CD30 antigen in non‐Hodgkin's lymphoma

Miyake, Kenji; Yoshino, Tadashi; Sarker, Ashit Baran; Teramoto, Norihiro; Akagi, Tadaatsu

doi:10.1111/j.1440-1827.1994.tb01706.x

Cited by 12 publications

(9 citation statements)

References 23 publications

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“…The Ki-1 (CD30) antigen is expressed by not only activated cells in non-neoplastic lymphoid tissues but tumor cells of Hodgkin' s disease and various non-Hodgkin' s lymphoma (7). ALCLis characterized by an increased number of the Ki-1 antigen positive cells and was incorporated into the updated Kiel classification (8).…”

Section: Discussionmentioning

confidence: 99%

Ki-1 (CD30)-positive Anaplastic Large Cell Lymphoma, Sarcomatoid Variant Accompanied by Spontaneously Regressing Lymphadenopathy.

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Ki-1 (CD30)-positive Anaplastic Large Cell Lymphoma, Sarcomatoid Variant Accompanied by Spontaneously Regressing Lymphadenopathy.

et al. 1999

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“…1,2,15 The metabolic fate of this membraneanchored receptor is characterized by 2 independent pathways, namely on the one hand the proteolytic cleavage of the CD30 ectodomain (sCD30) and its release into the cell environment and on the other hand the internalization of CD30. 16,17 The latter process is a prerequisite for the cytotoxic activity of anti-CD30 antibody-based immunotoxins toward CD30 ϩ lymphoma cells.…”

Section: Improved Cytotoxic Efficacy Of Ki-3dga By Inhibitor Bb-3644mentioning

confidence: 99%

Inhibition of metalloproteinases enhances the internalization of anti‐CD30 antibody Ki‐3 and the cytotoxic activity of Ki‐3 immunotoxin

Hansen

Matthey

Barth

et al. 2001

Intl Journal of Cancer

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Key words: CD30; metalloproteinase; hydroxamate inhibitor; internalization; immunotoxinCD30 is a 120 kDa type I transmembrane glycoprotein that is strongly expressed on the malignant Hodgkin and Reed-Sternberg (H-RS) cells of HodgkinЈs disease and several non-Hodgkin lymphomas such as the large-cell anaplastic lymphoma and the adult T-cell lymphoma. Normally, CD30 is only expressed on a small population of activated lymphocytes in reactive lymphoid tissue. 1,2 Owing to its restricted distribution, CD30 is regarded as a possible target for the treatment of CD30 ϩ malignancies with anti-CD30 antibody-based immunotoxins. 3,4 Although these immunotoxins can successfully kill CD30 ϩ tumor cells in vitro and in mouse models and were effective in killing residual H-RS cells after successful conventional therapy, 5,6 these constructs alone were not always able to cure patients with bulky tumors. 7 This limitation is in part due to shedding of the target protein, leading to high blood levels of soluble CD30 (sCD30) in active disease, 8,9 thus neutralizing the immunotoxins in the serum and diminishing their binding to the less accessible target cells located in the connective tissue. 10,11 Membrane-anchored CD30 is cleaved by tumor necrosis factor-␣ converting enzyme (TACE), a membrane-anchored metalloproteinase-disintegrin (ADAM), which results in the release of sCD30. 12 This cleavage can be influenced by anti-CD30 antibodies. The binding of most antibodies enhances the sCD30 release, e.g., Ki-1, Ki-2, Ki-3, HeFi-1 or M44. 13 To improve the therapy with immunoconjugates, we tested compounds that inhibit CD30 shedding. We found that the CD30 cleavage was effectively blocked by a panel of hydroxamic acid-based metalloproteinase inhibitors, of which BB-3644 was the most potent. This inhibition caused an increased internalization of Ki-3 MAb and an enhanced cytotoxicity of the anti-CD30 ricin A-chain immunotoxin Ki-3.dgA. MATERIAL AND METHODS Materials and cell cultureThe following anti-CD30 MAbs were used: Ki-1 (␥3,), Ki-2 (␥1,), ). 1,13 We used the synthetic hydroxamate inhibitors ,

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“…In fact, most of these cases may be reclassified as T-cell-marker+ ALCL [ 139]. However, several reports have confirmed the existence of monocyte/histiocytemarker+ and CD30+ THL/ALCL [16,19,22,98]. lt is usually difficult to separate these cases morphologically and biologically from the entities designated as null-celltype or histiocyte-type ALCL.…”

Section: Malignant Histiocytosis and True Histiocytic Lymphoma The Fmentioning

confidence: 94%

“…CD30 would be no exccption. In fact, CD30 has been detected in activatcd histiocytes, THL ceJls (and histiocytc-marker positive ALCL), myeloblastic lcukemia (AML) cells secondary to myelodysplastic syndrome (MDS) as weil as an NK cell line YT, a tri-phcnotypic cell line Deglis and a cell line K562 derived from CML in blast crisis [1,12,16,22,32,95,98]. Deglis ceJls express markers associated with all three lineages (i.e.…”

Section: Lack Of Lineage Specificity Of Most Cytokines and Cytokine Rmentioning

confidence: 99%

Hodgkin's Disease and Anaplastic Large Cell Lymphoma Revisited

Su-Ming¹,

Waldron²,

Xie³

et al. 1996

J Biomed Sci

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The true identity of Hodgkiri's mononuclear cells and Reed-Sternberg (H-RS) cells has been a subject of controversy for decades. Those who believe that Hodgkin's disease (HD) is a heterogeneous discase may consider it to constitute lymphomas of various origins. However, this theory seems incompatible with the finding of similar phenotypic, biologic, and immunologic properties among most HD. We believe that, in the majority of cases, HD, except for LP and some LD-type HD, is a homogeneous disease despite differences in the degree of fibrosis and/or cellular reaction. The heterogeneity in cellular reactions is a result of secrction of various cytokines by H-RS cells, which may or may not be influenced by the presence of EBV. H-RS cells, and anaplastic !arge cell lymphoma (ALCL) cells as well, can express a combination of cytokines and cytokine receptors that is not seen in other types oflymphomas. The unique cytokine/receptor profile ( e.g. the expression of c-kit-RICD 117), along with various properties associated with H-RS/ ALCL cells, leads to a hypothesis that H-RS/ ALCL cells are related to similar lymphohematopoietic progenitor cells with different etiologies and somewhat limited differentiation capacity. A number of H-RS cells may differentiate with limited capacity along the B-cell pathway and may be infected by EBV, which further complicates the biologic and immunologic properties ofthese cells. The majority of H-RS cells may also, however, differentiate along the antigen-presenting dendritic cell pathway, as indicated by the abundant expression of restin, CD 15, CD40, CD54, CD58, CD80, and CD86. The majority of ALCL cells clearly differentiate to T cells, but some may acquire B-cell or histiocyte phenotypes. The progenitor cell hypothesis may explain ( 1) the variable expression of CD 117, CD43, and CD34 as weil as the absence of CD27, CD45 and CD45RA in H-RS cells; (2) the inconsistent and irregular pattems of phenotype and genotype and the various, often very limited, degrees of differentiation among these two types oflymphoma cells; (3) the existence of secondary HD or ALCL associated with rare types of lymphomas or leukemias, or vice versa; (4) the absence of recombinase and of the B-specific transcription factors BSAP; and (5) the frequent expression ofIL- 7 and IL-9 in H-RS cells.

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CD30 antigen in non‐Hodgkin's lymphoma

Cited by 12 publications

References 23 publications

Ki-1 (CD30)-positive Anaplastic Large Cell Lymphoma, Sarcomatoid Variant Accompanied by Spontaneously Regressing Lymphadenopathy.

Ki-1 (CD30)-positive Anaplastic Large Cell Lymphoma, Sarcomatoid Variant Accompanied by Spontaneously Regressing Lymphadenopathy.

Inhibition of metalloproteinases enhances the internalization of anti‐CD30 antibody Ki‐3 and the cytotoxic activity of Ki‐3 immunotoxin

Hodgkin's Disease and Anaplastic Large Cell Lymphoma Revisited

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