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249 results on '"Lengerke, C"'

7. Ruxolitinib in corticosteroid-refractory graft-versus-host disease after allogeneic stem cell transplantation: a multicenter survey

Author

Zeiser, R, Burchert, A, Lengerke, C, Verbeek, M, Maas-Bauer, K, Metzelder, S K, Spoerl, S, Ditschkowski, M, Ecsedi, M, Sockel, K, Ayuk, F, Ajib, S, de Fontbrune, F S, Na, I-K, Penter, L, Holtick, U, Wolf, D, Schuler, E, Meyer, E, Apostolova, P, Bertz, H, Marks, R, Lübbert, M, Wäsch, R, Scheid, C, Stölzel, F, Ordemann, R, Bug, G, Kobbe, G, Negrin, R, Brune, M, Spyridonidis, A, Schmitt-Gräff, A, van der Velden, W, Huls, G, Mielke, S, Grigoleit, G U, Kuball, J, Flynn, R, Ihorst, G, Du, J, Blazar, B R, Arnold, R, Kröger, N, Passweg, J, Halter, J, Socié, G, Beelen, D, Peschel, C, Neubauer, A, Finke, J, Duyster, J, and von Bubnoff, N

Published
2015
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9. Allogene Stammzelltransplantation für Patienten über 70 Jahre

Author

Weller, J. F., Lengerke, C., de Wreede, L. C., Schroeder, T., Hirt, S., Fleischhauer, Katharina, and Christopeit, M.

Subjects
Medizin
Abstract

Weitere Verfasser:innen aus Einrichtungen außerhalb der Universität Duisburg-Essen sind nicht aufgeführt

Published
2022

11. OUTCOME DETERMINANTS OF COMMERCIAL CAR‐T CELL THERAPY FOR LARGE B‐CELL LYMPHOMA: RESULTS OF THE GLA/DRST REAL WORLD ANALYSIS

Author

Dreger, P., primary, Martus, P., additional, Holtick, U., additional, Ayuk, F., additional, Wagner‐Drouet, E. M., additional, Wulf, G., additional, Marks, R., additional, Penack, O., additional, Koenecke, C., additional, von Bonin, M., additional, von Tresckow, B., additional, Stelljes, M., additional, Baldus, C., additional, Vucinic, V., additional, Mougiakakos, D., additional, Topp, M., additional, Wolff, D., additional, Schroers, R., additional, Schmitt, M., additional, Schmitt, T., additional, Lengerke, C., additional, Thomas, S., additional, Beelen, D. W., additional, and Bethge, W., additional

Published
2021
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12. NCKAP1L defects lead to a novel syndrome combining immunodeficiency, lymphoproliferation and hyperinflammation Running title: NCKAP1L deficiency: NCKAP1L deficiency

Author

Castro, C. (Carla) N. (Noemi), Rosenzwajg, M. (Michelle), Carapito, R. (Raphaël), Shahrooei, M. (Mohammad), Konantz, M. (Martina), Khan, A. (Amjad), Miao, Z. (Zhichao), Gross, M. (Miriam), Tranchant, T. (Thibaud), Radosavljevic, M. (Mirjana), Paul, N. (Nicodème), Stemmelen, T. (Tristan), Pitoiset, F. (Fabien), Hirschler, A. (Aurélie), Nespola, B. (Benoit), Molitor, A. (Anne), Rolli, V. (Veronique), Pichot, A. (Angelique), Faletti, L. (Laura) E. (Eva), Rinaldi, B. (Bruno), Friant, S. (Sylvie), Mednikov, M. (Mark), Karauzum, H. (Hatice), Javad Aman, M. (M), Carapito, C. (Christine), Lengerke, C. (Claudia), Ziaee, V. (Vahid), Eyaid, W. (Wafaa), Ehl, S. (Stephan), Alroqi, F. (Fayhan), Parvaneh, N. (Nima), and Bahram, S. (Seiamak)

Subjects
hal-03024718, Aucun
Abstract

The Nck-associated protein 1-like (NCKAP1L) gene, alternatively called hematopoietic protein 1 (HEM-1), encodes a hematopoietic lineage-specific regulator of the actin cytoskeleton. Nckap1l-deficient mice have anomalies in lymphocyte development, phagocytosis, and neutrophil migration. Here we report, for the first time, NCKAP1L deficiency cases in humans. In two unrelated patients of Middle Eastern origin, recessive mutations in NCKAP1L abolishing protein expression led to immunodeficiency, lymphoproliferation, and hyperinflammation with features of hemophagocytic lymphohistiocytosis. Immunophenotyping showed an inverted CD4/CD8 ratio with a major shift of both CD4+ and CD8+ cells toward memory compartments, in line with combined RNA-seq/proteomics analyses revealing a T cell exhaustion signature. Consistent with the core function of NCKAP1L in the reorganization of the actin cytoskeleton, patients' T cells displayed impaired early activation, immune synapse morphology, and leading edge formation. Moreover, knockdown of nckap1l in zebrafish led to defects in neutrophil migration. Hence, NCKAP1L mutations lead to broad immune dysregulation in humans, which could be classified within actinopathies.

Published
2020

23. Sorafenib promotes graft-versus-leukemia activity in mice and humans through IL-15 production in FLT3-ITD-mutant leukemia cells

Author

Mathew, N.R., Baumgartner, F., Braun, L., O'Sullivan, D., Thomas, S., Waterhouse, M., Muller, T.A., Hanke, K., Taromi, S., Apostolova, P., Illert, A.L., Melchinger, W., Duquesne, S., Schmitt-Graeff, A., Osswald, L., Yan, K.L., Weber, A, Tugues, S., Spath, S., Pfeifer, D., Follo, M., Claus, R., Lubbert, M., Rummelt, C., Bertz, H., Wasch, R., Haag, J., Schmidts, A., Schultheiss, M., Bettinger, D., Thimme, R., Ullrich, E., Tanriver, Y., Vuong, G.L., Arnold, R., Hemmati, P., Wolf, D., Ditschkowski, M., Jilg, C., Wilhelm, K., Leiber, C., Gerull, S., Halter, J., Lengerke, C., Pabst, T., Schroeder, T., Kobbe, G., Rosler, W., Doostkam, S., Meckel, S., Stabla, K., Metzelder, S.K., Halbach, S., Brummer, T., Hu, Z, Dengjel, J., Hackanson, B., Schmid, C., Holtick, U., Scheid, C., Spyridonidis, A., Stolzel, F., Ordemann, R., Muller, L.P., Sicre-de-Fontbrune, F., Ihorst, G., Kuball, J., Ehlert, J.E., Feger, D., Wagner, E.M., Cahn, J.Y., Schnell, J., Kuchenbauer, F., Bunjes, D., Chakraverty, R., Richardson, S., Gill, S., Kroger, N., Ayuk, F., Vago, L., Ciceri, F., Muller, A.M., Kondo, T., Teshima, T., Klaeger, S., Kuster, B., Kim, D.D.H., Weisdorf, D., Velden, W.J. van der, Dorfel, D., Bethge, W., Hilgendorf, I., Hochhaus, A., Andrieux, G., Borries, M., Busch, H., Magenau, J., Reddy, P., Labopin, M., Antin, J.H., et al., Mathew, N.R., Baumgartner, F., Braun, L., O'Sullivan, D., Thomas, S., Waterhouse, M., Muller, T.A., Hanke, K., Taromi, S., Apostolova, P., Illert, A.L., Melchinger, W., Duquesne, S., Schmitt-Graeff, A., Osswald, L., Yan, K.L., Weber, A, Tugues, S., Spath, S., Pfeifer, D., Follo, M., Claus, R., Lubbert, M., Rummelt, C., Bertz, H., Wasch, R., Haag, J., Schmidts, A., Schultheiss, M., Bettinger, D., Thimme, R., Ullrich, E., Tanriver, Y., Vuong, G.L., Arnold, R., Hemmati, P., Wolf, D., Ditschkowski, M., Jilg, C., Wilhelm, K., Leiber, C., Gerull, S., Halter, J., Lengerke, C., Pabst, T., Schroeder, T., Kobbe, G., Rosler, W., Doostkam, S., Meckel, S., Stabla, K., Metzelder, S.K., Halbach, S., Brummer, T., Hu, Z, Dengjel, J., Hackanson, B., Schmid, C., Holtick, U., Scheid, C., Spyridonidis, A., Stolzel, F., Ordemann, R., Muller, L.P., Sicre-de-Fontbrune, F., Ihorst, G., Kuball, J., Ehlert, J.E., Feger, D., Wagner, E.M., Cahn, J.Y., Schnell, J., Kuchenbauer, F., Bunjes, D., Chakraverty, R., Richardson, S., Gill, S., Kroger, N., Ayuk, F., Vago, L., Ciceri, F., Muller, A.M., Kondo, T., Teshima, T., Klaeger, S., Kuster, B., Kim, D.D.H., Weisdorf, D., Velden, W.J. van der, Dorfel, D., Bethge, W., Hilgendorf, I., Hochhaus, A., Andrieux, G., Borries, M., Busch, H., Magenau, J., Reddy, P., Labopin, M., and Antin, J.H., et al.

Abstract

Contains fulltext : 190745.pdf (publisher's version ) (Closed access), Individuals with acute myeloid leukemia (AML) harboring an internal tandem duplication (ITD) in the gene encoding Fms-related tyrosine kinase 3 (FLT3) who relapse after allogeneic hematopoietic cell transplantation (allo-HCT) have a 1-year survival rate below 20%. We observed that sorafenib, a multitargeted tyrosine kinase inhibitor, increased IL-15 production by FLT3-ITD(+) leukemia cells. This synergized with the allogeneic CD8(+) T cell response, leading to long-term survival in six mouse models of FLT3-ITD(+) AML. Sorafenib-related IL-15 production caused an increase in CD8(+)CD107a(+)IFN-gamma(+) T cells with features of longevity (high levels of Bcl-2 and reduced PD-1 levels), which eradicated leukemia in secondary recipients. Mechanistically, sorafenib reduced expression of the transcription factor ATF4, thereby blocking negative regulation of interferon regulatory factor 7 (IRF7) activation, which enhanced IL-15 transcription. Both IRF7 knockdown and ATF4 overexpression in leukemia cells antagonized sorafenib-induced IL-15 production in vitro. Human FLT3-ITD(+) AML cells obtained from sorafenib responders following sorafenib therapy showed increased levels of IL-15, phosphorylated IRF7, and a transcriptionally active IRF7 chromatin state. The mitochondrial spare respiratory capacity and glycolytic capacity of CD8(+) T cells increased upon sorafenib treatment in sorafenib responders but not in nonresponders. Our findings indicate that the synergism of T cells and sorafenib is mediated via reduced ATF4 expression, causing activation of the IRF7-IL-15 axis in leukemia cells and thereby leading to metabolic reprogramming of leukemia-reactive T cells in humans. Therefore, sorafenib treatment has the potential to contribute to an immune-mediated cure of FLT3-ITD-mutant AML relapse, an otherwise fatal complication after allo-HCT.

Published
2018

24. A4GALT-related glycosphingolipids play a pivotal role in the reversible transition of mesenchymal and epithelial ovarian cancer cells and hence are important regulators of metastasis

Author

Jacob, F, additional, Alam, S, additional, Liang, CY, additional, Kohler, R, additional, Nonantz, M, additional, Everest-Dass, A, additional, Huang, YL, additional, Fedier, A, additional, Schötzau, A, additional, Nunez Lopez, M, additional, Packer, N, additional, Lengerke, C, additional, and Heinzelmann-Schwarz, V, additional

Published
2018
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26. Regulation of Glioma Cell Invasion by 3q26 Gene Products PIK3CA, SOX2, and OPA1

Author

Ramadoss, A., additional, Leu, S., additional, Schaefer, T., additional, Tintignac, L., additional, Tostado, C., additional, Moffa, G., additional, Bink, A., additional, Demougin, P., additional, Moes, S., additional, Stippich, C., additional, Falbo, S., additional, Neddersen, H., additional, Frank, S., additional, Lengerke, C., additional, Bucher, H., additional, Jenö, P., additional, Ritz, M., additional, Mariani, L., additional, and Boulay, J., additional

Published
2018
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27. GLA/DRST real-world outcome analysis of CAR-T cell therapies for large B-cell lymphoma in Germany

Author

Bethge, WA, Martus, P, Schmitt, M, Holtick, U, Subklewe, M, von Tresckow, B, Ayuk, F, Wagner-Drouet, EM, Wulf, G, Marks, R, Penack, O, Schnetzke, U, Koenecke, C, von Bonin, M, Stelljes, M, Glass, B, Baldus, CD, Vucinic, V, Mougiakakos, D, Topp, M, Fante, M, Schroers, R, Bayir, L, Borchmann, P, Buecklein, V, Hasenkamp, J, Hanoun, C, Thomas, S, Beelen, D, Lengerke, C, Kroeger, N, and Dreger, P

Abstract

CD19-directed chimeric antigen receptor (CAR) T cells have evolved as new standard-of-care (SOC) treatment in patients with relapsed/refractory large B-cell lymphoma (LBCL). Here, we report the first German real-world data on SOC CAR-T cell therapies with the aim to explore risk factors associated with outcome.

Published
2024
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28. Ecotropic viral integration site 1, a novel oncogene in prostate cancer

Author

Queisser, A, primary, Hagedorn, S, additional, Wang, H, additional, Schaefer, T, additional, Konantz, M, additional, Alavi, S, additional, Deng, M, additional, Vogel, W, additional, von Mässenhausen, A, additional, Kristiansen, G, additional, Duensing, S, additional, Kirfel, J, additional, Lengerke, C, additional, and Perner, S, additional

Published
2016
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30. Ruxolitinib in corticosteroid-refractory graft-versus-host disease after allogeneic stem cell transplantation: a multicenter survey

Author

Zeiser, R., Burchert, A., Lengerke, C., Verbeek, M.M., Maas-Bauer, K., Metzelder, S.K., Spoerl, S., Ditschkowski, M., Ecsedi, M., Sockel, K., Ayuk, F., Ajib, S., Fontbrune, F.S. de, Na, I.K., Penter, L., Holtick, U., Wolf, D., Schuler, E., Meyer, E., Apostolova, P., Bertz, H., Marks, R., Lubbert, M., Wasch, R., Scheid, C., Stolzel, F., Ordemann, R., Bug, G., Kobbe, G., Negrin, R., Brune, M., Spyridonidis, A., Schmitt-Graff, A., Velden, W.J. van der, Huls, G.A., Mielke, S., Grigoleit, G.U., Kuball, J., Flynn, R., Ihorst, G., Du, J., Blazar, B.R., Arnold, R., Kroger, N., Passweg, J., Halter, J., Socie, G., Beelen, D., Peschel, C., Neubauer, A., Finke, J., Duyster, J., Bubnoff, N. von, Zeiser, R., Burchert, A., Lengerke, C., Verbeek, M.M., Maas-Bauer, K., Metzelder, S.K., Spoerl, S., Ditschkowski, M., Ecsedi, M., Sockel, K., Ayuk, F., Ajib, S., Fontbrune, F.S. de, Na, I.K., Penter, L., Holtick, U., Wolf, D., Schuler, E., Meyer, E., Apostolova, P., Bertz, H., Marks, R., Lubbert, M., Wasch, R., Scheid, C., Stolzel, F., Ordemann, R., Bug, G., Kobbe, G., Negrin, R., Brune, M., Spyridonidis, A., Schmitt-Graff, A., Velden, W.J. van der, Huls, G.A., Mielke, S., Grigoleit, G.U., Kuball, J., Flynn, R., Ihorst, G., Du, J., Blazar, B.R., Arnold, R., Kroger, N., Passweg, J., Halter, J., Socie, G., Beelen, D., Peschel, C., Neubauer, A., Finke, J., Duyster, J., and Bubnoff, N. von

Abstract

Item does not contain fulltext, Despite major improvements in allogeneic hematopoietic cell transplantation over the past decades, corticosteroid-refractory (SR) acute (a) and chronic (c) graft-versus-host disease (GVHD) cause high mortality. Preclinical evidence indicates the potent anti-inflammatory properties of the JAK1/2 inhibitor ruxolitinib. In this retrospective survey, 19 stem cell transplant centers in Europe and the United States reported outcome data from 95 patients who had received ruxolitinib as salvage therapy for SR-GVHD. Patients were classified as having SR-aGVHD (n=54, all grades III or IV) or SR-cGVHD (n=41, all moderate or severe). The median number of previous GVHD-therapies was 3 for both SR-aGVHD (1-7) and SR-cGVHD (1-10). The overall response rate was 81.5% (44/54) in SR-aGVHD including 25 complete responses (46.3%), while for SR-cGVHD the ORR was 85.4% (35/41). Of those patients responding to ruxolitinib, the rate of GVHD-relapse was 6.8% (3/44) and 5.7% (2/35) for SR-aGVHD and SR-cGVHD, respectively. The 6-month-survival was 79% (67.3-90.7%, 95% confidence interval (CI)) and 97.4% (92.3-100%, 95% CI) for SR-aGVHD and SR-cGVHD, respectively. Cytopenia and cytomegalovirus-reactivation were observed during ruxolitinib treatment in both SR-aGVHD (30/54, 55.6% and 18/54, 33.3%) and SR-cGVHD (7/41, 17.1% and 6/41, 14.6%) patients. Ruxolitinib may constitute a promising new treatment option for SR-aGVHD and SR-cGVHD that should be validated in a prospective trial.

Published
2015

31. High response rates in patients treated with ruxolitinib for corticosteroid-refractory Graft-versus-host disease: analysis including 13 Transplant Centers

Author

Zeiser, R., Lengerke, C., Spoerl, S., Maas-Bauer, K., Ditschkowski, M., Ecsedi, M., Sockel, K., Ayuk, F., Sicre-de-Fontbrune, F., Na, I-K, Ajib, S., Verbeek, M., Nogai, H., Holtick, U., Wolf, D., Schuler, E., Meyer, E., Apostolova, P., Illert, L., Bertz, H., Marks, R., Waesch, R., Hackanson, B., Scheid, C., Ordemann, R., Bug, G., Kobbe, G., Negrin, R., Arnold, R., Kroeger, N., Passweg, J., Halter, J., Socie, G., Beelen, D., Finke, J., Peschel, C., Duyster, J., von Bubnoff, N., Zeiser, R., Lengerke, C., Spoerl, S., Maas-Bauer, K., Ditschkowski, M., Ecsedi, M., Sockel, K., Ayuk, F., Sicre-de-Fontbrune, F., Na, I-K, Ajib, S., Verbeek, M., Nogai, H., Holtick, U., Wolf, D., Schuler, E., Meyer, E., Apostolova, P., Illert, L., Bertz, H., Marks, R., Waesch, R., Hackanson, B., Scheid, C., Ordemann, R., Bug, G., Kobbe, G., Negrin, R., Arnold, R., Kroeger, N., Passweg, J., Halter, J., Socie, G., Beelen, D., Finke, J., Peschel, C., Duyster, J., and von Bubnoff, N.

Published
2015

32. Ruxolitinib for corticosteroid-refractory graft-versus-host disease: analysis of 95 patients treated at multiple medical centers

Author

Zeiser, R., Burchert, A., Lengerke, C., Verbeek, M., Maas-Bauer, K., Metzelder, S., Spoerl, S., Ditschkowski, M., Ecsedi, M., Sockel, K., Ayuk, F., Ajib, S., de Fontbrune, Sicre F., Na, I. -K, Penter, L., Holtick, U., Wolf, D., Schuler, E., Meyer, E., Apostolova, P., Bertz, H., Marks, R., Luebbert, M., Waesch, R., Scheid, C., Ordemann, R., Bug, G., Kobbe, G., Negrin, R., Brune, M., Spyridonidis, A., Schmitt-Graeff, A., van der Velden, W., Huls, G., Grigoleit, G. U., Kuball, J., Blazar, B. R., Arnold, R., Kroeger, N., Passweg, J., Halter, J., Socie, G., Beelen, D., Peschel, C., Neubauer, A., Finke, J., Duyster, J., von Bubnoff, N., Zeiser, R., Burchert, A., Lengerke, C., Verbeek, M., Maas-Bauer, K., Metzelder, S., Spoerl, S., Ditschkowski, M., Ecsedi, M., Sockel, K., Ayuk, F., Ajib, S., de Fontbrune, Sicre F., Na, I. -K, Penter, L., Holtick, U., Wolf, D., Schuler, E., Meyer, E., Apostolova, P., Bertz, H., Marks, R., Luebbert, M., Waesch, R., Scheid, C., Ordemann, R., Bug, G., Kobbe, G., Negrin, R., Brune, M., Spyridonidis, A., Schmitt-Graeff, A., van der Velden, W., Huls, G., Grigoleit, G. U., Kuball, J., Blazar, B. R., Arnold, R., Kroeger, N., Passweg, J., Halter, J., Socie, G., Beelen, D., Peschel, C., Neubauer, A., Finke, J., Duyster, J., and von Bubnoff, N.

Published
2015

33. The regulatory interaction of EVI1 with the TCL1A oncogene impacts cell survival and clinical outcome in CLL

Author

Vasyutina, E., Boucas, J. M., Bloehdorn, J., Aszyk, C., Crispatzu, G., Stiefelhagen, M., Breuer, A., Mayer, P., Lengerke, C., Doehner, H., Beutner, D., Rosenwald, A., Stilgenbauer, S., Hallek, M., Benner, A., Herling, M., Vasyutina, E., Boucas, J. M., Bloehdorn, J., Aszyk, C., Crispatzu, G., Stiefelhagen, M., Breuer, A., Mayer, P., Lengerke, C., Doehner, H., Beutner, D., Rosenwald, A., Stilgenbauer, S., Hallek, M., Benner, A., and Herling, M.

Abstract

Dysregulated T-cell leukemia/lymphoma-1A (TCL1A), a modulator in B-cell receptor (BCR) signaling, is causally implicated in chronic lymphocytic leukemia (CLL). However, the mechanisms of the perturbed TCL1A regulation are largely unknown. To characterize TCL1A-upstream networks, we functionally screened for TCL1A-repressive micro-RNAs (miRs) and their transcriptional regulators. We identified the novel miR-484 to target TCL1A's 3'-UTR and to be downregulated in CLL. In chromatin immunoprecipitations and reporter assays, the oncogenic transcription factor of myeloid cells, EVI1, bound and activated the miR-484 promoter. Most common in CLL was a pan-EVI1 transcript variant. EVI1 protein expression revealed distinct normal-tissue and leukemia-associated patterns of EVI1/TCL1A co-regulation. EVI1 levels were particularly low in TCL1A-high CLL or such cellular subsets. Global gene expression profiles from a 337-patient set linked EVI1 networks to BCR signaling and cell survival via TCL1A, BTK and other molecules of relevance in CLL. Enforced EVI1, as did miR-484, repressed TCL1A. Furthermore, it reduced phospho-kinase levels, impaired cell survival, mitigated BCR-induced Ca-flux and diminished the in vitro ibrutinib response. Moreover, TCL1A and EVI1 showed a strongly interactive hazard prediction in prospectively treated patients. Overall, we present regressive EVI1 as a novel regulatory signature in CLL. Through enhanced TCL1A and other EVI1-targeted hallmarks of CLL, this contributes to an aggressive cellular and clinical phenotype.

Published
2015

36. Differential requirements for Wnt and Notch signaling in hematopoietic versus thymic niches

Author

Roozen, P.P.C., Brugman, M.H., Staal, F.J.T., Kanz, L., Fibbe, W.E., Lengerke, C., and Dick, J.E.

Abstract

All blood cells are derived from multipotent stem cells, the so-called hematopoietic stem cells (HSCs), that in adults reside in the bone marrow. Most types of blood cells also develop there, with the notable exception of T lymphocytes that develop in the thymus. For both HSCs and developing T cells, interactions with the surrounding microenvironment are critical in regulating maintenance, differentiation, apoptosis, and proliferation. Such specialized regulatory microenvironments are referred to as niches and provide both soluble factors as well as cell-cell interactions between niche component cells and blood cells. Two pathways that are critical for early T cell development in the thymic niche are Wnt and Notch signaling. These signals also play important but controversial roles in the HSC niche. Here, we review the differences and similarities between the thymic and hematopoietic niches, with particular focus on Wnt and Notch signals, as well as the latest insights into regulation of these developmentally important pathways.

Published
2012

37. Epigenetic differences between sister chromatids?

Author

Lansdorp, Peter M., Falconer, Ester, Tao, Jiang, Brind'Amour, Julie, Naumann, Ulrike, Kanz, L, Fibbe, WE, Lengerke, C, Dick, JE, Faculteit Medische Wetenschappen/UMCG, and Damage and Repair in Cancer Development and Cancer Treatment (DARE)

Subjects
APC TUMOR-SUPPRESSOR, SELECTIVE SEGREGATION, DIVISION, IDENTIFICATION, METHYLATION, DNA replication, TEMPLATE DNA STRANDS, sister chromatids, CHROMOSOMES, TRANSCRIPTS, ADENOMATOUS POLYPOSIS-COLI, chromatin, EMBRYONIC STEM-CELLS, epigenetic marks
Abstract

Semi-conservative replication ensures that the DNA sequence of sister chromatids is identical except for replication errors and variation in the length of telomere repeats resulting from replicative losses and variable end processing. What happens with the various epigenetic marks during DNA replication is less clear. Many chromatin marks are likely to be copied onto both sister chromatids in conjunction with DNA replication, whereas others could be distributed randomly between sister chromatids. Epigenetic differences between sister chromatids could also emerge in a more predictable manner, for example, following processes that are associated with lagging strand DNA replication. The resulting epigenetic differences between sister chromatids could result in different gene expression patterns in daughter cells. This possibility has been difficult to test because techniques to distinguish between parental sister chromatids require analysis of single cells and are not obvious. Here, we briefly review the topic of sister chromatid epigenetics and discuss how the identification of sister chromatids in cells could change the way we think about asymmetric cell divisions and stochastic variation in gene expression between cells in general and paired daughter cells in particular.

Published
2012

38. Hematopoietic stem cell expansion: challenges and opportunities

Author

Walasek, Marta A., van Os, Ronald, de Haan, Gerald, Kanz, L, Fibbe, WE, Lengerke, C, Dick, JE, Damage and Repair in Cancer Development and Cancer Treatment (DARE), and Stem Cell Aging Leukemia and Lymphoma (SALL)

Subjects
small molecules, TRANS-RETINOIC ACID, SELF-RENEWAL CAPACITY, PROGENITOR CELLS, HSC expansion, cell-extrinsic factors, VALPROIC ACID, GROWTH-FACTOR-I, EX-VIVO EXPANSION, UMBILICAL-CORD BLOOD, MYELOID RECONSTITUTING ABILITY, WNT GENE FAMILY, COPPER CHELATOR TETRAETHYLENEPENTAMINE
Abstract

Attempts to improve hematopoietic reconstitution and engraftment potential of ex vivo-expanded hematopoietic stem and progenitor cells (HSPCs) have been largely unsuccessful due to the inability to generate sufficient stem cell numbers and to excessive differentiation of the starting cell population. Although hematopoietic stem cells (HSCs) will rapidly expand after in vivo transplantation, experience from in vitro studies indicates that control of HSPC self-renewal and differentiation in culture remains difficult. Protocols that are based on hematopoietic cytokines have failed to support reliable amplification of immature stem cells in culture, suggesting that additional factors are required. In recent years, several novel factors, including developmental factors and chemical compounds, have been reported to affect HSC self-renewal and improve ex vivo stem cell expansion protocols. Here, we highlight early expansion attempts and review recent development in the extrinsic control of HSPC fate in vitro.

Published
2012

39. SOX2 gene amplification and protein overexpression are associated with better outcome in squamous cell lung cancer

Author

Wilbertz, T, Wagner, P, Petersen, K, Stiedl, A C, Scheble, V J, Maier, S, Reischl, M, Mikut, R, Altorki, N K, Moch, H, Fend, F, Staebler, A, Bass, A J, Meyerson, M, Rubin, M A, Soltermann, A, Lengerke, C, Perner, S, University of Zurich, and Perner, S

Subjects
2734 Pathology and Forensic Medicine, 10049 Institute of Pathology and Molecular Pathology, 610 Medicine & health
Published
2011

42. EVI-1 modulates leukemogenic potential and apoptosis sensitivity in human acute lymphoblastic leukemia

Author

Konantz, M, primary, André, M C, additional, Ebinger, M, additional, Grauer, M, additional, Wang, H, additional, Grzywna, S, additional, Rothfuss, O C, additional, Lehle, S, additional, Kustikova, O S, additional, Salih, H R, additional, Handgretinger, R, additional, Fend, F, additional, Baum, C, additional, Kanz, L, additional, Quintanilla-Martinez, L, additional, Schulze-Osthoff, K, additional, Essmann, F, additional, and Lengerke, C, additional

Published
2012
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44. Monitoring the glioma tropism of bone marrow-derived progenitor cells by 2-photon laser scanning microscopy and positron emission tomography

Author

Hasenbach, K., primary, Wiehr, S., additional, Herrmann, C., additional, Mannheim, J., additional, Cay, F., additional, von Kurthy, G., additional, Bolmont, T., additional, Grathwohl, S. A., additional, Weller, M., additional, Lengerke, C., additional, Pichler, B. J., additional, and Tabatabai, G., additional

Published
2012
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45. Expression of the embryonic stem cell marker SOX2 in breast carcinoma

Author

Fehm, T, primary, Kurth, R, additional, Lengerke, C, additional, Bareiss, PM, additional, Scheble, V, additional, Müller, F, additional, Schneider, F, additional, Wallwiener, D, additional, Kanz, L, additional, Fend, F, additional, Perner, S, additional, Staebler, A, additional, and Neubauer, H, additional

Published
2011
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49. Prospective comparison of PCR-based vs late mRNA-based preemptive antiviral therapy for HCMV infection in patients after allo-SCT

Author

Hebart, H, primary, Lengerke, C, additional, Ljungman, P, additional, Paya, C V, additional, Klingebiel, T, additional, Loeffler, J, additional, Pfaffenrath, S, additional, Lewensohn-Fuchs, I, additional, Barkholt, L, additional, Tomiuk, J, additional, Meisner, C, additional, Lunenberg, J, additional, Top, B, additional, Razonable, R R, additional, Patel, R, additional, Litzow, M R, additional, Jahn, G, additional, and Einsele, H, additional

Published
2010
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50. Safety and Efficacy of a Combination of Imatinib and Pegylated Interferon α2a (Pegasys®) in Newly Diagnosed Patients with Chronic Myelogenous Leukemia - A Phase II Cohort Study.

Author

Hochhaus, Andreas, primary, Neubauer, A., additional, Mueller, M.C., additional, Fischer, T., additional, Waller, C., additional, Bruemmendorf, T.H., additional, Bostel, T., additional, Lengerke, C., additional, Hehlmann, R., additional, and Burchert, A., additional

Published
2007
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