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19.04.2022 | Hodgkin-Lymphom | Leitthema

Neues aus Pathologie und Pathophysiologie des Hodgkin-Lymphoms

verfasst von: Elena Gerhard-Hartmann, Sarah Reinke, Andreas Rosenwald, Wolfram Klapper

Erschienen in: Die Onkologie | Ausgabe 10/2022

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Zusammenfassung

Hintergrund

Die letzten Jahre ergaben neue Einblicke in die Pathomechanismen der Tumorzellen des Hodgkin-Lymphoms, aber auch in die Bedeutung des Begleitinfiltrats.

Fragestellung

Das Ziel der Übersichtsarbeit ist die Darstellung neuer Erkenntnisse über die Pathobiologie von Hodgkin-Lymphomen in den letzten Jahren.

Material und Methoden

Es erfolgte eine selektive Literaturrecherche unter Berücksichtigung eigener Erfahrungen als Forschende auf dem Gebiet der Hodgkin-Lymphome.

Ergebnisse

Molekulare Eigenschaften der neoplastischen Zellen zeigen eine gestörte Interaktion mit dem Immunsystem. Das ausgeprägte Begleitinfiltrat benigner Zellen eröffnet Möglichkeiten in der Immuncheckpointtherapie. Die Wirkmechanismen dieser Therapie beim Hodgkin-Lymphom scheinen sich jedoch von den Mechanismen in anderen Tumorentitäten zu unterscheiden.

Schlussfolgerungen

Das Begleitinfiltrat benigner Immunzellen stellen eine therapeutische Zielstruktur dar, obwohl die Wirkmechanismen eine Immuncheckpointtherapie im Hodgkin-Lymphom unzureichend verstanden sind. Die pathologische Diagnostik und wird durch neueste Erkenntnisse noch nicht beeinflusst; prognostische oder prädiktive Biomarker aus dem Begleitinfiltrat stehen derzeit noch nicht zur Verfügung.
Literatur
1.
Zurück zum Zitat International Agency for Reaserch on Cancer (2018) WHO classification of tumors of haematopoietic and lymphoid tissues, 4. Aufl. International Agency for Reaserch on Cancer (2018) WHO classification of tumors of haematopoietic and lymphoid tissues, 4. Aufl.
4.
Zurück zum Zitat Kanzler H et al (1996) Hodgkin and Reed-Sternberg cells in Hodgkin’s disease represent the outgrowth of a dominant tumor clone derived from (crippled) germinal center B cells. J Exp Med 184(4):1495–1505PubMedCrossRef Kanzler H et al (1996) Hodgkin and Reed-Sternberg cells in Hodgkin’s disease represent the outgrowth of a dominant tumor clone derived from (crippled) germinal center B cells. J Exp Med 184(4):1495–1505PubMedCrossRef
5.
Zurück zum Zitat Marafioti T et al (2000) Hodgkin and reed-sternberg cells represent an expansion of a single clone originating from a germinal center B‑cell with functional immunoglobulin gene rearrangements but defective immunoglobulin transcription. Blood 95(4):1443–1450PubMedCrossRef Marafioti T et al (2000) Hodgkin and reed-sternberg cells represent an expansion of a single clone originating from a germinal center B‑cell with functional immunoglobulin gene rearrangements but defective immunoglobulin transcription. Blood 95(4):1443–1450PubMedCrossRef
6.
Zurück zum Zitat Schwering I et al (2003) Loss of the B‑lineage-specific gene expression program in Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma. Blood 101(4):1505–1512PubMedCrossRef Schwering I et al (2003) Loss of the B‑lineage-specific gene expression program in Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma. Blood 101(4):1505–1512PubMedCrossRef
7.
Zurück zum Zitat Joos S et al (2002) Classical Hodgkin lymphoma is characterized by recurrent copy number gains of the short arm of chromosome 2. Blood 99(4):1381–1387PubMedCrossRef Joos S et al (2002) Classical Hodgkin lymphoma is characterized by recurrent copy number gains of the short arm of chromosome 2. Blood 99(4):1381–1387PubMedCrossRef
8.
Zurück zum Zitat Martin-Subero JI et al (2002) Recurrent involvement of the REL and BCL11A loci in classical Hodgkin lymphoma. Blood 99(4):1474–1477PubMedCrossRef Martin-Subero JI et al (2002) Recurrent involvement of the REL and BCL11A loci in classical Hodgkin lymphoma. Blood 99(4):1474–1477PubMedCrossRef
9.
Zurück zum Zitat Green MR et al (2010) Integrative analysis reveals selective 9p24.1 amplification, increased PD‑1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B‑cell lymphoma. Blood 116(17):3268–3277PubMedPubMedCentralCrossRef Green MR et al (2010) Integrative analysis reveals selective 9p24.1 amplification, increased PD‑1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B‑cell lymphoma. Blood 116(17):3268–3277PubMedPubMedCentralCrossRef
10.
Zurück zum Zitat Roemer MG et al (2016) PD-L1 and PD-L2 genetic alterations define classical Hodgkin lymphoma and predict outcome. J Clin Oncol 34(23):2690–2697PubMedPubMedCentralCrossRef Roemer MG et al (2016) PD-L1 and PD-L2 genetic alterations define classical Hodgkin lymphoma and predict outcome. J Clin Oncol 34(23):2690–2697PubMedPubMedCentralCrossRef
11.
Zurück zum Zitat Wienand K et al (2019) Genomic analyses of flow-sorted Hodgkin Reed-Sternberg cells reveal complementary mechanisms of immune evasion. Blood Adv 3(23):4065–4080PubMedPubMedCentralCrossRef Wienand K et al (2019) Genomic analyses of flow-sorted Hodgkin Reed-Sternberg cells reveal complementary mechanisms of immune evasion. Blood Adv 3(23):4065–4080PubMedPubMedCentralCrossRef
13.
Zurück zum Zitat Reichel J et al (2015) Flow sorting and exome sequencing reveal the oncogenome of primary Hodgkin and Reed-Sternberg cells. Blood 125(7):1061–1072PubMedCrossRef Reichel J et al (2015) Flow sorting and exome sequencing reveal the oncogenome of primary Hodgkin and Reed-Sternberg cells. Blood 125(7):1061–1072PubMedCrossRef
14.
Zurück zum Zitat Weniger MA, Kuppers R (2016) NF-kappaB deregulation in Hodgkin lymphoma. Semin Cancer Biol 39:32–39PubMedCrossRef Weniger MA, Kuppers R (2016) NF-kappaB deregulation in Hodgkin lymphoma. Semin Cancer Biol 39:32–39PubMedCrossRef
16.
Zurück zum Zitat Kapatai G, Murray P (2007) Contribution of the Epstein Barr virus to the molecular pathogenesis of Hodgkin lymphoma. J Clin Pathol 60(12):1342–1349PubMedPubMedCentralCrossRef Kapatai G, Murray P (2007) Contribution of the Epstein Barr virus to the molecular pathogenesis of Hodgkin lymphoma. J Clin Pathol 60(12):1342–1349PubMedPubMedCentralCrossRef
17.
Zurück zum Zitat Murray P, Bell A (2015) Contribution of the Epstein-Barr virus to the pathogenesis of Hodgkin lymphoma. Curr Top Microbiol Immunol 390(1):287–313PubMed Murray P, Bell A (2015) Contribution of the Epstein-Barr virus to the pathogenesis of Hodgkin lymphoma. Curr Top Microbiol Immunol 390(1):287–313PubMed
18.
Zurück zum Zitat Montgomery ND et al (2016) Karyotypic abnormalities associated with Epstein-Barr virus status in classical Hodgkin lymphoma. Cancer Genet 209(9):408–416PubMedCrossRef Montgomery ND et al (2016) Karyotypic abnormalities associated with Epstein-Barr virus status in classical Hodgkin lymphoma. Cancer Genet 209(9):408–416PubMedCrossRef
19.
Zurück zum Zitat Schmitz R et al (2009) TNFAIP3 (A20) is a tumor suppressor gene in Hodgkin lymphoma and primary mediastinal B cell lymphoma. J Exp Med 206(5):981–989PubMedPubMedCentralCrossRef Schmitz R et al (2009) TNFAIP3 (A20) is a tumor suppressor gene in Hodgkin lymphoma and primary mediastinal B cell lymphoma. J Exp Med 206(5):981–989PubMedPubMedCentralCrossRef
20.
Zurück zum Zitat Liu D et al (2019) Integrative molecular and clinical modeling of clinical outcomes to PD1 blockade in patients with metastatic melanoma. Nat Med 25(12):1916–1927PubMedPubMedCentralCrossRef Liu D et al (2019) Integrative molecular and clinical modeling of clinical outcomes to PD1 blockade in patients with metastatic melanoma. Nat Med 25(12):1916–1927PubMedPubMedCentralCrossRef
21.
Zurück zum Zitat Ansell SM et al (2015) PD‑1 blockade with nivolumab in relapsed or refractory Hodgkin’s lymphoma. N Engl J Med 372(4):311–319PubMedCrossRef Ansell SM et al (2015) PD‑1 blockade with nivolumab in relapsed or refractory Hodgkin’s lymphoma. N Engl J Med 372(4):311–319PubMedCrossRef
22.
Zurück zum Zitat Nijland M et al (2017) HLA dependent immune escape mechanisms in B‑cell lymphomas: implications for immune checkpoint inhibitor therapy? OncoImmunology 6(4):e1295202PubMedPubMedCentralCrossRef Nijland M et al (2017) HLA dependent immune escape mechanisms in B‑cell lymphomas: implications for immune checkpoint inhibitor therapy? OncoImmunology 6(4):e1295202PubMedPubMedCentralCrossRef
23.
Zurück zum Zitat Cader FZ et al (2018) Mass cytometry of Hodgkin lymphoma reveals a CD4(+) regulatory T‑cell-rich and exhausted T‑effector microenvironment. Blood 132(8):825–836PubMedPubMedCentralCrossRef Cader FZ et al (2018) Mass cytometry of Hodgkin lymphoma reveals a CD4(+) regulatory T‑cell-rich and exhausted T‑effector microenvironment. Blood 132(8):825–836PubMedPubMedCentralCrossRef
24.
Zurück zum Zitat Aoki T et al (2020) Single-cell transcriptome analysis reveals disease-defining T‑cell subsets in the tumor microenvironment of classic Hodgkin lymphoma. Cancer Discov 10(3):406–421PubMedCrossRef Aoki T et al (2020) Single-cell transcriptome analysis reveals disease-defining T‑cell subsets in the tumor microenvironment of classic Hodgkin lymphoma. Cancer Discov 10(3):406–421PubMedCrossRef
25.
Zurück zum Zitat Patel SS et al (2019) The microenvironmental niche in classic Hodgkin lymphoma is enriched for CTLA-4-positive T cells that are PD-1-negative. Blood 134(23):2059–2069PubMedPubMedCentral Patel SS et al (2019) The microenvironmental niche in classic Hodgkin lymphoma is enriched for CTLA-4-positive T cells that are PD-1-negative. Blood 134(23):2059–2069PubMedPubMedCentral
26.
Zurück zum Zitat Cader FZ et al (2020) A peripheral immune signature of responsiveness to PD‑1 blockade in patients with classical Hodgkin lymphoma. Nat Med 26(9):1468–1479PubMedCrossRef Cader FZ et al (2020) A peripheral immune signature of responsiveness to PD‑1 blockade in patients with classical Hodgkin lymphoma. Nat Med 26(9):1468–1479PubMedCrossRef
27.
Zurück zum Zitat Roemer MGM et al (2018) Major histocompatibility complex class II and programmed death ligand 1 expression predict outcome after programmed death 1 blockade in classic Hodgkin lymphoma. J Clin Oncol 36(10):942–950PubMedPubMedCentralCrossRef Roemer MGM et al (2018) Major histocompatibility complex class II and programmed death ligand 1 expression predict outcome after programmed death 1 blockade in classic Hodgkin lymphoma. J Clin Oncol 36(10):942–950PubMedPubMedCentralCrossRef
28.
Zurück zum Zitat Brockelmann PJ et al (2020) Efficacy of nivolumab and AVD in early-stage unfavorable classic Hodgkin lymphoma: the randomized phase 2 German Hodgkin study group NIVAHL trial. JAMA Oncol 6(6):872–880PubMedCrossRef Brockelmann PJ et al (2020) Efficacy of nivolumab and AVD in early-stage unfavorable classic Hodgkin lymphoma: the randomized phase 2 German Hodgkin study group NIVAHL trial. JAMA Oncol 6(6):872–880PubMedCrossRef
29.
Zurück zum Zitat Reinke S et al (2020) Tumor and microenvironment response but no cytotoxic T‑cell activation in classic Hodgkin lymphoma treated with anti-PD1. Blood 136(25):2851–2863PubMedCrossRef Reinke S et al (2020) Tumor and microenvironment response but no cytotoxic T‑cell activation in classic Hodgkin lymphoma treated with anti-PD1. Blood 136(25):2851–2863PubMedCrossRef
30.
31.
Zurück zum Zitat Jachimowicz RD et al (2021) Whole-slide image analysis of the tumor microenvironment identifies low B‑cell content as a predictor of adverse outcome in patients with advanced-stage classical Hodgkin lymphoma treated with BEACOPP. Haematologica 106(6):1684–1692PubMedCrossRef Jachimowicz RD et al (2021) Whole-slide image analysis of the tumor microenvironment identifies low B‑cell content as a predictor of adverse outcome in patients with advanced-stage classical Hodgkin lymphoma treated with BEACOPP. Haematologica 106(6):1684–1692PubMedCrossRef
33.
35.
Zurück zum Zitat El Halabi L et al (2021) Expression of the immune checkpoint regulators LAG‑3 and TIM‑3 in classical Hodgkin lymphoma. Clin Lymphoma Myeloma Leuk 21(4):257–266.e3PubMedCrossRef El Halabi L et al (2021) Expression of the immune checkpoint regulators LAG‑3 and TIM‑3 in classical Hodgkin lymphoma. Clin Lymphoma Myeloma Leuk 21(4):257–266.e3PubMedCrossRef
36.
Zurück zum Zitat Roemer MG et al (2016) Classical Hodgkin lymphoma with reduced β2M/MHC class I expression is associated with inferior outcome independent of 9p24.1 status. Cancer Immunol Res 4(11):910–916PubMedPubMedCentralCrossRef Roemer MG et al (2016) Classical Hodgkin lymphoma with reduced β2M/MHC class I expression is associated with inferior outcome independent of 9p24.1 status. Cancer Immunol Res 4(11):910–916PubMedPubMedCentralCrossRef
37.
Zurück zum Zitat Diepstra A et al (2005) Association with HLA class I in Epstein-Barr-virus-positive and with HLA class III in Epstein-Barr-virus-negative Hodgkin’s lymphoma. Lancet 365(9478):2216–2224PubMedCrossRef Diepstra A et al (2005) Association with HLA class I in Epstein-Barr-virus-positive and with HLA class III in Epstein-Barr-virus-negative Hodgkin’s lymphoma. Lancet 365(9478):2216–2224PubMedCrossRef
38.
Zurück zum Zitat McAulay KA, Jarrett RF (2015) Human leukocyte antigens and genetic susceptibility to lymphoma. Tissue Antigens 86(2):98–113PubMedCrossRef McAulay KA, Jarrett RF (2015) Human leukocyte antigens and genetic susceptibility to lymphoma. Tissue Antigens 86(2):98–113PubMedCrossRef
39.
Zurück zum Zitat Diepstra A et al (2007) HLA class II expression by Hodgkin Reed-Sternberg cells is an independent prognostic factor in classical Hodgkin’s lymphoma. J Clin Oncol 25(21):3101–3108PubMedCrossRef Diepstra A et al (2007) HLA class II expression by Hodgkin Reed-Sternberg cells is an independent prognostic factor in classical Hodgkin’s lymphoma. J Clin Oncol 25(21):3101–3108PubMedCrossRef
40.
Zurück zum Zitat Nagasaki J et al (2020) The critical role of CD4+ T cells in PD‑1 blockade against MHC-II-expressing tumors such as classic Hodgkin lymphoma. Blood Adv 4(17):4069–4082PubMedPubMedCentralCrossRef Nagasaki J et al (2020) The critical role of CD4+ T cells in PD‑1 blockade against MHC-II-expressing tumors such as classic Hodgkin lymphoma. Blood Adv 4(17):4069–4082PubMedPubMedCentralCrossRef
41.
42.
Zurück zum Zitat Kraman M et al (2020) FS118, a bispecific antibody targeting LAG‑3 and PD-L1, enhances T‑cell activation resulting in potent antitumor activity. Clin Cancer Res 26(13):3333–3344PubMedCrossRef Kraman M et al (2020) FS118, a bispecific antibody targeting LAG‑3 and PD-L1, enhances T‑cell activation resulting in potent antitumor activity. Clin Cancer Res 26(13):3333–3344PubMedCrossRef
43.
Zurück zum Zitat Schuhmacher B et al (2019) JUNB, DUSP2, SGK1, SOCS1 and CREBBP are frequently mutated in T‑cell/histiocyte-rich large B‑cell lymphoma. Haematologica 104(2):330–337PubMedPubMedCentralCrossRef Schuhmacher B et al (2019) JUNB, DUSP2, SGK1, SOCS1 and CREBBP are frequently mutated in T‑cell/histiocyte-rich large B‑cell lymphoma. Haematologica 104(2):330–337PubMedPubMedCentralCrossRef
44.
Zurück zum Zitat Al-Mansour M et al (2010) Transformation to aggressive lymphoma in nodular lymphocyte-predominant Hodgkin’s lymphoma. J Clin Oncol 28(5):793–799PubMedCrossRef Al-Mansour M et al (2010) Transformation to aggressive lymphoma in nodular lymphocyte-predominant Hodgkin’s lymphoma. J Clin Oncol 28(5):793–799PubMedCrossRef
45.
Zurück zum Zitat Fan Z et al (2003) Characterization of variant patterns of nodular lymphocyte predominant hodgkin lymphoma with immunohistologic and clinical correlation. Am J Surg Pathol 27(10):1346–1356PubMedCrossRef Fan Z et al (2003) Characterization of variant patterns of nodular lymphocyte predominant hodgkin lymphoma with immunohistologic and clinical correlation. Am J Surg Pathol 27(10):1346–1356PubMedCrossRef
46.
Zurück zum Zitat Hartmann S et al (2013) The prognostic impact of variant histology in nodular lymphocyte-predominant Hodgkin lymphoma: a report from the German Hodgkin study group (GHSG). Blood 122(26):4246–4252 (quiz 4292)PubMedCrossRef Hartmann S et al (2013) The prognostic impact of variant histology in nodular lymphocyte-predominant Hodgkin lymphoma: a report from the German Hodgkin study group (GHSG). Blood 122(26):4246–4252 (quiz 4292)PubMedCrossRef
47.
Zurück zum Zitat Hartmann S et al (2019) The time to relapse correlates with the histopathological growth pattern in nodular lymphocyte predominant Hodgkin lymphoma. Am J Hematol 94(11):1208–1213PubMedCrossRef Hartmann S et al (2019) The time to relapse correlates with the histopathological growth pattern in nodular lymphocyte predominant Hodgkin lymphoma. Am J Hematol 94(11):1208–1213PubMedCrossRef
48.
Zurück zum Zitat Kuppers R et al (1994) Hodgkin disease: Hodgkin and Reed-Sternberg cells picked from histological sections show clonal immunoglobulin gene rearrangements and appear to be derived from B cells at various stages of development. Proc Natl Acad Sci U S A 91(23):10962–10966PubMedPubMedCentralCrossRef Kuppers R et al (1994) Hodgkin disease: Hodgkin and Reed-Sternberg cells picked from histological sections show clonal immunoglobulin gene rearrangements and appear to be derived from B cells at various stages of development. Proc Natl Acad Sci U S A 91(23):10962–10966PubMedPubMedCentralCrossRef
49.
Zurück zum Zitat Braeuninger A et al (1997) Hodgkin and Reed-Sternberg cells in lymphocyte predominant Hodgkin disease represent clonal populations of germinal center-derived tumor B cells. Proc Natl Acad Sci U S A 94(17):9337–9342PubMedPubMedCentralCrossRef Braeuninger A et al (1997) Hodgkin and Reed-Sternberg cells in lymphocyte predominant Hodgkin disease represent clonal populations of germinal center-derived tumor B cells. Proc Natl Acad Sci U S A 94(17):9337–9342PubMedPubMedCentralCrossRef
50.
Zurück zum Zitat Brune V et al (2008) Origin and pathogenesis of nodular lymphocyte-predominant Hodgkin lymphoma as revealed by global gene expression analysis. J Exp Med 205(10):2251–2268PubMedPubMedCentralCrossRef Brune V et al (2008) Origin and pathogenesis of nodular lymphocyte-predominant Hodgkin lymphoma as revealed by global gene expression analysis. J Exp Med 205(10):2251–2268PubMedPubMedCentralCrossRef
51.
Zurück zum Zitat Mottok A et al (2007) Somatic hypermutation of SOCS1 in lymphocyte-predominant Hodgkin lymphoma is accompanied by high JAK2 expression and activation of STAT6. Blood 110(9):3387–3390PubMedCrossRef Mottok A et al (2007) Somatic hypermutation of SOCS1 in lymphocyte-predominant Hodgkin lymphoma is accompanied by high JAK2 expression and activation of STAT6. Blood 110(9):3387–3390PubMedCrossRef
52.
Zurück zum Zitat Bakhirev AG et al (2014) Fluorescence immunophenotyping and interphase cytogenetics (FICTION) detects BCL6 abnormalities, including gene amplification, in most cases of nodular lymphocyte-predominant Hodgkin lymphoma. Arch Pathol Lab Med 138(4):538–542PubMedCrossRef Bakhirev AG et al (2014) Fluorescence immunophenotyping and interphase cytogenetics (FICTION) detects BCL6 abnormalities, including gene amplification, in most cases of nodular lymphocyte-predominant Hodgkin lymphoma. Arch Pathol Lab Med 138(4):538–542PubMedCrossRef
53.
Zurück zum Zitat Renne C et al (2005) Molecular cytogenetic analyses of immunoglobulin loci in nodular lymphocyte predominant Hodgkin’s lymphoma reveal a recurrent IGH-BCL6 juxtaposition. J Mol Diagn 7(3):352–356PubMedPubMedCentralCrossRef Renne C et al (2005) Molecular cytogenetic analyses of immunoglobulin loci in nodular lymphocyte predominant Hodgkin’s lymphoma reveal a recurrent IGH-BCL6 juxtaposition. J Mol Diagn 7(3):352–356PubMedPubMedCentralCrossRef
54.
Zurück zum Zitat Wlodarska I et al (2003) Frequent occurrence of BCL6 rearrangements in nodular lymphocyte predominance Hodgkin lymphoma but not in classical Hodgkin lymphoma. Blood 101(2):706–710PubMedCrossRef Wlodarska I et al (2003) Frequent occurrence of BCL6 rearrangements in nodular lymphocyte predominance Hodgkin lymphoma but not in classical Hodgkin lymphoma. Blood 101(2):706–710PubMedCrossRef
55.
Zurück zum Zitat Huppmann AR et al (2014) EBV may be expressed in the LP cells of nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL) in both children and adults. Am J Surg Pathol 38(3):316–324PubMedPubMedCentralCrossRef Huppmann AR et al (2014) EBV may be expressed in the LP cells of nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL) in both children and adults. Am J Surg Pathol 38(3):316–324PubMedPubMedCentralCrossRef
56.
Zurück zum Zitat Paschold L et al (2021) Evolutionary clonal trajectories in nodular lymphocyte-predominant Hodgkin lymphoma with high risk of transformation. Haematologica 106(10):2654–2666PubMedPubMedCentralCrossRef Paschold L et al (2021) Evolutionary clonal trajectories in nodular lymphocyte-predominant Hodgkin lymphoma with high risk of transformation. Haematologica 106(10):2654–2666PubMedPubMedCentralCrossRef
57.
Zurück zum Zitat Thurner L et al (2020) Lymphocyte predominant cells detect moraxella catarrhalis-derived antigens in nodular lymphocyte-predominant Hodgkin lymphoma. Nat Commun 11(1):2465PubMedPubMedCentralCrossRef Thurner L et al (2020) Lymphocyte predominant cells detect moraxella catarrhalis-derived antigens in nodular lymphocyte-predominant Hodgkin lymphoma. Nat Commun 11(1):2465PubMedPubMedCentralCrossRef
Metadaten
Titel
Neues aus Pathologie und Pathophysiologie des Hodgkin-Lymphoms
verfasst von
Elena Gerhard-Hartmann
Sarah Reinke
Andreas Rosenwald
Wolfram Klapper
Publikationsdatum
19.04.2022
Verlag
Springer Medizin
Erschienen in
Die Onkologie / Ausgabe 10/2022
Print ISSN: 2731-7226
Elektronische ISSN: 2731-7234
DOI
https://doi.org/10.1007/s00761-022-01155-2

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