell behaviour: Control and mechanism of motility. Princeton, NJ: Princeton University Press, 1999.

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Preston, Terence M. The cytoskeleton and cell motility. Glasgow: Blackie, 1990.

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Buchteile zum Thema "Motility of leukemia cells"

1

Wozniak, Marcin J., und Victoria J. Allan. „Carrier Motility“. In Trafficking Inside Cells, 233–53. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-93877-6_12.

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Raff, Thorsten, und Monika Brüggemann. „Leukemia-Initiating Cells in Acute Lymphoblastic Leukemia“. In Cancer Stem Cells, 161–70. Hoboken, NJ: John Wiley & Sons, 2014. http://dx.doi.org/10.1002/9781118356203.ch12.

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Lane, Steven W., und David A. Williams. „Leukemia Stem Cells“. In Advances in Cancer Stem Cell Biology, 85–103. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0809-3_6.

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Müschen, Markus. „Leukemia Stem Cells“. In Stem Cell Biology in Health and Disease, 281–94. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3040-5_13.

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Konopleva, Marina, und Lina Han. „Leukemia Stem Cells“. In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-27841-9_7164-3.

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Konopleva, Marina, und Lina Han. „Leukemia Stem Cells“. In Encyclopedia of Cancer, 2476–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_7164.

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Lynch, R. G. „Lymphoid Tumor Stem Cells and Their Regulation“. In Leukemia, 83–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69722-7_6.

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Krivtsov, Andrei V., Yingzi Wang, Zhaohui Feng und Scott A. Armstrong. „Gene Expression Profiling of Leukemia Stem Cells“. In Leukemia, 231–46. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_11.

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Bonnet, Dominique. „Humanized Model to Study Leukemic Stem Cells“. In Leukemia, 247–62. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_12.

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Preston, Terence M., Conrad A. King und Jeremy S. Hyams. „Movement within Cells“. In The Cytoskeleton and Cell Motility, 70–86. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0393-7_3.

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Konferenzberichte zum Thema "Motility of leukemia cells"

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Marquerie, G., A. Duperray, G. Uzan und R. Berthier. „BIOSYNTHETIC PATHWAYS OF THE PLATELET FIBRINOGEN RECEPTOR IN HUMAN MEGAKARYOCYTES“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642954.

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Interaction between cells and between cells and extracellular matrices are critical for a number of biological processes, including organ development, cell differenciation, cell motility, and the inimune' response. These interactions are mediated by a family of adhesion receptors that recognize short sequences such as Arg-Gly-Asp (RGD). These receptors share similar structural properties. They are heterodimers composed of a and B subunits and sometime express common epitopes. This suggests that the structural and functional relationship of these receptors may result from the transcription of related genes or may arise from cell specific post-transcriptional events. Thus, analysis of the biosynthesis and processing of these receptors would provide valuable insights into the molecular mechanism which control their expression at the surface,of different cells. Platelet membrane glycoprotein (GP) IIb-IIIa is a member of this receptor family. This protein is a non covalent heterodimer composed of two distinct polypeptides, Glib which consists of two subunits Ilba and IlbB (Mr = 116 kD, Mr = 25 kD) and GPIIIa (Mr = 100 kD, reduced). GPIIb-IIIa functions at site of platelet aggregation and serves as receptor for RGD containing factors including fibrinogen, fibronectin and von Willebrand factor. We report here on the investigation of the biosynthetic pathways of this RGD receptor in human megakaryocytes. High number of megakaryocytic cells from the megakaryoblastic stage to the polyploid mature megakaryocyte were obtained from liquid culture of cryopreserved leukocyte stem cell concentrates from patients with chronic myelogenous leukemia (CML). After sorting, using a FACS IV and indirect immunofluores-cent labeling with monoclonal antibodies anti-GPIIb-IIIa, 95 % of the cells in culture were of the megakaryocytic lineage. These megakarocytes represented an excellent tool to delineate at the molecular level events associated with the biosynthesis of GPIIb-IIIa.Metabolic labeling and pulse-chase experiments indicated that GPIIb and GPIIIa are synthesized from separate mRNA and that the two subunits of GPIIb derive from a common precursor. This was further confirmed by cell-free translation of megakaryocyte mRNA and the identification of separate cDNA containing sequences coding for the pro-GPIIb and for GPIIIa. These cDNA were isolated from a Xgt11 expression library constructed with purified megakaryocyte RNA, and were used to size the messengers coding for the two polypeptides. A single mRNA species of 3.9 kB was found to encode the pro-GPIIb, whereas two different mRNA species of 2.9 kB and 4. 1 kB were identified with the GPIIIa cDNA.The newly synthesized GPIIIa associates early with the pro-GPIIb in the rough endoplasmic reticulum. Examination of the glycosylation pathways with endoglycosidase H, tunicamycin and monensin indicated that high mannose oligosaccharides are added to the GPIIIa and pro-GPIIb polypeptide backbone. The pro-GPIIb is then processed with conversion of high mannose to the complex type carbohydrate, whereas GPIIIa remains endoH sensitive. Glycosylation of pro-GPIIb-IIIa and processing of oligosaccharides are prerequisite for proteolytic maturation of pro-GPIIb and the expression of the mature complex at the surface of the cell. Thus post-translational processing of GPIIb-IIIa requires an early assembly of the complex. This may have important implications in the maturation of megakaryocyte granules and in the molecular mechanism underlying the Glanzmann thrombastenic disease.
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Yunardi, Riky Tri, Agung Budianto Achmad und Qurrotul A'yun. „Imaging Motility Pattern Analyzer Based on Optical Flow on Mice Sperm Cells Motility“. In 2020 10th Electrical Power, Electronics, Communications, Controls and Informatics Seminar (EECCIS). IEEE, 2020. http://dx.doi.org/10.1109/eeccis49483.2020.9263448.

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Liu, Zhuolin, Kazuhiro Kurokawa, Furu Zhang und Donald T. Miller. „Characterizing motility dynamics in human RPE cells“. In SPIE BiOS, herausgegeben von Fabrice Manns, Per G. Söderberg und Arthur Ho. SPIE, 2017. http://dx.doi.org/10.1117/12.2256144.

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Pramanik, Rocky, Xia Sheng und Steven D. Mittelman. „Abstract 5173: Adipocytes attract leukemia 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.am10-5173.

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Xiao, Lifu, Xiaoying Liao, Lisheng Lin, Huifang Huang, Yuanzhong Chen und Buhong Li. „Autofluorescence characteristics of human leukemia cells and mononuclear cells“. In Photonics Asia 2010, herausgegeben von Qingming Luo, Ying Gu und Xingde Li. SPIE, 2010. http://dx.doi.org/10.1117/12.870282.

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Yu-Chiu Kao, Chau-Hwang Lee und Po-Ling Kuo. „Increased hydrostatic pressure enhances motility of lung cancer cells“. In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6944236.

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Burgett, Monica E., Russell S. Tipps, Justin D. Lathia, Shideng Bao, Jeremy N. Rich und Candece L. Gladson. „Abstract 5288: Glioma stem cells stimulate the motility of brain endothelial cells: Identification of cell-adhesion molecules mediating motility and direct interaction“. 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.am2012-5288.

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Popescu, Gabriel, Kamran Badizadegan, Ramachandra R. Dasari und Michael S. Feld. „Motility of Live Cancer Cells Quantified by Fourier Phase Microscopy“. In European Conference on Biomedical Optics. Washington, D.C.: OSA, 2005. http://dx.doi.org/10.1364/ecbo.2005.md4.

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Lu, Ling-Chao, Cheng-Kai Xuan und Yue-Min Ding. „Dibutyl Phthalate Inhibits Motility and Neurite Outgrowth in Neuronal Cells“. In 2015 International Conference on Medicine and Biopharmaceutical. WORLD SCIENTIFIC, 2016. http://dx.doi.org/10.1142/9789814719810_0047.

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Karl, Ilonka, und Juergen Bereiter-Hahn. „Scanning acoustic microscopy reveals distinct motility domains in living cells“. In 6th Annual International Symposium on NDE for Health Monitoring and Diagnostics, herausgegeben von Tribikram Kundu. SPIE, 2001. http://dx.doi.org/10.1117/12.434181.

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Berichte der Organisationen zum Thema "Motility of leukemia cells"

1

Segall, Jeffrey E. Molecular Analysis of Motility in Metastatic Mammary Adenocarcinoma Cells. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada300010.

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Segall, Jeffrey E. Molecular Analysis of Motility in Metastatic Mammary Adenocarcinoma Cells. Fort Belvoir, VA: Defense Technical Information Center, September 1998. http://dx.doi.org/10.21236/ada361091.

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Segall, Jeffrey E. Molecular Analysis of Motility in Metastatic Mammary Adenocarcinoma Cells. Fort Belvoir, VA: Defense Technical Information Center, September 1997. http://dx.doi.org/10.21236/ada343279.

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Muller-Sieburg, Christa. Myeloid-Biased Stem Cells as Potential Targets for Chronic Myelogeneous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada447669.

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Wang, Fang. Inhibition of Invasiveness and Motility of Human Breast Cancer Cells by Sphingosine-1-Phosphate. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada382431.

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Wang, Fang. Inhibition of Invasiveness and Motility of Human Breast Cancer Cells by Sphingosine-1-Phosphate. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada359261.

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Fort Belvoir, VA: Defense Technical Information Center, Juni 2005. http://dx.doi.org/10.21236/ada439284.

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurotibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Fort Belvoir, VA: Defense Technical Information Center, Oktober 2002. http://dx.doi.org/10.21236/ada411714.

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Fort Belvoir, VA: Defense Technical Information Center, Oktober 2003. http://dx.doi.org/10.21236/ada422403.

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Vogel, Kristine S. Cell Motility and Invasiveness of Neurofibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines. Addendum. Fort Belvoir, VA: Defense Technical Information Center, Juni 2006. http://dx.doi.org/10.21236/ada458421.

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