ArticleLeukemia2009
CMC-544 (inotuzumab ozogamicin), an anti-CD22 immuno-conjugate of calicheamicin, alters the levels of target molecules of malignant B-cells.
Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
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- Preparing for CAR T cell therapy: patient selection, bridging therapies and lymphodepletion.Nature reviews. Clinical oncology · 2022Review
- Site-selective lysine conjugation methods and applications towards antibody-drug conjugates.Chemical communications (Cambridge, England) · 2021Review
- Combining Biology and Chemistry for a New Take on Chemotherapy: Antibody-Drug Conjugates in Hematologic Malignancies.Current hematologic malignancy reports · 2018Review
- Antibody-drug conjugates: Promising and efficient tools for targeted cancer therapy.Journal of cellular physiology · 2018Review
- Efficacy and resistance of gemtuzumab ozogamicin for acute myeloid leukemia.International journal of hematology · 2013Review
- Article
- Ongoing development of monoclonal antibodies and antibody drug-conjugates in lymphoma.Current oncology reports · 2011Article
- Treatment strategies for nodal and gastrointestinal follicular lymphoma: current status and future development.World journal of gastroenterology · 2010Review
- CD22 EXON 12 deletion as a pathogenic mechanism of human B-precursor leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We studied the effect of CMC-544, the calicheamicin-conjugated anti-CD22 monoclonal antibody, used alone and in combination with rituximab, analyzing the quantitative alteration of target molecules, that is, CD20, CD22, CD55 and CD59, in Daudi and Raji cells as well as in cells obtained from patients with B-cell malignancies (BCM). Antibody inducing direct antiproliferative and apoptotic effect, complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) were tested separately. In Daudi and Raji cells, the CDC effect of rituximab significantly increased within 12 h following incubation with CMC-544. The levels of CD22 and CD55 were significantly reduced (P<0.001 in both cells) after incubation with CMC-544, but CD20 level remained constant or increased for 12 h. Similar results were obtained in cells from 12 patients with BCM. The antiproliferative and apoptotic effect of CMC-544 were greater than that of rituximab. The ADCC of rituximab was not enhanced by CMC-544. Thus, the combination of CMC-544 and rituximab increased the in vitro cytotoxic effect in BCM cells, and sequential administration for 12 h proceeded by CMC-544 was more effective. The reduction of CD55 and the preservation of CD20 after incubation with CMC-544 support the rationale for the combined use of CMC-544 and rituximab.
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