Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The transmembrane receptor CD30 (TNFRSF8) and its ligand CD30L (CD153, TNFSF8) are members of the tumor necrosis factor (TNF) superfamily and display restricted expression in subpopulations of activated T-and B-cells in nonpathologic conditions. CD30 expression is upregulated in various hematological malignancies, including Reed-Sternberg cells in Hodgkin's disease (HD), anaplastic large cell lymphoma (ALCL) and subsets of Non-Hodgkin's lymphomas (NHLs). Increased CD30L expression was found on mast cells within HD tumors and preclinical and clinical studies with compounds targeting the CD30/ CD30L system in HD and ALCL demonstrated therapeutic benefit. Upregulation of CD30 and CD30L is also linked to leukocytes in patients with chronic inflammatory diseases, including lupus erythematosus, asthma, rheumatoid arthritis and atopic dermatitis (AD). Preclinical studies conducted with transgenic mice or biologic compounds suggested important regulatory functions of the CD30-CD30L system in various aspects of the immune system. Such key regulatory roles and their low expression in normal conditions combined with increased expression in malignant tissues provided a strong rationale to investigate CD30 and CD30L as therapeutic targets in hematologic malignancies, autoimmune and inflammatory diseases. In this report, we review the pharmacodynamic effects of specific therapeutic compounds targeting the CD30/CD30L system in preclinical- and clinical studies.
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PMID:Targeting CD30/CD30L in oncology and autoimmune and inflammatory diseases. 1976 74

Anaplastic large-cell lymphomas (ALCLs) are a group of clinically and biologically heterogeneous diseases including the ALK(+) and ALK(-) systemic forms. Whereas ALK(+) ALCLs are molecularly characterized and can be readily diagnosed, specific immunophenotypic or genetic features to define ALK(-) ALCL are missing, and their distinction from other T-cell non-Hodgkin lymphomas (T-NHLs) remains controversial. In the present study, we undertook a transcriptional profiling meta-analysis of 309 cases, including ALCL and other primary T-NHL samples. Pathway discovery and prediction analyses defined a minimum set of genes capable of recognizing ALK(-) ALCL. Application of quantitative RT-PCR in independent datasets from cryopreserved and formalin-fixed paraffin-embedded samples validated a 3-gene model (TNFRSF8, BATF3, and TMOD1) able to successfully separate ALK(-) ALCL from peripheral T-cell lymphoma not otherwise specified, with overall accuracy near 97%. In conclusion, our data justify the possibility of translating quantitative RT-PCR protocols to routine clinical settings as a new approach to objectively dissect T-NHL and to select more appropriate therapeutic protocols.
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PMID:Identification of a 3-gene model as a powerful diagnostic tool for the recognition of ALK-negative anaplastic large-cell lymphoma. 2274 Apr 51

CD30 is a cytokine receptor belonging to the TNF superfamily (TNFRSF8) that acts as a regulator of apoptosis. The presence of CD30 antigen is important in the diagnosis of Hodgkin disease and anaplastic large cell lymphoma. There have been sporadic reports of CD30 expression in nonlymphoid tumors, including malignant mesothelioma. Given the remarkable success of brentuximab vedotin, an antibody-drug conjugate directed against CD30 antigen, in lymphoid malignancies, we undertook a study to examine the incidence of CD30 in mesothelioma and to investigate the ability to target CD30 antigen in mesothelioma. Mesothelioma tumor specimens (N = 83) were examined for CD30 expression by IHC. Positive CD30 expression was noted in 13 mesothelioma specimens, primarily those of epithelial histology. There was no significant correlation of CD30 positivity with tumor grade, stage, or survival. Examination of four mesothelioma cell lines (H28, H2052, H2452, and 211H) for CD30 expression by both FACS analysis and confocal microscopy showed that CD30 antigen localized to the cell membrane. Brentuximab vedotin treatment of cultured mesothelioma cells produced a dose-dependent decrease in cell growth and viability at clinically relevant concentrations. Our studies validate the presence of CD30 antigen in a subgroup of epithelial-type mesothelioma tumors and indicate that selected mesothelioma patients may derive benefit from brentuximab vedotin treatment.
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PMID:CD30 is a potential therapeutic target in malignant mesothelioma. 2558 94

Hodgkin lymphoma is a cancer that can be cured using standard chemotherapy with or without radiation. Although it accounts for only 0.6% of all malignancy worldwide, but it usually affects young adults with median age of 38 years. About 60 to 90% cases can be cured depending on its stage and 5 to 10% cases are refractory to the first-line chemotherapy; while 20 to 30% patients experiencing relapse after receiving the first-line chemotherapy. The relapse causes new problem in treatment. A monoclonal antibody-chemotherapy conjugate, Brentuximab vedotin, was approved by Food Drug Association and European Medicine since 2011 dan was approved by European Medicine Agency since 2012 to treat relapsed classical Hodgkin lymphoma and anaplastic large cell lymphoma (ALCL). Brentuximab vedotin has also been known as anti-CD30.CD30 or Ki-1 or TNFRSF8 is a 120-kD glycoprotein, which is a trans-membrane receptor of Hodgkin lymphoma cells. The glycoprotein was first identified in 1982 using monoclonal antibody against Hodgkin lymphoma-derived cell lines. The glycoprotein was then cloned and recognized as a member of tumor necrosis factor receptor (TNFR) superfamily, which has intracellular, transcellular and extracellular domains. The monoclonal antibody obviously does cause a reaction not only with the Reed-Sternberg (RS) cells of Hodgkin lymphoma, but also with a small number of normal lymphocytes subset, which are located at perifollicular zone as well as lymphoid tumor such as anaplastic large cell lymphoma (ALCL) and other non-lymphoid tumor such as embryonic and pancreas carcinoma, undifferentiated nasopharyngeal carcinoma and malignant melanoma. Therefore, CD30 monoclonal antibody alone to confirm the diagnosis of Hodgkin lymphoma is ineffective as it must be used together with other panel of immunohistochemistry antibodies such as cytokeratins, carcinoma embryonic antigen, melanoma-associated antigen and placental alkaline phosphatide.The expression of CD30 molecules in Reed-Sternberg cells of Hodgkin lymphoma has been demonstrated in over 98% of classical Hodgkin lymphoma cases; however, there is a difference in staining intensity among various cases or even in one case.
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PMID:The Role of Reed-Sternberg CD30 Receptor and Lymphocytes in Pathogenesis of Disease and Its Implication for Treatment. 2995 May 26