Serum levels of the soluble form of CD30 molecule as a tumor marker in CD30+ anaplastic large-cell lymphoma.

Nadali, Gianpaolo; Vinante, Fabrizio; Stein, Harald; Todeschini, Giuseppe; Tecchio, Cristina; Morosato, L.; Chilosi, Marco; Menestrina, Fabio; Kinney, Marsha C.; Jp, Greer

doi:10.1200/jco.1995.13.6.1355

Cited by 58 publications

(36 citation statements)

References 18 publications

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“…It is part of the nerve growth factor/tumor necrosis factor superfamily, and the gene encoding CD30 is found on chromosome 1p36 (11). The CD30 antigen is found in elevated levels in the serum of patients with HD and other CD30-expressing malignancies (12,13).…”

Section: Historical Backgroundmentioning

confidence: 99%

Anaplastic Large Cell Lymphoma: The Shifting Sands of Diagnostic Hematopathology

2001

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Anaplastic large cell lymphoma (ALCL) is a paradigm for the process used to define new disease entities, and provides a model that is applicable to all areas of pathology. ALCL was first recognized based on characteristic histologic features (sinusoidal invasion) and a distinctive immunophenotype (CD30؉). However, neither sinusoidal invasion nor CD30-positivity proved to be entirely specific. Subsequently, a characteristic cytogenetic abnormality was identified, the t(2;5), that led to identification of the genes involved in the translocation (NPM/ALK) and insights into the pathogenesis. Generation of monoclonal antibodies to the aberrantly expressed anaplastic large cell lymphoma kinase (ALK) such as ALK-1 can be used diagnostically, and have led to improved definition of the diagnostic entity with important clinical and prognostic implications. These studies also have clarified the relationship of ALCL to Hodgkin's disease, another lymphoid malignancy associated with CD30 expression. We have learned that the ultimate histologic spectrum of ALCL is both narrower and broader than originally believed. The small cell and lymphohistiocytic variants of ALCL are ALK-positive, and are an accepted part of the disease entity, although the neoplastic cells may appear neither large nor anaplastic. Conversely, most cases of Hodgkin's-like ALCL have proved to be more closely related to true Hodgkin's disease, and are unrelated to ALCL.

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Section: Historical Backgroundmentioning

confidence: 99%

Anaplastic Large Cell Lymphoma: The Shifting Sands of Diagnostic Hematopathology

2001

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“…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.…”

mentioning

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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“…35 The CD30 ligand is expressed on resting B and activated T lymphocytes, and can induce apoptosis in CD30ϩ cell lines. 36 Levels of soluble CD30 are also elevated in ALCL, 37 and may explain the B symptoms that patients with the disease experience. 38,39 Furthermore, elevated soluble CD30 is thought to protect against CD30 ligand-mediated cell death, and may correlate with a poor prognosis.…”

Section: Discussionmentioning

confidence: 99%

Ki-1 anaplastic large-cell lymphoma occurring at the site of ileocolonic anastomosis in a patient treated surgically for colonic adenocarcinoma: Case report and review of the literature

Cooperberg

Fiedler

2001

Annals of Diagnostic Pathology

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Systemic anaplastic large-cell lymphoma is an uncommon type of non-Hodgkin lymphoma characterized by strong expression of the Ki-1 (CD30) antigen. Gastrointestinal involvement typically is less common than in other types of non-Hodgkin's lymphoma. We report a case of CD30-positive anaplastic large-cell lymphoma occurring at the site of colonic anastomosis in an elderly patient who had been treated for colonic adenocarcinoma by right hemicolectomy 10 years previously. The lymphoma was a 2-cm mass composed of large, atypical cells infiltrating the mucosa, submucosa, and muscularis propria. Immunoperoxidase stain was strongly positive for Ki-1, and negative for LeuM1, L26, UCHL1, EMA, and cytokeratin. There have been numerous reports of unusual extranodal presentations of systemic anaplastic large-cell lymphoma; the only previously reported case involving the colon, however, occurred in the context of ulcerative colitis. Anastomotic recurrence is a relatively common complication of surgical therapy for adenocarcinoma, but the recurrent tumors are invariably adenocarcinomas. We are aware of no cases of lymphoma of any type occurring at the site of anastomosis after resection for adenocarcinoma.

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Serum levels of the soluble form of CD30 molecule as a tumor marker in CD30+ anaplastic large-cell lymphoma.

Abstract: sCD30 appears to be a new biologic serum tumor marker of possible use in the clinical setting of CD30+ ALCL.

Cited by 58 publications

References 18 publications

Anaplastic Large Cell Lymphoma: The Shifting Sands of Diagnostic Hematopathology

Anaplastic Large Cell Lymphoma: The Shifting Sands of Diagnostic Hematopathology

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

Ki-1 anaplastic large-cell lymphoma occurring at the site of ileocolonic anastomosis in a patient treated surgically for colonic adenocarcinoma: Case report and review of the literature

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