Search

Your search keyword '"Herling M"' showing total 307 results
Start Over Author "Herling M"
307 results on '"Herling M"'

1. Deregulation and epigenetic modification of BCL2-family genes cause resistance to venetoclax in hematologic malignancies

Author

Thomalla, D., Beckmann, L., Grimm, C., Oliverio, M., Meder, L., Herling, C.D., Nieper, P., Feldmann, T., Merkel, O., Lorsy, E., da Palma Guerreiro, A., von Jan, J., Kisis, I., Wasserburger, E., Claasen, J., Faitschuk-Meyer, E., Altmüller, J., Nürnberg, P., Yang, T.-P., Lienhard, M., Herwig, R., Kreuzer, K.-A., Pallasch, C.P., Büttner, R., Schäfer, S.C., Hartley, J., Abken, H., Peifer, M., Kashkar, H., Knittel, G., Eichhorst, B., Ullrich, R.T., Herling, M., Reinhardt, H.C., Hallek, M., Schweiger, M.R., and Frenzel, L.P.

Published
2022
Full Text
View/download PDF

2. Noncanonical effector functions of the T-memory–like T-PLL cell are shaped by cooperative TCL1A and TCR signaling

Author

Oberbeck, S., Schrader, A., Warner, K., Jungherz, D., Crispatzu, G., von Jan, J., Chmielewski, M., Ianevski, A., Diebner, H.H., Mayer, P., Kondo Ados, A., Wahnschaffe, L., Braun, T., Müller, T.A., Wagle, P., Bouska, A., Neumann, T., Pützer, S., Varghese, L., Pflug, N., Thelen, M., Makalowski, J., Riet, N., Göx, H.J.M., Rappl, G., Altmüller, J., Kotrová, M., Persigehl, T., Hopfinger, G., Hansmann, M.L., Schlößer, H., Stilgenbauer, S., Dürig, J., Mougiakakos, D., von Bergwelt-Baildon, M., Roeder, I., Hartmann, S., Hallek, M., Moriggl, R., Brüggemann, M., Aittokallio, T., Iqbal, J., Newrzela, S., Abken, H., and Herling, M.

Published
2020
Full Text
View/download PDF

5. Cellular dynamics and their impact on outcome in patients with mantle cell lymphoma during treatment with chimeric antigen receptor (CAR) T cells

Author

Weiss, R., primary, Fernandez, C. P., additional, Boldt, A., additional, Hoffmann, S., additional, Krauss, S., additional, Bach, E., additional, Kirchberg, J., additional, Kurch, L., additional, Merz, M., additional, Metzeler, K., additional, Herling, C., additional, Jentzsch, M., additional, Schwind, S., additional, Petermann, N., additional, Franz, P., additional, Herling, M., additional, Denecke, T., additional, Sabri, O., additional, Fricke, S., additional, Kluge, R., additional, Sack, U., additional, Franke, G., additional, Koehl, U., additional, Platzbecker, U., additional, Georgi, T., additional, and Vucinic, V., additional

Published
2023
Full Text
View/download PDF

13. P1381: EARLY FULL DONOR CHIMERISM AFTER FLAMSA RIC BASED ALLOGENEIC HSCT BUT NOT PRESENCE OF MORPHOLOGICAL REMISSION ASSOCIATES WITH OUTCOMES IN R/R AML PATIENTS

Author

Ussmann, J., primary, Hell, S., additional, Schetschorke, B., additional, Friedrich, G., additional, Pfrepper, C., additional, Schwind, S., additional, Jentzsch, M., additional, Vucinic, V., additional, Herling, M., additional, Platzbecker, U., additional, and Franke, G.-N., additional

Published
2022
Full Text
View/download PDF

14. S287: FACTORS INFLUENCING AUTOLOGOUS LYMPHOCYTE COLLECTIONS FOR CHIMERIC ANTIGEN RECEPTOR (CAR) T-CELLS – THE ROLE OF T-CELL SENESCENCE

Author

Vucinic, V., primary, Tumewu, T., additional, Brückner, M., additional, Jentzsch, M., additional, Ramdohr, F., additional, Buhmann, R., additional, Remane, Y., additional, Hoffmann, S., additional, Janz, M., additional, Penack, O., additional, Vogtmann, G., additional, Ruschpler, E., additional, Bullinger, L., additional, Keller, U., additional, Cross, M., additional, Schwind, S., additional, Herling, M., additional, Franke, G.-N., additional, Bach, E., additional, Reinhard, H., additional, and Platzbecker, U., additional

Published
2022
Full Text
View/download PDF

20. Brain metastases-Interdisciplinary approach towards a personalized treatment

Author

Grau, S., Herling, M., Mauch, C., Galldiks, N., Golla, H., Schlamann, M., Scheel, A. H., Celik, E., Ruge, M., Goldbrunner, R., Grau, S., Herling, M., Mauch, C., Galldiks, N., Golla, H., Schlamann, M., Scheel, A. H., Celik, E., Ruge, M., and Goldbrunner, R.

Abstract

The incidence, treatment and prognosis of patients with brain metastases have substantially changed during the last decades. While the survival time after diagnosis of cerebral metastases was on average a maximum of 3-6 months only 10 years ago, the survival time could be significantly improved due to novel surgical, radiotherapeutic and systemic treatment modalities. Only a few years ago, the occurrence of brain metastases led to a withdrawal from systemic oncological treatment and the exclusion of drug therapy studies and to a purely palliatively oriented treatment in the sense of whole brain radiation therapy (WBRT) with or without surgery. The increasing availability of targeted and immunomodulatory drugs as well as adapted radio-oncological procedures enable increasingly more personalized treatment approaches. The aim of this review article is to demonstrate the progress and complexity of the treatment of brain metastases in the context of modern comprehensive interdisciplinary concepts.

Published
2021

25. Reinstated p53 response and high anti-T-cell leukemia activity by the novel alkylating deacetylase inhibitor tinostamustine

Author

Puetzer, S., Varghese, L., von Jan, J., Braun, T., Giri, A. K., Mayer, P., Riet, N., Timonen, S., Oberbeck, S., Kuusanmaki, H., Mustjoki, S., Stern, M. -H., Aittokallio, T., Newrzela, S., Schrader, A., Herling, M., Puetzer, S., Varghese, L., von Jan, J., Braun, T., Giri, A. K., Mayer, P., Riet, N., Timonen, S., Oberbeck, S., Kuusanmaki, H., Mustjoki, S., Stern, M. -H., Aittokallio, T., Newrzela, S., Schrader, A., and Herling, M.

Published
2020

27. Interdisciplinary guideline on diagnosis, therapy, and follow-up of adult patients with monoclonal gammopathy of undetermined significance or multiple myeloma

Author

Piechotta, V, John, L., Jung, J., Graziani, G., Reinhardt, H., Holtick, U., Semrau, R., Trog, D., Voelker, L. A., Herling, M., Fend, F., Harder, L., Weinhold, N., Kriegsmann, K., Merz, M., Delorme, S., Derlin, T., Raab, M. S., Goede, V, Schubert, M., Hohloch, K., Senf, B., Simon, S. T., Baumann, W., Fetscher, S., Schinke, M., Holtkamp, U., Einsele, H., Engelhardt, M., Goldschmidt, H., Scheid, C., Skoetz, N., Piechotta, V, John, L., Jung, J., Graziani, G., Reinhardt, H., Holtick, U., Semrau, R., Trog, D., Voelker, L. A., Herling, M., Fend, F., Harder, L., Weinhold, N., Kriegsmann, K., Merz, M., Delorme, S., Derlin, T., Raab, M. S., Goede, V, Schubert, M., Hohloch, K., Senf, B., Simon, S. T., Baumann, W., Fetscher, S., Schinke, M., Holtkamp, U., Einsele, H., Engelhardt, M., Goldschmidt, H., Scheid, C., and Skoetz, N.

Published
2020

30. Corrections: Reinstated p53 response and high anti-T-cell leukemia activity by the novel alkylating deacetylase inhibitor tinostamustine

Author

Pützer, S., primary, Varghese, L., additional, von Jan, J., additional, Braun, T., additional, Giri, A. K., additional, Mayer, P., additional, Riet, N., additional, Timonen, S., additional, Oberbeck, S., additional, Kuusanmäki, H., additional, Mustjoki, S., additional, Stern, M.-H., additional, Aittokallio, T., additional, Newrzela, S., additional, Schrader, A., additional, and Herling, M., additional

Published
2020
Full Text
View/download PDF

35. Fibroblasts in Nodular Sclerosing Classical Hodgkin Lymphoma Are Defined by a Specific Phenotype and Protect Tumor Cells from Brentuximab-Vedotin Induced Injury

Author

Bankov K, Döring C, Ustaszewski A, Giefing M, Herling M, Cencioni C, Spallotta F, Gaetano C, Küppers R, Hansmann ML, and Hartmann S.

Subjects
polycyclic compounds, food and beverages, macromolecular substances, classical Hodgkin lymphoma, fibroblasts, gene expression analysis, luteolin, methylation profiling, nodular sclerosis
Abstract

Classical Hodgkin lymphoma (cHL) is one of the most common malignant lymphomas in Western Europe. The nodular sclerosing subtype of cHL (NS cHL) is characterized by a proliferation of fibroblasts in the tumor microenvironment, leading to fibrotic bands surrounding the lymphoma infiltrate. Several studies have described a crosstalk between the tumour cells of cHL, the Hodgkin- and Reed-Sternberg (HRS) cells, and cancer-associated fibroblasts. However, to date a deep molecular characterization of these fibroblasts is lacking. Thus, the aim of the present study is a comprehensive characterization of these fibroblasts. Gene expression profiling and methylation profiles of fibroblasts isolated from primary lymph node suspensions revealed persistent differences between fibroblasts obtained from NS cHL and lymphadenitis. NS cHL derived fibroblasts exhibit a myofibroblastic phenotype characterized by myocardin (MYOCD) expression. Moreover, TIMP3, an inhibitor of matrix metalloproteinases, was strongly upregulated in NS cHL fibroblasts, likely contributing to the accumulation of collagen in sclerotic bands of NS cHL. As previously shown for other types of cancer-associated fibroblasts, treatment by luteolin could reverse this fibroblast phenotype and decrease TIMP3 secretion. NS cHL fibroblasts showed enhanced proliferation when they were exposed to soluble factors released from HRS cells. For HRS cells, soluble factors from fibroblasts were not sufficient to protect them from Brentuximab-Vedotin induced cell death. However, HRS cells adherent to fibroblasts were protected from Brentuximab-Vedotin induced injury. In summary, we confirm the importance of fibroblasts for HRS cell survival and identify TIMP3 which probably contributes as a major factor to the typical fibrosis observed in NS cHL.

Published
2019
Full Text
View/download PDF

40. Actionable perturbations of damage responses by TCL1/ATM and epigenetic lesions form the basis of T-PLL

Author

Schrader, A., Crispatzu, G., Oberbeck, S., Mayer, P., Putzer, S., von Jan, J., Vasyutina, E., Warner, K., Weit, N., Pflug, N., Braun, T., Andersson, E. I., Yadav, B., Riabinska, A., Maurer, B., Ferreira, M. S. Ventura, Beier, F., Altmueller, J., Lanasa, M., Herling, C. D., Haferlach, T., Stilgenbauer, S., Hopfinger, G., Peifer, M., Bruemmendorf, T. H., Nuernberg, P., Elenitoba-Johnson, K. S. J., Zha, S., Hallek, M., Moriggl, R., Reinhardt, H. C., Stern, M. -H., Mustjoki, S., Newrzela, S., Frommolt, P., Herling, M., Schrader, A., Crispatzu, G., Oberbeck, S., Mayer, P., Putzer, S., von Jan, J., Vasyutina, E., Warner, K., Weit, N., Pflug, N., Braun, T., Andersson, E. I., Yadav, B., Riabinska, A., Maurer, B., Ferreira, M. S. Ventura, Beier, F., Altmueller, J., Lanasa, M., Herling, C. D., Haferlach, T., Stilgenbauer, S., Hopfinger, G., Peifer, M., Bruemmendorf, T. H., Nuernberg, P., Elenitoba-Johnson, K. S. J., Zha, S., Hallek, M., Moriggl, R., Reinhardt, H. C., Stern, M. -H., Mustjoki, S., Newrzela, S., Frommolt, P., and Herling, M.

Abstract

T-cell prolymphocytic leukemia (T-PLL) is a rare and poor-prognostic mature T-cell malignancy. Here we integrated large-scale profiling data of alterations in gene expression, allelic copy number (CN), and nucleotide sequences in 111 well-characterized patients. Besides prominent signatures of T-cell activation and prevalent clonal variants, we also identify novel hot-spots for CN variability, fusion molecules, alternative transcripts, and progression-associated dynamics. The overall lesional spectrum of T-PLL is mainly annotated to axes of DNA damage responses, T-cell receptor/cytokine signaling, and histone modulation. We formulate a multi-dimensional model of T-PLL pathogenesis centered around a unique combination of TCL1 overexpression with damaging ATM aberrations as initiating core lesions. The effects imposed by TCL1 cooperate with compromised ATM toward a leukemogenic phenotype of impaired DNA damage processing. Dysfunctional ATM appears inefficient in alleviating elevated redox burdens and telomere attrition and in evoking a p53-dependent apoptotic response to genotoxic insults. As non-genotoxic strategies, synergistic combinations of p53 reactivators and deacetylase inhibitors reinstate such cell death execution.

Published
2018

41. Discovery of novel drug sensitivities in T-PLL by high-throughput ex vivo drug testing and mutation profiling

Author

Andersson, E. I., Puetzer, S., Yadav, B., Dufva, O., Khan, S., He, L., Sellner, L., Schrader, A., Crispatzu, G., Oles, M., Zhang, H., Adnan-Awad, S., Lagstrom, S., Bellanger, D., Mpindi, J. P., Eldfors, S., Pemovska, T., Pietarinen, P., Lauhio, A., Tomska, K., Cuesta-Mateos, C., Faber, E., Koschmieder, S., Bruemmendorf, T. H., Kytola, S., Savolainen, E-R, Siitonen, T., Ellonen, P., Kallioniemi, O., Wennerberg, K., Ding, W., Stern, M-H, Huber, W., Anders, S., Tang, J., Aittokallio, T., Zenz, T., Herling, M., Mustjoki, S., Andersson, E. I., Puetzer, S., Yadav, B., Dufva, O., Khan, S., He, L., Sellner, L., Schrader, A., Crispatzu, G., Oles, M., Zhang, H., Adnan-Awad, S., Lagstrom, S., Bellanger, D., Mpindi, J. P., Eldfors, S., Pemovska, T., Pietarinen, P., Lauhio, A., Tomska, K., Cuesta-Mateos, C., Faber, E., Koschmieder, S., Bruemmendorf, T. H., Kytola, S., Savolainen, E-R, Siitonen, T., Ellonen, P., Kallioniemi, O., Wennerberg, K., Ding, W., Stern, M-H, Huber, W., Anders, S., Tang, J., Aittokallio, T., Zenz, T., Herling, M., and Mustjoki, S.

Abstract

T-cell prolymphocytic leukemia (T-PLL) is a rare and aggressive neoplasm of mature T-cells with an urgent need for rationally designed therapies to address its notoriously chemo-refractory behavior. The median survival of T-PLL patients is <2 years and clinical trials are difficult to execute. Here we systematically explored the diversity of drug responses in T-PLL patient samples using an ex vivo drug sensitivity and resistance testing platform and correlated the findings with somatic mutations and gene expression profiles. Intriguingly, all T-PLL samples were sensitive to the cyclin-dependent kinase inhibitor SNS-032, which overcame stromal-cell-mediated protection and elicited robust p53-activation and apoptosis. Across all patients, the most effective classes of compounds were histone deacetylase, phosphoinositide-3 kinase/ AKT/mammalian target of rapamycin, heat-shock protein 90 and BH3-family protein inhibitors as well as p53 activators, indicating previously unexplored, novel targeted approaches for treating T-PLL. Although Janus-activated kinase-signal transducer and activator of transcription factor (JAK-STAT) pathway mutations were common in T-PLL (71% of patients), JAK-STAT inhibitor responses were not directly linked to those or other T-PLL-specific lesions. Overall, we found that genetic markers do not readily translate into novel effective therapeutic vulnerabilities. In conclusion, novel classes of compounds with high efficacy in T-PLL were discovered with the comprehensive ex vivo drug screening platform warranting further studies of synergisms and clinical testing.

Published
2018

42. Actionable perturbations of damage responses by TCL1/ATM and epigenetic lesions form the basis of T-PLL

Author

Schrader, A., primary, Crispatzu, G., additional, Oberbeck, S., additional, Mayer, P., additional, Pützer, S., additional, von Jan, J., additional, Vasyutina, E., additional, Warner, K., additional, Weit, N., additional, Pflug, N., additional, Braun, T., additional, Andersson, E. I., additional, Yadav, B., additional, Riabinska, A., additional, Maurer, B., additional, Ventura Ferreira, M. S., additional, Beier, F., additional, Altmüller, J., additional, Lanasa, M., additional, Herling, C. D., additional, Haferlach, T., additional, Stilgenbauer, S., additional, Hopfinger, G., additional, Peifer, M., additional, Brümmendorf, T. H., additional, Nürnberg, P., additional, Elenitoba-Johnson, K. S. J., additional, Zha, S., additional, Hallek, M., additional, Moriggl, R., additional, Reinhardt, H. C., additional, Stern, M.-H., additional, Mustjoki, S., additional, Newrzela, S., additional, Frommolt, P., additional, and Herling, M., additional

Published
2018
Full Text
View/download PDF

44. Targeting transcription-coupled nucleotide excision repair overcomes resistance in chronic lymphocytic leukemia

Author

Lohmann, G., Vasyutina, E., Bloehdorn, J., Reinart, N., Schneider, J. I., Babu, V., Knittel, G., Crispatzu, G., Mayer, P., Prinz, C., Muenzner, J. K., Biersack, B., Efremov, D. G., Chessa, L., Herling, C. D., Stilgenbauer, S., Hallek, M., Schobert, R., Reinhardt, H. C., Schumacher, B., Herling, M., Lohmann, G., Vasyutina, E., Bloehdorn, J., Reinart, N., Schneider, J. I., Babu, V., Knittel, G., Crispatzu, G., Mayer, P., Prinz, C., Muenzner, J. K., Biersack, B., Efremov, D. G., Chessa, L., Herling, C. D., Stilgenbauer, S., Hallek, M., Schobert, R., Reinhardt, H. C., Schumacher, B., and Herling, M.

Abstract

Treatment resistance becomes a challenge at some point in the course of most patients with chronic lymphocytic leukemia (CLL). This applies to fludarabine-based regimens, and is also an increasing concern in the era of more targeted therapies. As cells with low-replicative activity rely on repair that triggers checkpoint-independent noncanonical pathways, we reasoned that targeting the nucleotide excision repair (NER) reaction addresses a vulnerability of CLL and might even synergize with fludarabine, which blocks the NER gap-filling step. We interrogated here especially the replication-independent transcription-coupled-NER ((TC)-NER) in prospective trial patients, primary CLL cultures, cell lines and mice. We screen selected (TC)-NER-targeting compounds as experimental (illudins) or clinically approved (trabectedin) drugs. They inflict transcription-stalling DNA lesions requiring TC-NER either for their removal (illudins) or for generation of lethal strand breaks (trabectedin). Genetically defined systems of NER deficiency confirmed their specificity. They selectively and efficiently induced cell death in CLL, irrespective of high-risk cytogenetics, IGHV status or clinical treatment history, including resistance. The substances induced ATM/p53-independent apoptosis and showed marked synergisms with fludarabine. Trabectedin additionally perturbed stromal-cell protection and showed encouraging antileukemic profiles even in aggressive and transforming murine CLL. This proof-of-principle study established (TC)-NER as a mechanism to be further exploited to resensitize CLL cells.

Published
2017

47. Novel models of high-risk CLL reveal an actionable PARP1 dependence in ATM-defective CLL in vivo

Author

Knittel, G., Korovkina, D., Liedgens, P., Rehkaemper, T., Fritz, C., Torgovnick, A., Al-Baldawi, Y., Al-Maarri, M., Cun, Y., Fedorchenko, O., Riabinska, A., Beleggia, F., Nguyen, P. -H., Wunderlich, F. T., Ortmann, M., Montesinos-Rongen, M., Tausch, E., Stilgenbauer, S., Frenzel, L., Herling, M., Herling, C., Bahlo, J., Hallek, M., Peifer, M., Buettner, R., Persigehl, T., Reinhardt, H. C., Knittel, G., Korovkina, D., Liedgens, P., Rehkaemper, T., Fritz, C., Torgovnick, A., Al-Baldawi, Y., Al-Maarri, M., Cun, Y., Fedorchenko, O., Riabinska, A., Beleggia, F., Nguyen, P. -H., Wunderlich, F. T., Ortmann, M., Montesinos-Rongen, M., Tausch, E., Stilgenbauer, S., Frenzel, L., Herling, M., Herling, C., Bahlo, J., Hallek, M., Peifer, M., Buettner, R., Persigehl, T., and Reinhardt, H. C.

Published
2017

48. Discovery of novel drug sensitivities in T-PLL by high-throughput ex vivo drug testing and mutation profiling

Author

Andersson, E I, primary, Pützer, S, additional, Yadav, B, additional, Dufva, O, additional, Khan, S, additional, He, L, additional, Sellner, L, additional, Schrader, A, additional, Crispatzu, G, additional, Oleś, M, additional, Zhang, H, additional, Adnan-Awad, S, additional, Lagström, S, additional, Bellanger, D, additional, Mpindi, J P, additional, Eldfors, S, additional, Pemovska, T, additional, Pietarinen, P, additional, Lauhio, A, additional, Tomska, K, additional, Cuesta-Mateos, C, additional, Faber, E, additional, Koschmieder, S, additional, Brümmendorf, T H, additional, Kytölä, S, additional, Savolainen, E-R, additional, Siitonen, T, additional, Ellonen, P, additional, Kallioniemi, O, additional, Wennerberg, K, additional, Ding, W, additional, Stern, M-H, additional, Huber, W, additional, Anders, S, additional, Tang, J, additional, Aittokallio, T, additional, Zenz, T, additional, Herling, M, additional, and Mustjoki, S, additional

Published
2017
Full Text
View/download PDF

49. DRUG PERTURBATION BASED STRATIFICATION OF LYMPHOPROLIFERATIVE DISORDERS

Author

Dietrich, S., primary, Oleś, M., additional, Sellner, L., additional, Anders, S., additional, Lu, J., additional, Velten, B., additional, Mock, A., additional, Oakes, C., additional, Sutton, L., additional, Young, E., additional, Rosenquist, R., additional, Rossi, D., additional, Zirlik, K., additional, Herling, M., additional, Nguyen-Khac, F., additional, Plass, C., additional, von Kalle, C., additional, Dürig, J., additional, Ringshausen, I., additional, Huber, W., additional, and Zenz, T., additional

Published
2017
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results