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395 results on '"Hartmann, Sylvia"'

2. Mediastinal large B cell lymphoma and surrounding gray areas: a report of the lymphoma workshop of the 20th meeting of the European Association for Haematopathology

Author

Gibson, Sarah E., Dojcinov, Stefan, Dotlic, Snjezana, Hartmann, Sylvia, Hsi, Eric D., Klimkowska, Monika, Melle, Federica, Pileri, Stefano A., Ramsower, Colleen A., Rech, Karen, Rimsza, Lisa M., Rodriguez-Pinilla, Socorro Maria, Tousseyn, Thomas A., de Jong, Daphne, and Sabattini, Elena

Published
2023
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4. Novel insights into the pathogenesis of follicular lymphoma by molecular profiling of localized and systemic disease forms

Author

Kalmbach, Sabrina, Grau, Michael, Zapukhlyak, Myroslav, Leich, Ellen, Jurinovic, Vindi, Hoster, Eva, Staiger, Annette M., Kurz, Katrin S., Weigert, Oliver, Gaitzsch, Erik, Passerini, Verena, Engelhard, Marianne, Herfarth, Klaus, Beiske, Klaus, Micci, Francesca, Möller, Peter, Bernd, Heinz-Wolfram, Feller, Alfred C., Klapper, Wolfram, Stein, Harald, Hansmann, Martin-Leo, Hartmann, Sylvia, Dreyling, Martin, Holte, Harald, Lenz, Georg, Rosenwald, Andreas, Ott, German, and Horn, Heike

Published
2023
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6. Hyperactive STAT5 hijacks T cell receptor signaling and drives immature T cell acute lymphoblastic leukemia

Author

Suske, Tobias, Sorger, Helena, Manhart, Gabriele, Ruge, Frank, Prutsch, Nicole, Zimmerman, Mark W., Eder, Thomas, Abdallah, Diaaeldin I., Maurer, Barbara, Wagner, Christina, Schonefeldt, Susann, Spirk, Katrin, Pichler, Alexander, Pemovska, Tea, Schweicker, Carmen, Poloske, Daniel, Hubanic, Emina, Jungherz, Dennis, Muller, Tony Andreas, Aung, Myint Myat Khine, Orlova, Anna, Pham, Ha Thi Thanh, Zimmel, Kerstin, Krausgruber, Thomas, Bock, Christoph, Muller, Mathias, Dahlhoff, Maik, Boersma, Auke, Rulicke, Thomas, Fleck, Roman, de Araujo, Elvin Dominic, Gunning, Patrick Thomas, Aittokallio, Tero, Mustjoki, Satu, Sanda, Takaomi, Hartmann, Sylvia, Grebien, Florian, Hoermann, Gregor, Haferlach, Torsten, Staber, Philipp Bernhard, Neubauer, Heidi Anne, Look, Alfred Thomas, Herling, Marco, and Moriggl, Richard

Subjects
Tyrosine -- Comparative analysis -- Genetic aspects, T cells -- Comparative analysis -- Genetic aspects, Genes -- Comparative analysis -- Genetic aspects, Acute lymphocytic leukemia -- Development and progression -- Genetic aspects, Health care industry
Abstract

T cell acute lymphoblastic leukemia (T-ALL) is an aggressive immature T cell cancer. Mutations in IL7R have been analyzed genetically, but downstream effector functions such as STAT5A and STAT5B hyperactivation are poorly understood. Here, we studied the most frequent and clinically challenging [STAT5B.sup.N642H] driver in T cell development and immature T cell cancer onset and compared it with STAT5A hyperactive variants in transgenic mice. Enhanced STAT5 activity caused disrupted T cell development and promoted an early T cell progenitor-ALL phenotype, with upregulation of genes involved in T cell receptor (TCR) signaling, even in absence of surface TCR. Importantly, TCR pathway genes were overexpressed in human T-ALL and mature T cell cancers and activation of TCR pathway kinases was STAT5 dependent. We confirmed STAT5 binding to these genes using ChIP-Seq analysis in human T-ALL cells, which were sensitive to pharmacologic inhibition by dual STAT3/5 degraders or ZAP70 tyrosine kinase blockers in vitro and in vivo. We provide genetic and biochemical proof that STAT5A and STAT5B hyperactivation can initiate T-ALL through TCR pathway hijacking and suggest similar mechanisms for other T cell cancers. Thus, STAT5 or TCR component blockade are targeted therapy options, particularly in patients with chemoresistant clones carrying [STAT5B.sup.N642H]., Introduction Acute lymphoblastic leukemia (ALL) is subdivided into B and T cell acute lymphoblastic leukemia (T-ALL), of which T-ALL represents up to 15% of pediatric and 25% of adult ALL [...]

Published
2024
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8. Correction to: Mediastinal large B cell lymphoma and surrounding gray areas: a report of the lymphoma workshop of the 20th meeting of the European Association for Haematopathology

Author

Gibson, Sarah E., Dojcinov, Stefan, Dotlic, Snjezana, Hartmann, Sylvia, Hsi, Eric D., Klimkowska, Monika, Melle, Federica, Pileri, Stefano A., Ramsower, Colleen A., Rech, Karen, Rimsza, Lisa M., Rodriguez‑Pinilla, Socorro Maria, Tousseyn, Thomas A., de Jong, Daphne, and Sabattini, Elena

Published
2024
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10. Correction: “The 5th edition of The World Health Organization Classification of Haematolymphoid Tumours: Lymphoid Neoplasms” Leukemia. 2022 Jul;36(7):1720–1748

Author

Alaggio, Rita, Amador, Catalina, Anagnostopoulos, Ioannis, Attygalle, Ayoma D., de Oliveira Araujo, Iguaracyra Barreto, Berti, Emilio, Bhagat, Govind, Borges, Anita Maria, Boyer, Daniel, Calaminici, Mariarita, Chadburn, Amy, Chan, John K. C., Cheuk, Wah, Chng, Wee-Joo, Choi, John K., Chuang, Shih-Sung, Coupland, Sarah E., Czader, Magdalena, Dave, Sandeep S., de Jong, Daphne, Di Napoli, Arianna, Du, Ming-Qing, Elenitoba-Johnson, Kojo S., Ferry, Judith, Geyer, Julia, Gratzinger, Dita, Guitart, Joan, Gujral, Sumeet, Harris, Marian, Harrison, Christine J., Hartmann, Sylvia, Hochhaus, Andreas, Jansen, Patty M., Karube, Kennosuke, Kempf, Werner, Khoury, Joseph, Kimura, Hiroshi, Klapper, Wolfram, Kovach, Alexandra E., Kumar, Shaji, Lazar, Alexander J., Lazzi, Stefano, Leoncini, Lorenzo, Leung, Nelson, Leventaki, Vasiliki, Li, Xiao-Qiu, Lim, Megan S., Liu, Wei-Ping, Louissaint, Jr, Abner, Marcogliese, Andrea, Medeiros, L. Jeffrey, Michal, Michael, Miranda, Roberto N., Mitteldorf, Christina, Montes-Moreno, Santiago, Morice, William, Nardi, Valentina, Naresh, Kikkeri N., Natkunam, Yasodha, Ng, Siok-Bian, Oschlies, Ilske, Ott, German, Parrens, Marie, Pulitzer, Melissa, Rajkumar, S. Vincent, Rawstron, Andrew C., Rech, Karen, Rosenwald, Andreas, Said, Jonathan, Sarkozy, Clémentine, Sayed, Shahin, Saygin, Caner, Schuh, Anna, Sewell, William, Siebert, Reiner, Sohani, Aliyah R., Suzuki, Ritsuro, Tooze, Reuben, Traverse-Glehen, Alexandra, Vega, Francisco, Vergier, Beatrice, Wechalekar, Ashutosh D., Wood, Brent, Xerri, Luc, and Xiao, Wenbin

Published
2023
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11. Transcriptional reprogramming by mutated IRF4 in lymphoma

Author

Schleussner, Nikolai, Cauchy, Pierre, Franke, Vedran, Giefing, Maciej, Fornes, Oriol, Vankadari, Naveen, Assi, Salam A., Costanza, Mariantonia, Weniger, Marc A., Akalin, Altuna, Anagnostopoulos, Ioannis, Bukur, Thomas, Casarotto, Marco G., Damm, Frederik, Daumke, Oliver, Edginton-White, Benjamin, Gebhardt, J. Christof M., Grau, Michael, Grunwald, Stephan, Hansmann, Martin-Leo, Hartmann, Sylvia, Huber, Lionel, Kärgel, Eva, Lusatis, Simone, Noerenberg, Daniel, Obier, Nadine, Pannicke, Ulrich, Fischer, Anja, Reisser, Anja, Rosenwald, Andreas, Schwarz, Klaus, Sundararaj, Srinivasan, Weilemann, Andre, Winkler, Wiebke, Xu, Wendan, Lenz, Georg, Rajewsky, Klaus, Wasserman, Wyeth W., Cockerill, Peter N., Scheidereit, Claus, Siebert, Reiner, Küppers, Ralf, Grosschedl, Rudolf, Janz, Martin, Bonifer, Constanze, and Mathas, Stephan

Published
2023
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18. Imaging bridges pathology and radiology

Author

Hansmann, Martin-Leo, Klauschen, Frederick, Samek, Wojciech, Müller, Klaus-Robert, Donnadieu, Emmanuel, Scharf, Sonja, Hartmann, Sylvia, Koch, Ina, Ackermann, Jörg, Pantanowitz, Liron, Schäfer, Hendrik, and Wurzel, Patrick

Published
2023
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21. The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Lymphoid Neoplasms

Author

Alaggio, Rita, Amador, Catalina, Anagnostopoulos, Ioannis, Attygalle, Ayoma D., Araujo, Iguaracyra Barreto de Oliveira, Berti, Emilio, Bhagat, Govind, Borges, Anita Maria, Boyer, Daniel, Calaminici, Mariarita, Chadburn, Amy, Chan, John K. C., Cheuk, Wah, Chng, Wee-Joo, Choi, John K., Chuang, Shih-Sung, Coupland, Sarah E., Czader, Magdalena, Dave, Sandeep S., de Jong, Daphne, Du, Ming-Qing, Elenitoba-Johnson, Kojo S., Ferry, Judith, Geyer, Julia, Gratzinger, Dita, Guitart, Joan, Gujral, Sumeet, Harris, Marian, Harrison, Christine J., Hartmann, Sylvia, Hochhaus, Andreas, Jansen, Patty M., Karube, Kennosuke, Kempf, Werner, Khoury, Joseph, Kimura, Hiroshi, Klapper, Wolfram, Kovach, Alexandra E., Kumar, Shaji, Lazar, Alexander J., Lazzi, Stefano, Leoncini, Lorenzo, Leung, Nelson, Leventaki, Vasiliki, Li, Xiao-Qiu, Lim, Megan S., Liu, Wei-Ping, Louissaint, Jr., Abner, Marcogliese, Andrea, Medeiros, L. Jeffrey, Michal, Michael, Miranda, Roberto N., Mitteldorf, Christina, Montes-Moreno, Santiago, Morice, William, Nardi, Valentina, Naresh, Kikkeri N., Natkunam, Yasodha, Ng, Siok-Bian, Oschlies, Ilske, Ott, German, Parrens, Marie, Pulitzer, Melissa, Rajkumar, S. Vincent, Rawstron, Andrew C., Rech, Karen, Rosenwald, Andreas, Said, Jonathan, Sarkozy, Clémentine, Sayed, Shahin, Saygin, Caner, Schuh, Anna, Sewell, William, Siebert, Reiner, Sohani, Aliyah R., Tooze, Reuben, Traverse-Glehen, Alexandra, Vega, Francisco, Vergier, Beatrice, Wechalekar, Ashutosh D., Wood, Brent, Xerri, Luc, and Xiao, Wenbin

Published
2022
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23. Intrathecal IgM synthesis as a diagnostic marker in patients with suspected CNS lymphoma.

Author

Reinecke, Raphael, Jahnke, Kolja, Foltyn‐Dumitru, Martha, Lachner, Karsten, Armbrust, Moritz, Weber, Katharina J., Zeiner, Pia S., Czabanka, Marcus, Brunnberg, Uta, Hartmann, Sylvia, Steinbach, Joachim P., and Ronellenfitsch, Michael W.

Subjects
IMMUNOGLOBULIN M, RECEIVER operating characteristic curves, RESOURCE-limited settings, LYMPHOMAS
Abstract

For CNS lymphomas (CNSL), there is a high need for minimally invasive and easily obtainable diagnostic markers. Intrathecal IgM synthesis can easily be determined in routine CSF diagnostics. The aim of this study was to systematically investigate the diagnostic potential of intrathecal IgM synthesis in primary and secondary CNSL (PCNSL and SCNSL). In this retrospective study, patients with a biopsy‐proven diagnosis of PCNSL or SCNSL were compared with patients with other neurological diseases in whom CNSL was initially the primary radiological differential diagnosis based on MRI. Sensitivity and specificity of intrathecal IgM synthesis were calculated using receiver operating characteristic curves. Seventy patients with CNSL were included (49 PCNSL and 21 SCNSL) and compared to 70 control patients. The sensitivity and specificity for the diagnosis of CNSL were 49% and 87%, respectively, for the entire patient population and 66% and 91% after selection for cases with tumor access to the CSF system and isolated intrathecal IgM synthesis. In cases with MRI‐based radiological suspicion of CNSL, intrathecal IgM synthesis has good specificity but limited sensitivity. Because of its low‐threshold availability, analysis of intrathecal IgM synthesis has the potential to lead to higher diagnostic accuracy, especially in resource‐limited settings, and deserves further study. [ABSTRACT FROM AUTHOR]

Published
2024
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28. Hyper-N-glycosylated SAMD14 and neurabin-I as driver autoantigens of primary central nervous system lymphoma

Author

Thurner, Lorenz, Preuss, Klaus-Dieter, Bewarder, Moritz, Kemele, Maria, Fadle, Natalie, Regitz, Evi, Altmeyer, Sarah, Schormann, Claudia, Poeschel, Viola, Ziepert, Marita, Walter, Silke, Roth, Patrick, Weller, Michael, Szczepanowski, Monika, Klapper, Wolfram, Monoranu, Camelia, Rosenwald, Andreas, Möller, Peter, Hartmann, Sylvia, Hansmann, Martin-Leo, Mackensen, Andreas, Schäfer, Henning, Schorb, Elisabeth, Illerhaus, Gerald, Buslei, Rolf, Bohle, Rainer Maria, Stilgenbauer, Stephan, Kim, Yoo-Jin, and Pfreundschuh, Michael

Published
2018
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29. Duodenal-type and nodal follicular lymphomas differ by their immune microenvironment rather than their mutation profiles

Author

Hellmuth, Johannes C., Louissaint, Abner, Jr, Szczepanowski, Monika, Haebe, Sarah, Pastore, Alessandro, Alig, Stefan, Staiger, Annette M., Hartmann, Sylvia, Kridel, Robert, Ducar, Matthew D., Koch, Peter, Dreyling, Martin, Hansmann, Martin-Leo, Ott, German, Rosenwald, Andreas, Gascoyne, Randy D., Weinstock, David M., Hiddemann, Wolfgang, Klapper, Wolfram, and Weigert, Oliver

Published
2018
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31. LRPAP1 is a frequent proliferation-inducing antigen of BCRs of mantle cell lymphomas and can be used for specific therapeutic targeting

Author

Thurner, Lorenz, Hartmann, Sylvia, Fadle, Natalie, Kemele, Maria, Bock, Theresa, Bewarder, Moritz, Regitz, Evi, Neumann, Frank, Nimmesgern, Anna, von Müller, Lutz, Pott, Christiane, Kim, Yoo-Jin, Bohle, Rainer Maria, Wasik, Mariusz, Schuster, Stephen J., Hansmann, Martin-Leo, Preuss, Klaus-Dieter, and Pfreundschuh, Michael

Published
2019
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34. Lymphocyte predominant cells detect Moraxella catarrhalis-derived antigens in nodular lymphocyte-predominant Hodgkin lymphoma

Author

Thurner, Lorenz, Hartmann, Sylvia, Fadle, Natalie, Regitz, Evi, Kemele, Maria, Kim, Yoo-Jin, Bohle, Rainer Maria, Nimmesgern, Anna, von Müller, Lutz, Kempf, Volkhard A. J., Weniger, Marc A., Neumann, Frank, Schneider, Nadine, Vornanen, Martine, Sundström, Christer, de Leval, Laurence, Engert, Andreas, Eichenauer, Dennis A., Küppers, Ralf, Preuss, Klaus-Dieter, Hansmann, Martin-Leo, and Pfreundschuh, Michael

Published
2020
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35. miRNA expression profiling divides follicular dendritic cell sarcomas into two groups, related to fibroblasts and myopericytomas or Castleman's disease

Author

Hartmann, Sylvia, Döring, Claudia, Agostinelli, Claudio, Portscher-Kim, Soo-Jeong, Lonardi, Silvia, Lorenzi, Luisa, Fuligni, Fabio, Martinez, Daniel, Mehta, Jay, Borges, Anita, Hackstein, Holger, Kippenberger, Stefan, Piccaluga, Pier Paolo, Simonitsch-Klupp, Ingrid, Cabeçadas, José, Campo, Elias, Facchetti, Fabio, Pileri, Stefano A., and Hansmann, Martin-Leo

Published
2016
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36. Identification of two unannotated miRNAs in classic Hodgkin lymphoma cell lines

Author

Ustaszewski Adam, Paczkowska Julia, Janiszewska Joanna, Bernhart Stephan H., Bein Julia, Russiñol Núria, Hansmann Martin-Leo, Chapaprieta Vicente, Martín-Subero José I., Siebert Reiner, Hartmann Sylvia, and Giefing Maciej

Subjects
Classic Hodgkin lymphoma (cHL), novel miRNA, loss of epigenetic control
Abstract

MicroRNAs (miRNAs) are small non coding RNAs responsible for posttranscriptional regulation of gene expression. Even though almost 2000 precursors have been described so far, additional miRNAs are still being discovered in normal as well as malignant cells. Alike protein coding genes, miRNAs may acquire oncogenic properties in consequence of altered expression or presence of gain or loss of function mutations. In this study we mined datasets from miRNA expression profiling (miRNA-seq) of 7 classic Hodgkin Lymphoma (cHL) cell lines, 10 non-Hodgkin lymphoma (NHL) cell lines and 56 samples of germinal center derived B-cell lymphomas. Our aim was to discover potential novel cHL oncomiRs not reported in miRBase (release 22.1) and expressed in cHL cell lines but no other B-cell lymphomas. We identified six such miRNA candidates in cHL cell lines and verified the expression of two of them encoded at chr2:212678788-212678849 and chr5:168090507-168090561 (GRCh38). Interestingly, we showed that one of the validated miRNAs (located in an intron of the TENM2 gene) is expressed together with its host gene. TENM2 is characterized by hypomethylation and open chromatin around its TSS in cHL cell lines in contrast to NHL cell lines and germinal centre B-cells respectively. It indicates an epigenetic mechanism responsible for aberrant expression of both, the TENM2 gene and the novel miRNA in cHL cell lines.

Published
2023

38. Molecular characteristics of diffuse large B-cell lymphoma in the Positron Emission Tomography-Guided Therapy of Aggressive Non-Hodgkin lymphomas (PETAL) trial: correlation with interim PET and outcome

Author

Richter, Julia, Hüttmann, Andreas, Rekowski, Jan, Schmitz, Christine, Gärtner, Selina, Rosenwald, Andreas, Hansmann, Martin-Leo, Hartmann, Sylvia, Möller, Peter, Wacker, Hans-Heinrich, Feller, Alfred, Thorns, Christoph, Müller, Stefan, Dührsen, Ulrich, and Klapper, Wolfram

Published
2019
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39. Clonal composition and differentiation stage of human CD30+ B cells in reactive lymph nodes.

Author

Küppers, Ralf, Budeus, Bettina, Hartmann, Sylvia, and Hansmann, Martin-Leo

Subjects
B cells, B cell differentiation, LYMPH nodes, LYMPHADENITIS, HODGKIN'S disease
Abstract

Introduction: Normal CD30+ B cells represent a distinct B-cell differentiation stage with features of strong activation. We lack an in depth understanding of these cells, because they are not present in peripheral blood and are typically very rare in reactive lymphoid organs. CD30+ B cells have been discussed as a potential precursor population for the malignant CD30+ Hodgkin and Reed-Sternberg cells in classical Hodgkin lymphoma. As CD30+ B cells can be more numerous in some cases of reactive lymphadenitis, we aimed to characterize these CD30+ B cells in terms of their differentiation stage and clonal composition, also as a means to clarify whether such CD30+ B-cell populations may represent potential precursor lesions of Hodgkin lymphoma. Methods: We microdissected single CD30+ B cells from tissue sections of eight reactive lymph nodes with substantial numbers of such cells and sequenced their rearranged immunoglobulin (Ig) heavy chain V region (IGHV) genes. Results: The CD30+ B cells were polyclonal B cells in all instances, and they not only encompass post-germinal center (GC) B cells with mutated IGHV genes, but also include a substantial fraction of pre-germinal center B cells with unmutated IGHV genes. In five of the lymph nodes, mostly small clonal expansions were detected among the CD30+ B cells. Most of the expanded clones carried somatically mutated IGHV genes and about half of the mutated clones showed intraclonal diversity. Discussion: We conclude that in human reactive lymph nodes with relatively many CD30+ B cells, these cells are a heterogenous population of polyclonal B cells encompassing activated pre-GC B cells as well as GC and post-GC B cells, with some clonal expansions. Because of their polyclonality and frequent pre-GC differentiation stage, there is no indication that such cell-rich CD30+ B-cell populations represent precursor lesions of Hodgkin lymphoma. [ABSTRACT FROM AUTHOR]

Published
2023
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45. The RHOA Mutation G17V Does Not Lead to Increased Migration of Human Malignant T Cells but Is Associated with Matrix Remodelling.

Author

Merk-Ahmad, Katrin, Bein, Julia, Scharf, Sonja, Schäfer, Hendrik, Bexte, Tobias, Ullrich, Evelyn, Loth, Andreas G., Flinner, Nadine, Senff, Tina, Schneider, Olga, Hansmann, Martin-Leo, Piel, Matthieu, Häupl, Björn, Oellerich, Thomas, Donnadieu, Emmanuel, and Hartmann, Sylvia

Subjects
GENETIC mutation, ALLELES, CELL motility, COMPARATIVE studies, RESEARCH funding, T cells, LYMPHOPROLIFERATIVE disorders, CELL lines, EXTRACELLULAR space, T helper cells
Abstract

Simple Summary: The aim of this study was to understand if the presence of a RHOA-G17V mutation in angioimmunoblastic T-cell lymphoma is responsible for the typical clinical presentation with early dissemination of tumor cells. Overexpression of RHOA-G17V in malignant T cells did not enhance their migration capacity neither in microfluidics microchannels, 3D collagen gel or primary human lymphoid tissue. In contrast, RHOA-G17V overexpressing cells from the HH cell line presented increased numbers of cells surrounded by cleaved collagen. Primary AITL cases showed a correlation between RHOA-G17V mutation allele frequency and collagen fibrosis of the tissue, suggesting that mechanisms leading to extracellular matrix degradation contribute to the early spread of AITL tumor cells. Nodal T-follicular helper cell lymphoma, angioimmunoblastic-type (AITL), is characterized by constitutional symptoms, advanced-stage disease, and generalized lymphadenopathy. A genetic hallmark of this lymphoma is the frequent occurrence of the RHOA mutation G17V in neoplastic cells, which is observed in around 60% of patients. Because RHOA is involved in both T-cell receptor downstream signalling and cell migration, we hypothesized that the characteristic presentation of AITL could be the result of enhanced tumor cell migration. Therefore, this study aimed to elucidate the impact of the RHOA variant G17V on the migration of neoplastic T cells. We transfected the T-cell lymphoma cell lines HH and HuT78 to stably express the RHOA-G17V variant. RHOA-G17V-expressing T cells did not exhibit enhanced motility compared to empty-vector-transfected cells in microchannels, a 3D collagen gel, or primary human lymphatic tissue. Cells of the HH cell line expressing RHOA-G17V had an increased number of cells with cleaved collagen compared with the empty-vector-transfected cells. Therefore, we hypothesized that the early spread of AITL tumor cells may be related to remodelling of the extracellular matrix. Accordingly, we observed a significant negative correlation between the relative area of collagen in histological sections from 18 primary AITL and the allele frequency of the RHOA-G17V mutation. In conclusion, our results suggest that the characteristic presentation of AITL with early, widespread dissemination of lymphoma cells is not the result of an enhanced migration capacity due to the RHOA-G17V mutation; instead, this feature may rather be related to extracellular matrix remodelling. [ABSTRACT FROM AUTHOR]

Published
2023
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46. The prognostic impact of variant histology in nodular lymphocyte-predominant Hodgkin lymphoma: a report from the German Hodgkin Study Group (GHSG)

Author

Hartmann, Sylvia, Eichenauer, Dennis A., Plütschow, Annette, Mottok, Anja, Bob, Roshanak, Koch, Karoline, Bernd, Heinz-Wolfram, Cogliatti, Sergio, Hummel, Michael, Feller, Alfred C., Ott, German, Möller, Peter, Rosenwald, Andreas, Stein, Harald, Hansmann, Martin-Leo, Engert, Andreas, and Klapper, Wolfram

Published
2013
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