The purpose of this article is to review the pathologic and clinical spectrum of ALCL, including the borderline with Hodgkin's disease and lymphomatoid papulosis and to discuss the use of the t(2;5) in better defining a more specific molecular pathologic entity within this group of diseases with CD30 expression.
This confirms previous immunohistological data indicating that non-Hodgkin's lymphomas which express the Ki-1 antigen may be of either T-cell or B-cell origin.
In order to contribute to the characterization of the molecular mechanisms of this disease, cDNAs coding for the HD characteristic antigen CD30 were cloned from expression libraries of the human HUT-102 cell line using the monoclonal antibodies Ki-1 and Ber-H2.
We compared the gene expression profiles of ALCL with those of another CD30+ neoplasm, Hodgkin's disease (HD), and found that BCL3 is expressed at higher levels in ALCL than in HD.
Expression and signaling of CD30, a tumor necrosis factor receptor family member, is up-regulated in numerous lymphoid-derived neoplasias, most notably anaplastic large-cell lymphoma (ALCL) and Hodgkin's lymphoma.
The results of this study indicate that Epstein-Barr virus genomes might be identified in more than 50% of the evaluated high grade non-Hodgkin's lymphomas; this association occurred significantly more often in the small noncleaved cell lymphomas resembling endemic Burkitt's lymphoma (60%) and with ALC CD30/BerH2+ lymphomas (77.8%).
Constitutive AP-1 activity and EBV infection induce PD-L1 in Hodgkin lymphomas and posttransplant lymphoproliferative disorders: implications for targeted therapy.
Hodgkin lymphoma (HL) and Anaplastic Large Cell Lymphoma (ALCL), are forms of malignant lymphoma defined by unique morphologic, immunophenotypic, genotypic, and clinical characteristics, but both overexpress CD30.
The CD30 antigen has been characterized as a marker for cultured and primary Hodgkin and Reed-Sternberg cells, and was found to be overexpressed in Hodgkin disease and a subgroup of non-Hodgkin lymphomas including large cell anaplastic lymphomas and Burkitt lymphomas.
CD30 is a member of the tumor necrosis factor receptor superfamily whose expression is up-regulated on anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) cells.
The CD30 expression at Hodgkin and Reed-Sternberg level can give us supplementary information in differential diagnostic and can be used as progressive disease factor.
Histologic features of the patient's biopsy concluded on classical CD15/CD30-positive Hodgkin's disease without expression of Epstein-Barr virus proteins.
Our interest lies in understanding the control of CD30 expression, particularly as its over-expression provides a diagnostic marker for a subset of non-Hodgkin's lymphomas, particularly anaplastic large cell lymphoma (ALCL), and because anti-CD30 treatment has been shown to be efficacious.
Expression of CD30 is a distinct feature of B- or T-cell activation, found in Hodgkin's disease, large cell anaplastic lymphoma, lymphomatoid papulosis, as well as in certain viral infections such as human T-lymphotropic virus type I, HIV, hepatitis B and C virus, and Epstein-Barr virus.
Here, we describe the isolation of viable H/RS cells from HD affected tissues by high gradient magnetic cell sorting (MACS) according to expression of CD30.
In most advanced cancers, except Hodgkin lymphoma (which has high PD-L1/L2 expression) and melanoma (which has high tumor mutational burden), the objective response rate with anti-PD-1/PD-L1 monotherapy is only ~20%, and immune-related toxicities and hyperprogression can occur in a small subset of patients during PD-1/PD-L1 blockade therapy.
Increased levels of serum CD30 are observed in Hodgkin's disease patients and are a good marker for predicting a poor prognosis and a poor response to therapy.