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A strong host response and lack of MYC expression are characteristic for diffuse large B cell lymphoma transformed from nodular lymphocyte predominant Hodgkin lymphoma.
Schuhmacher, Bianca; Rengstl, Benjamin; Döring, Claudia; Bein, Julia; Newrzela, Sebastian; Brunnberg, Uta; Kvasnicka, Hans Michael; Vornanen, Martine; Küppers, Ralf; Hansmann, Martin-Leo; Hartmann, Sylvia.
Afiliación
  • Schuhmacher B; Dr. Senckenberg Institute of Pathology, Goethe University, Frankfurt am Main, Germany.
  • Rengstl B; Dr. Senckenberg Institute of Pathology, Goethe University, Frankfurt am Main, Germany.
  • Döring C; Dr. Senckenberg Institute of Pathology, Goethe University, Frankfurt am Main, Germany.
  • Bein J; Dr. Senckenberg Institute of Pathology, Goethe University, Frankfurt am Main, Germany.
  • Newrzela S; Dr. Senckenberg Institute of Pathology, Goethe University, Frankfurt am Main, Germany.
  • Brunnberg U; Department of Internal Medicine 2, Hospital of the J. W. Goethe University, Frankfurt am Main, Germany.
  • Kvasnicka HM; Dr. Senckenberg Institute of Pathology, Goethe University, Frankfurt am Main, Germany.
  • Vornanen M; Department of Pathology, Tampere University Hospital and University of Tampere, Tampere, Finland.
  • Küppers R; Institute of Cell Biology (Cancer Research), Faculty of Medicine, University of Duisburg-Essen, Essen, Germany.
  • Hansmann ML; Dr. Senckenberg Institute of Pathology, Goethe University, Frankfurt am Main, Germany.
  • Hartmann S; Dr. Senckenberg Institute of Pathology, Goethe University, Frankfurt am Main, Germany.
Oncotarget ; 7(44): 72197-72210, 2016 Nov 01.
Article en En | MEDLINE | ID: mdl-27708232
Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is an indolent lymphoma, but can transform into diffuse large B cell lymphoma (DLBCL), showing a more aggressive clinical behavior. Little is known about these cases on the molecular level. Therefore, the aim of the present study was to characterize DLBCL transformed from NLPHL (LP-DLBCL) by gene expression profiling (GEP). GEP revealed an inflammatory signature pinpointing to a specific host response. In a coculture model resembling this host response, DEV tumor cells showed an impaired growth behavior. Mechanisms involved in the reduced tumor cell proliferation included a downregulation of MYC and its target genes. Lack of MYC expression was also confirmed in 12/16 LP-DLBCL by immunohistochemistry. Furthermore, CD274/PD-L1 was upregulated in DEV tumor cells after coculture with T cells or monocytes and its expression was validated in 12/19 cases of LP-DLBCL. Thereby, our data provide new insights into the pathogenesis of LP-DLBCL and an explanation for the relatively low tumor cell content. Moreover, the findings suggest that treatment of these patients with immune checkpoint inhibitors may enhance an already ongoing host response in these patients.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedad de Hodgkin / Regulación Neoplásica de la Expresión Génica / Transformación Celular Neoplásica / Proteínas Proto-Oncogénicas c-myc / Linfoma de Células B Grandes Difuso / Inflamación Tipo de estudio: Prognostic_studies Límite: Adult / Aged / Female / Humans / Male / Middle aged Idioma: En Revista: Oncotarget Año: 2016 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedad de Hodgkin / Regulación Neoplásica de la Expresión Génica / Transformación Celular Neoplásica / Proteínas Proto-Oncogénicas c-myc / Linfoma de Células B Grandes Difuso / Inflamación Tipo de estudio: Prognostic_studies Límite: Adult / Aged / Female / Humans / Male / Middle aged Idioma: En Revista: Oncotarget Año: 2016 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos