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1. Guerrero MA, Kebebew E: Adrenocortical carcinoma and synchronous malignancies. J Cancer; 2010;1:108-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenocortical carcinoma and synchronous malignancies.
  • OBJECTIVE: Adrenocortical carcinoma (ACC) is an aggressive tumor that accounts for 0.02% of all reported cancers.

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  • (PMID = 20842232.001).
  • [ISSN] 1837-9664
  • [Journal-full-title] Journal of Cancer
  • [ISO-abbreviation] J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Other-IDs] NLM/ PMC2938073
  • [Keywords] NOTNLM ; Adrenocortical carcinoma / Ovarian cancer / Synchronous malignancies / Uterine cancer / and Hereditary syndrome
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2. Kawaguchi Y, Kono K, Mizukami Y, Mimura K, Fujii H: Mechanisms of escape from trastuzumab-mediated ADCC in esophageal squamous cell carcinoma: relation to susceptibility to perforin-granzyme. Anticancer Res; 2009 Jun;29(6):2137-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of escape from trastuzumab-mediated ADCC in esophageal squamous cell carcinoma: relation to susceptibility to perforin-granzyme.
  • BACKGROUND: The escape mechanisms leading to trastuzumab-resistance are under investigation, but no report has yet described the mechanisms of escape from trastuzumab-mediated antibody-dependent cellular cytotoxicity (ADCC).
  • In the present study, the mechanisms of escape from trastuzumab-mediated ADCC were elucidated using esophageal squamous cell carcinoma (SCC) cell clones.
  • MATERIALS AND METHODS: The esophageal SCC cell line TE4, which is highly susceptible to trastuzumab-mediated ADCC, was cloned by limited dilution, resulting in SCC clones with different sensitivities to trastuzumab-mediated ADCC.
  • RESULTS: There was no significant correlation between human epidermal growth factor receptor (HER) 2-expression on the tumor and the sensitivity to trastuzumab-mediated ADCC.
  • Altered major histocompatibility complex (MHC) class I expression treated by IFN-gamma or the blocking of natural killer (NK) cell inhibitory receptors did not induce significant changes in sensitivity to trastuzumab-mediated ADCC.
  • However, the tumor clones with a lower sensitivity to trastuzumab-mediated ADCC showed a reduced susceptibility to the perforin-granzyme system compared to those with a greater sensitivity to trastuzumab-mediated ADCC.
  • CONCLUSION: Lower susceptibility to the perforin-granzyme system is one of the important mechanisms explaining escape from trastuzumab-mediated ADCC.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibody-Dependent Cell Cytotoxicity. Antineoplastic Agents / therapeutic use. Carcinoma, Squamous Cell / immunology. Esophageal Neoplasms / immunology. Granzymes / metabolism. Perforin / metabolism


3. Inagaki A, Ishida T, Yano H, Ishii T, Kusumoto S, Ito A, Ri M, Mori F, Ding J, Komatsu H, Iida S, Ueda R: Expression of the ULBP ligands for NKG2D by B-NHL cells plays an important role in determining their susceptibility to rituximab-induced ADCC. Int J Cancer; 2009 Jul 1;125(1):212-21
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  • [Title] Expression of the ULBP ligands for NKG2D by B-NHL cells plays an important role in determining their susceptibility to rituximab-induced ADCC.
  • Antibody-dependent cellular cytotoxicity (ADCC) is a major antitumor mechanism of action of therapeutic monoclonal antibodies (mAbs).
  • The aim of this study was to identify tumor-associated factors which determine susceptibility to rituximab-induced ADCC.
  • Thirty different CD20+ non-Hodgkin lymphoma cell lines were phenotyped for characteristics such as level of expression of NKG2D ligands, and the influence thereof on susceptibility to rituximab-induced ADCC was established.
  • The present study demonstrated that tumor cell susceptibility to rituximab-induced ADCC was determined by 3 major tumor-associated factors: (i) the amount of the target molecule, CD20;.
  • In conclusion, this is the first report to show the importance for rituximab-induced ADCC of ULBPs expressed on tumor cells.

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  • (PMID = 19358282.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 0 / GPI-Linked Proteins; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I; 0 / Intercellular Signaling Peptides and Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / KLRK1 protein, human; 0 / Membrane Proteins; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / ULBP1 protein, human; 0 / ULBP3 protein, human; 4F4X42SYQ6 / Rituximab; EC 3.4.22.1 / Cathepsin B
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4. Natsume A, Niwa R, Satoh M: Improving effector functions of antibodies for cancer treatment: Enhancing ADCC and CDC. Drug Des Devel Ther; 2009;3:7-16
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  • [Title] Improving effector functions of antibodies for cancer treatment: Enhancing ADCC and CDC.
  • Recently, to improve MAb activity in humans, effector functions have been subjects of focus, especially antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC).
  • For this aim, we have recently developed a successful combination composed of ADCC-enhancing modification by the fucose depletion from Fc-linked oligosaccharides and CDC-enhancing modification by IgG1 and IgG3 isotype shuffling in heavy chains, which could be of great value for the development of third-generation antibody therapeutics.

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  • (PMID = 19920917.001).
  • [ISSN] 1177-8881
  • [Journal-full-title] Drug design, development and therapy
  • [ISO-abbreviation] Drug Des Devel Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2769226
  • [Keywords] NOTNLM ; ADCC / CDC / Fc oligosaccharides / IgG isotypes / effector functions / nonfucosylated IgG
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5. Soon PS, McDonald KL, Robinson BG, Sidhu SB: Molecular markers and the pathogenesis of adrenocortical cancer. Oncologist; 2008 May;13(5):548-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular markers and the pathogenesis of adrenocortical cancer.
  • Adrenal tumors are common, with an estimated incidence of 7.3% in autopsy cases, while adrenocortical carcinomas (ACCs) are rare, with an estimated prevalence of 4-12 per million population.
  • Because the prognoses for adrenocortical adenomas (ACAs) and ACCs are vastly different, it is important to be able to accurately differentiate the two tumor types.
  • Adrenocortical tumors (ACTs) occur as a component of several hereditary tumor syndromes, which include the Li-Fraumeni syndrome, Beckwith-Wiedemann syndrome, multiple endocrine neoplasia 1, Carney complex, and congenital adrenal hyperplasia.
  • The adrenocorticotropic hormone-cAMP-protein kinase A and Wnt pathways are also implicated in adrenocortical tumorigenesis.
  • The aim of this review is to summarize the current knowledge on the molecular mechanisms involved in adrenocortical tumorigenesis, including results of comparative genomic hybridization, loss of heterozygosity, and microarray gene-expression profiling studies.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Adrenocortical Carcinoma / genetics. Neoplastic Syndromes, Hereditary / genetics

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  • (PMID = 18515740.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 135
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6. Chung A, Rollman E, Johansson S, Kent SJ, Stratov I: The utility of ADCC responses in HIV infection. Curr HIV Res; 2008 Nov;6(6):515-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The utility of ADCC responses in HIV infection.
  • There is growing evidence that HIV-specific antibodies that mediate their activity via the Fc-receptor, such as antibody dependent cellular cytotoxicity (ADCC), have an important role in controlling HIV infection.
  • Newer assays are being developed that enable HIV-specific ADCC responses to be finely mapped.
  • In turn, this should allow a more definitive analysis of the effectiveness of HIV-specific ADCC antibodies.
  • However, progressive dysfunction of effector cells that mediate ADCC responses, such as NK cells, combined with immune escape variants that emerge from effective ADCC responses, likely undermine the utility of ADCC responses during chronic HIV infection.
  • Nonetheless the utility of ADCC responses in preventing HIV infection requires urgent consideration.

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  • (PMID = 18991616.001).
  • [ISSN] 1873-4251
  • [Journal-full-title] Current HIV research
  • [ISO-abbreviation] Curr. HIV Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 49
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7. Weitzman J, Betancur M, Boissel L, Rabinowitz AP, Klein A, Klingemann H: Variable contribution of monoclonal antibodies to ADCC in patients with chronic lymphocytic leukemia. Leuk Lymphoma; 2009 Aug;50(8):1361-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Variable contribution of monoclonal antibodies to ADCC in patients with chronic lymphocytic leukemia.
  • Here we determined (i) the extent of antibody-dependent cellular cytotoxicity (ADCC) of four different mAbs against primary CLL cells, (ii) whether ADCC correlates with antigen density on CLL cells, and (iii) whether allogeneic natural killer (NK) cells display superior ADCC than autologous.
  • Effector cells for ADCC were (i) NK-92 cells not expressing FcR, (ii) NK-92 cells transfected with a high-affinity Fc receptor, (iii) autologous NK cells from patients with CLL, (iv) allogeneic NK cells.
  • Results suggest that ADCC contributes to killing of CLL cells by anti-CD20 antibodies (rituximab and veltuzumab), whereas mAbs against CD22 (epratuzumab) and CD23 (lumiliximab) showed minimal ADCC.
  • The magnitude of anti-CD20 mediated ADCC did not correlate with antigen density of CD20.
  • ADCC was not influenced by the FcR genotype expressed by autologous NK cells.

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  • (PMID = 19562616.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD; 0 / Antigens, CD20; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD22 protein, human; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Receptors, IgG; 0 / Recombinant Fusion Proteins; 0 / Sialic Acid Binding Ig-like Lectin 2; 0 / epratuzumab; 0 / lumiliximab; 0 / veltuzumab; 4F4X42SYQ6 / Rituximab
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8. Soon PS, Sidhu SB: Molecular basis of adrenocortical carcinomas. Minerva Endocrinol; 2009 Jun;34(2):137-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular basis of adrenocortical carcinomas.
  • Adrenocortical carcinomas (ACCs) are rare tumors associated with poor prognosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Mutation. Neoplastic Syndromes, Hereditary / genetics

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  • (PMID = 19471238.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Number-of-references] 88
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9. Szabó D, Zsippai A, Bendes M, Tömböl Z, Szabó PM, Rácz K, Igaz P: [Pathogenesis of adrenocortical cancer]. Orv Hetil; 2010 Jul 18;151(29):1163-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pathogenesis of adrenocortical cancer].
  • [Transliterated title] A mellékvesekéreg-carcinoma molekuláris patogenezise.
  • Adrenocortical cancer is a rare tumor with poor prognosis.
  • Whereas most cases occur in a sporadic setting, there are very rare hereditary forms that are important for the understanding of tumor pathogenesis.
  • The hereditary syndromes associated with adrenocortical cancer are: Li-Fraumeni's syndrome, Beckwith-Wiedemann's syndrome and familial adenomatous polyposis, whereas multiple endocrine neoplasia type 1, Carney's complex and McCune-Albright's syndrome mostly predispose to benign adrenocortical tumors.
  • Options for medical treatment of adrenocortical cancer are rather limited.
  • In this study, the pathogenesis of hereditary tumor syndromes, the alterations in sporadic tumors and the most recent molecular-bioinformatical observations are discussed.

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  • (PMID = 20591784.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 67763-97-7 / Insulin-Like Growth Factor II
  • [Number-of-references] 37
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10. Volante M, Buttigliero C, Greco E, Berruti A, Papotti M: Pathological and molecular features of adrenocortical carcinoma: an update. J Clin Pathol; 2008 Jul;61(7):787-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathological and molecular features of adrenocortical carcinoma: an update.
  • The pathological diagnosis of adrenocortical carcinoma (ACC), which is based on gross and microscopic criteria, is subjective.
  • The classification of oncocytic and paediatric adrenocortical tumours is even more challenging, as not all of the above morphological parameters are predictors of malignancy in these tumour types.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Carcinoma / pathology
  • [MeSH-minor] Algorithms. Biomarkers, Tumor / metabolism. Chromosome Aberrations. Diagnosis, Differential. Humans. Immunophenotyping. Neoplastic Syndromes, Hereditary / genetics

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  • (PMID = 18430754.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 75
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11. Shiokawa M, Takahashi T, Murakami A, Kita S, Ito M, Sugamura K, Ishii N: In vivo assay of human NK-dependent ADCC using NOD/SCID/gammac(null) (NOG) mice. Biochem Biophys Res Commun; 2010 Sep 3;399(4):733-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo assay of human NK-dependent ADCC using NOD/SCID/gammac(null) (NOG) mice.
  • One of the mechanisms used by antibodies to kill tumor cells is antibody-dependent cellular cytotoxicity (ADCC), in which natural killer cells (NK) are the main mediator.
  • The capacity to induce ADCC has conventionally been assessed in the human-mouse xeno-graft model, in which human peripheral blood mononuclear cells (PBMC), containing NK cells along with antibodies, are administered to tumor-bearing immunodeficient mice.
  • In this study, we established a new NK-dependent ADCC assay model using a supra-immunodeficient strain of mice, NOD/SCID/gammac(null) (NOG).

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20696130.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
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12. Tamura K, Shimizu C, Koizumi F, Kouno T, Katsumata N, Kinoshita T, Aogi K, Nishio K, Ando M, Fujiwara Y: Correlation of FcγR IIa-H131R and IIIa-V158F polymorphisms and clinical outcome of trastuzumab in both neoadjuvant and metastatic setting in patients with HER-2 positive breast cancer. J Clin Oncol; 2009 May 20;27(15_suppl):1100

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 1100 Background: The antibody dependent cell mediated cytotoxicity (ADCC) affects an efficacy of Immunoglobulin G1 antibody, including trastuzumab which is a humanized anti-HER-2 monoclonal antibody, through fragment C receptor (FcγR) polymorphisms.

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  • (PMID = 27962180.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Cortés J, Baselga J, Petrella T, Gelmon K, Fumoleau P, Verma S, Pivot X, Ross G, Szado T, Gianni L: Pertuzumab monotherapy following trastuzumab-based treatment: Activity and tolerability in patients with advanced HER2- positive breast cancer. J Clin Oncol; 2009 May 20;27(15_suppl):1022

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 1022 Background: Pertuzumab binds to the dimerization epitope of the HER2 receptor, inhibits HER dimerization and signal transduction, and induces ADCC.

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  • (PMID = 27961043.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Valerius T, Dechant M, Lammerts van Bueren JJ, Schneider-Merck T, Berger S, Beyer T, Gramatzki M, Bleeker WK, Parren PW, van de Winkel JG: Effect of the epidermal growth factor receptor antibody panitumumab on triggering of ADCC. J Clin Oncol; 2009 May 20;27(15_suppl):11055

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of the epidermal growth factor receptor antibody panitumumab on triggering of ADCC.
  • Both antibodies had similar binding characteristics, but differed in induction of antibody- dependent cellular cytotoxicity (ADCC).
  • Zalutumumab induced potent MNC-mediated ADCC via FcgRIII (CD16), which was poorly triggered by panitumumab.
  • Interestingly, not only zalutumumab but also panitumumab recruited neutrophils for ADCC.
  • Thus, panitumumab- mediated ADCC was more effective by neutrophils from FcgRIIa-131H homozygous individuals than from -131R individuals.
  • ADCC induced by the IgG1 antibody zalutumumab was not affected by this polymorphism.
  • In an experimental metastasis model in mice, both zalutumumab and panitumumab prevented establishment of metastases at low antibody concentrations which allowed the induction of ADCC but not the inhibition of signalling.
  • Our results may implicate neutrophil- mediated ADCC in the in vivo mechanisms of action of EGF-R- directed antibodies, and suggest that heterogeneity in clinical responses due to the FcgRIIa-131R/H polymorphism can be expected for panitumumab.

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  • (PMID = 27963162.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Lin S, Chiang E, Tsai Y, Lee S, Kuo B, Lin R: Effect of AbGn-7, a glycotope-specific monoclonal antibody, on apoptosis in colon cancer cells and tumor growth in xenograft models. J Clin Oncol; 2009 May 20;27(15_suppl):e15118

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In addition, AbGn-7 elicited potent complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC) in a dose-dependent manner.

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  • (PMID = 27960845.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Barriere J, Fischel J, Formento P, Renée N, Francoual M, Formento J, Chefrour M, Etienne-Grimaldi M, François E, Milano G: Cetuximab-mediated antibody-dependent cellular cytotoxicity (ADCC) against tumor cell lines characterized for EGFR expression and K-ras mutation. J Clin Oncol; 2009 May 20;27(15_suppl):e14583

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cetuximab-mediated antibody-dependent cellular cytotoxicity (ADCC) against tumor cell lines characterized for EGFR expression and K-ras mutation.
  • However, cetuximab is also able to mediate ADCC, which may be part of the clinical response.
  • The aim of this ex-vivo study was to quantify cetuximab-mediated ADCC on various human cancer cell lines characterized for EGFR-expression and K-ras mutation.
  • METHODS: Two K-ras mutated cell lines over-expressing EGFR and resistant to anti-EGFR tyrosine kinase inhibitor were tested (Capan-1 and Capan-2, pancreatic), along with 2 K-ras wild-type cell lines over- expressing EGFR (CAL166, head and neck; A431, epidermoid carcinoma) and an EGFR-negative cell line (OCM1, uveal melanoma).
  • ADCC (<sup>51</sup>Cr release assay) was performed using freshly- isolated peripheral blood mononuclear cells from a healthy donor.
  • RESULTS: Cetuximab mediates ADCC against EGFR-over-expressing cell lines CAL166 (38.4 ± 3.1 %), A431 (13.5 ± 1.7 %), Capan-1 (31.2 ± 0.8 %) and Capan-2 (27.8 ± 8.6 %) irrespective of the K-ras mutational status, but not against EGFR-negative OCM-1 (6.2 ± 1 %).
  • Conversely, unlike IgG1 cetuximab, the anti-EGFR IgG2 panitumumab and the irrelevant antibody rituximab were both unable to induce significant ADCC (< 10 % on all tested cell lines).
  • CONCLUSIONS: Cetuximab-mediated ADCC is independent of the K-ras mutational status of the tumor cell lines.
  • Immunostimulation, as well as new generation anti-EGFR mAbs with improved ability to induce ADCC, may be promising in the management of K-ras-mutated patients.

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  • (PMID = 27963753.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Shimizu C, Tamura K, Koizumi F, Komori O, Pritchard M, Mollah MH, Eguchi S, Fujiwara Y: Prediction of the benefit of trastuzumab (T)-based therapy by the change of gene expression of peripheral blood mononuclear cells (PBMC). J Clin Oncol; 2009 May 20;27(15_suppl):e14578

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Antibody-dependent cell-mediated cytotoxicity (ADCC) is suggested as one of the main mechanism of action of T.

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  • (PMID = 27963657.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Ritesh P, Pahuja S, Chavez J, Braddy W, Skipper M, Bernstein ZP, Chanan-Khan A, Ramanarayanan J, Czuczman MS, Hernandez-Ilizaliturri FJ: Correlation of surface expression of CD11b or CD32 in polymorphonuclear cells (PMNs) and CD69 in natural killer cells (NK) with progression-free survival (PFS) following chemoimmunotherapy with rituximab and liposomal doxorubicin (LD) in patients (pts) with relapsed or refractory B-cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8583

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 8583 Antibody dependent cellular citotoxicity (ADCC) play a significant role in rituximab's anti-tumor activity.
  • Serum or PBMC's were isolated from each patient and used <sup>51</sup>Cr release assays to study rituximab-associated complement mediated cytotoxicity (CMC) or ADCC.
  • Surface expression of CD11b and CD32 in the PMN's correlated with a longer PFS (P = 0.040 and P = 0.015, respectively).There was a non-statistically significant trend towards an improved in PFS in those patients whom their PBMC's exhibited a higher degree of ex-vivo rituximab ADCC.

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  • (PMID = 27962271.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Santin A, Bellone S, El-Sahwi K, Buza N, Tavassoli FA, Silasi D, Azodi M, Schwartz PE, Rutherford TJ, Pecorelli S: Potential therapeutic activity of adecatumumab (MT201), a fully human monoclonal antibody, against epithelial cell adhesion molecule (EpCAM) in uterine serous papillary carcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):e16502

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential therapeutic activity of adecatumumab (MT201), a fully human monoclonal antibody, against epithelial cell adhesion molecule (EpCAM) in uterine serous papillary carcinoma.
  • : e16502 Background: Uterine serous papillary carcinoma (USPC) represents a variant of endometrial cancer characterized by a highly aggressive biologic behavior and inborn resistance to chemotherapy.
  • Sensitivity to MT201 antibody dependent cellular cytotoxicity (ADCC) and complement dependent cytotoxicity (CDC) was tested in standard 4-hour chromium (<sup>51</sup>Cr) release cytotoxicity assays.
  • Importantly, while primary USPC cell lines were highly resistant to natural killer dependent cytotoxicity in vitro, EpCAM positive cell lines were found highly sensitive to MT201-mediated ADCC.
  • CONCLUSIONS: These results demonstrate for the first time high EpCAM expression in uterine serous carcinoma at mRNA and protein levels and high sensitivity to MT201-mediated cytotoxicity in vitro by primary USPC cell lines.

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  • (PMID = 27960768.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Wong A, Mitra S, Gupta P: Targeting brain tumor stem cells using a bispecific antibody directed against CD133+ and EGFRvIII. J Clin Oncol; 2009 May 20;27(15_suppl):2022

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Di-CD133 was the least effective at inducing ADCC.
  • Finally, we studied the ability of the BsAb to induce ADCC on tumor spheres and normal neurospheres.

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  • (PMID = 27964602.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Timmerman J, Betting D, Yamada R, Hurvitz S, Steward K, Said J, van Rooijen N, Kafi K: In vivo activity of rituximab-CpG oligodeoxynucleotide conjugate against rituximab-resistant human CD20+ B-cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8529

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 8529 Background: The anti-CD20 monoclonal antibody rituximab (R) is a mainstay in the treatment of B cell non-Hodgkin's lymphoma (NHL), exerting anti-tumor effects via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity, and apoptosis induction.
  • Toll-like receptor 9 agonist CpG oligodeoxynucleotides (CpG) are potent activators of ADCC and T cell immunity, and have been studied for anti-NHL effects when administered by systemic or intratumoral routes.
  • Mechanistic studies indicated that both natural killer cells and complement participated in the cure of tumors by intratumoral CpG + R, by increasing tumor cell sensitivity to complement and ADCC lysis, and by augmenting the cytotoxicity of ADCC effectors.

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  • (PMID = 27960908.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Rosen L, Gordon MS, Hurwitz HI, Wong MK, Adams BJ, Alvarez D, Seon BK, Leigh BR, Theuer CP: Early evidence of tolerability and clinical activity from a phase I study of TRC105 (anti-CD105 antibody) in patients with advanced refractory cancer. J Clin Oncol; 2009 May 20;27(15_suppl):3518

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • TRC105 is a human/murine chimeric IgG1 anti-CD105 monoclonal antibody that inhibits angiogenesis and tumor growth via endothelial cell growth inhibition, ADCC, and apoptosis.

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  • (PMID = 27961300.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Etienne-Grimaldi M, Bennouna J, Formento J, Douillard J, Francoual M, François E, Faroux R, El Hannani C, Jacob J, Milano G: Prospective pharmacogenetic analysis in advanced colorectal cancer (CRC) patients receiving first-line cetuximab-UFT-irinotecan therapy: Importance of gene polymorphisms related to antibody-dependent cellular cytotoxicity (ADCC). J Clin Oncol; 2009 May 20;27(15_suppl):4069

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prospective pharmacogenetic analysis in advanced colorectal cancer (CRC) patients receiving first-line cetuximab-UFT-irinotecan therapy: Importance of gene polymorphisms related to antibody-dependent cellular cytotoxicity (ADCC).
  • CONCLUSIONS: Present data suggest the importance of ADCC in cetuximab pharmacodynamics, as outlined by the role of FCGR gene polymorphisms on toxicity, responsiveness and survival.

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  • (PMID = 27961604.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. van Berkel PH, Gerritsen J, van Voskuilen E, Perdok G, Vink T, van de Winkel JG, Parren PW: Rapid production of recombinant human IgG With improved ADCC effector function in a transient expression system. Biotechnol Bioeng; 2010 Feb 1;105(2):350-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapid production of recombinant human IgG With improved ADCC effector function in a transient expression system.
  • Rapid production of recombinant human IgG with improved antibody dependent cell-mediated cytotoxicity (ADCC) effector function is presented.
  • IgG1 transiently produced in kifunensine- treated HEK-293F cells has improved affinity for the FcgammaRIIIA molecule as measured in an ELISA based assay, and almost eightfold enhanced ADCC using primary peripheral blood mononuclear effector cells.

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  • [Copyright] 2009 Wiley Periodicals, Inc.
  • (PMID = 19739094.001).
  • [ISSN] 1097-0290
  • [Journal-full-title] Biotechnology and bioengineering
  • [ISO-abbreviation] Biotechnol. Bioeng.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkaloids; 0 / FCGR3A protein, human; 0 / Immunoglobulin G; 0 / Receptors, IgG; 0 / Recombinant Proteins; 109944-15-2 / kifunensine; EC 3.2.1.- / Glycoside Hydrolases
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25. Iida S, Kuni-Kamochi R, Mori K, Misaka H, Inoue M, Okazaki A, Shitara K, Satoh M: Two mechanisms of the enhanced antibody-dependent cellular cytotoxicity (ADCC) efficacy of non-fucosylated therapeutic antibodies in human blood. BMC Cancer; 2009;9:58
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Two mechanisms of the enhanced antibody-dependent cellular cytotoxicity (ADCC) efficacy of non-fucosylated therapeutic antibodies in human blood.
  • BACKGROUND: Antibody-dependent cellular cytotoxicity (ADCC) has recently been identified as one of the critical mechanisms underlying the clinical efficacy of therapeutic antibodies, especially anticancer antibodies.
  • Therapeutic antibodies fully lacking the core fucose of the Fc oligosaccharides have been found to exhibit much higher ADCC in humans than their fucosylated counterparts.
  • However, data which show how fully non-fucosylated antibodies achieve such a high ADCC in human whole blood have not yet been disclosed.
  • The precise mechanisms responsible for the high ADCC mediated by fully non-fucosylated therapeutic antibodies, even in the presence of human plasma, should be explained based on direct evidence of non-fucosylated antibody action in human blood.
  • METHODS: Using a human ex vivo B-cell depletion assay with non-fucosylated and fucosylated anti-CD20 IgG1s rituximab, we monitored the binding of the therapeutic agents both to antigens on target cells (target side interaction) and to leukocyte receptors (FcgammaR) on effector cells (effector side interaction), comparing the intensities of ADCC in human blood.
  • Simple competition for binding to the antigens on target B cells between fucosylated and non-fucosylated anti-CD20s was detected in human blood to cause inhibition of the enhanced ADCC of non-fucosylated anti-CD20 by fucosylated anti-CD20.
  • The core fucosylation levels of individual serum IgG1 from healthy donors was found to be so slightly different that it did not affect the inhibitory effect on the ADCC of fucosylated anti-CD20.
  • CONCLUSION: Our results demonstrate that removal of fucosylated antibody ingredients from antibody therapeutics elicits high ADCC in human blood by two mechanisms: namely, by evading the inhibitory effects both of plasma IgG on FcgammaRIIIa binding (effector side interaction) and of fucosylated antibodies on antigen binding (target side interaction).

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  • (PMID = 19226457.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD20; 0 / Immunoglobulin G; 3713-31-3 / Fucose
  • [Other-IDs] NLM/ PMC2649154
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26. Joshi T, Ganesan LP, Cheney C, Ostrowski MC, Muthusamy N, Byrd JC, Tridandapani S: The PtdIns 3-kinase/Akt pathway regulates macrophage-mediated ADCC against B cell lymphoma. PLoS One; 2009;4(1):e4208
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The PtdIns 3-kinase/Akt pathway regulates macrophage-mediated ADCC against B cell lymphoma.
  • However, the signaling pathways that regulate macrophage-induced ADCC are poorly defined.
  • To understand the regulation of macrophage-mediated ADCC, we used human B cell lymphoma coated with Rituximab as the tumor target and murine macrophages primed with IFNgamma as the effectors.
  • Our data demonstrate that the PtdIns 3-kinase/Akt pathway is activated during macrophage-induced ADCC and that the inhibition of PtdIns 3-kinase results in the inhibition of macrophage-mediated cytotoxicity.
  • Interestingly, downstream of PtdIns 3-kinase, expression of constitutively active Akt (Myr-Akt) in macrophages significantly enhanced their ability to mediate ADCC.
  • Further analysis revealed that in this model, macrophage-mediated ADCC is dependent upon the release of nitric oxide (NO).
  • Taken together, these findings illustrate that the PtdIns 3-kinase/Akt pathway plays a critical role in macrophage ADCC through its influence on conjugate formation between macrophages and antibody-coated tumor cells.

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  • (PMID = 19148288.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA095426; United States / NIAID NIH HHS / AI / R01 AI059406; United States / NCI NIH HHS / CA / R01 CA053271
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 31C4KY9ESH / Nitric Oxide; 4F4X42SYQ6 / Rituximab; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC2615217
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27. Moreno M, Mol BM, von Mensdorff-Pouilly S, Verheijen RH, von Blomberg BM, van den Eertwegh AJ, Scheper RJ, Bontkes HJ: Toll-like receptor agonists and invariant natural killer T-cells enhance antibody-dependent cell-mediated cytotoxicity (ADCC). Cancer Lett; 2008 Dec 8;272(1):70-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Toll-like receptor agonists and invariant natural killer T-cells enhance antibody-dependent cell-mediated cytotoxicity (ADCC).
  • huHMFG-1 (AS1402) is a humanised IgG1 against MUC1, which exerts tumour cell killing through antibody-dependent cellular cytotoxicity (ADCC) mediated by natural killer (NK) cells.
  • Here, we explored the capacity of invariant NKT (iNKT) cells, which are known to activate NK cells, and toll-like receptor (TLR) ligands which activate both iNKT and NK cells, to enhance huHMFG-1-ADCC.

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  • (PMID = 18684557.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / CD69 antigen; 0 / Immunoglobulin G; 0 / Lectins, C-Type; 0 / Mucin-1; 0 / Toll-Like Receptors; 0 / pemtumomab; EC 3.4.21.- / Granzymes
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28. Nakano K, Orita T, Nezu J, Yoshino T, Ohizumi I, Sugimoto M, Furugaki K, Kinoshita Y, Ishiguro T, Hamakubo T, Kodama T, Aburatani H, Yamada-Okabe H, Tsuchiya M: Anti-glypican 3 antibodies cause ADCC against human hepatocellular carcinoma cells. Biochem Biophys Res Commun; 2009 Jan 9;378(2):279-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-glypican 3 antibodies cause ADCC against human hepatocellular carcinoma cells.
  • Glypican 3 (GPC3), a GPI-anchored heparan sulfate proteoglycan, is expressed in the majority of hepatocellular carcinoma (HCC) tissues.
  • All mAbs that induced antibody-dependent cellular cytotoxicity (ADCC) and/or complement-dependent cytotoxicity (CDC) against cells expressing GPC3 recognized the 30-kDa fragment, indicating that the C-terminal region of GPC3 serves as an epitope for mAb with ADCC and/or CDC inducing activities.
  • Chimeric GC33 induced not only ADCC against GPC3-positive human HCC cells but also was efficacious against the Huh-7 human HCC xenograft.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibody-Dependent Cell Cytotoxicity. Carcinoma, Hepatocellular / drug therapy. Glypicans / antagonists & inhibitors. Liver Neoplasms / drug therapy. Neoplasm Proteins / antagonists & inhibitors

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  • (PMID = 19022220.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / GPC3 protein, human; 0 / Glypicans; 0 / Immunodominant Epitopes; 0 / Neoplasm Proteins
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29. Clémenceau B, Congy-Jolivet N, Gallot G, Vivien R, Gaschet J, Thibault G, Vié H: Antibody-dependent cellular cytotoxicity (ADCC) is mediated by genetically modified antigen-specific human T lymphocytes. Blood; 2006 Jun 15;107(12):4669-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antibody-dependent cellular cytotoxicity (ADCC) is mediated by genetically modified antigen-specific human T lymphocytes.
  • In contrast, treatments based on monoclonal antibodies (Abs) have been clinically successful and have demonstrated the clinical relevance of several antigens as therapeutic targets and the importance of the antibody-dependent cellular cytotoxicity (ADCC) pathway.
  • In the present study, we considered the possibility of arming specific T cells with a receptor that would enable them to mediate ADCC.
  • When tested against the autologous B-lymphoblastoid cell line (BLCL) coated with anti-CD20 mAb, the newly expressed Fc receptor enabled the T cells to kill the BLCL through ADCC.

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  • (PMID = 16514054.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, CD; 0 / FCGR3B protein, human; 0 / GPI-Linked Proteins; 0 / Receptors, IgG
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30. Kanda Y, Yamane-Ohnuki N, Sakai N, Yamano K, Nakano R, Inoue M, Misaka H, Iida S, Wakitani M, Konno Y, Yano K, Shitara K, Hosoi S, Satoh M: Comparison of cell lines for stable production of fucose-negative antibodies with enhanced ADCC. Biotechnol Bioeng; 2006 Jul 5;94(4):680-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of cell lines for stable production of fucose-negative antibodies with enhanced ADCC.
  • Several methods have been described to enhance antibody-dependent cellular cytotoxicity (ADCC) using different host cells that produce antibody with reduced levels of fucose on their carbohydrates.
  • Our results demonstrate that FUT8 knockout has the essential characteristics of host cells for robust manufacture of fucose-negative therapeutic antibodies with enhanced ADCC.

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  • [Copyright] (c) 2006 Wiley Periodicals, Inc.
  • (PMID = 16609957.001).
  • [ISSN] 0006-3592
  • [Journal-full-title] Biotechnology and bioengineering
  • [ISO-abbreviation] Biotechnol. Bioeng.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Serum-Free; 0 / DNA, Complementary; 0 / Monosaccharides; 0 / Oligosaccharides; 3713-31-3 / Fucose; EC 2.4.1.- / Fucosyltransferases
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31. Oganesyan V, Damschroder MM, Leach W, Wu H, Dall'Acqua WF: Structural characterization of a mutated, ADCC-enhanced human Fc fragment. Mol Immunol; 2008 Apr;45(7):1872-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structural characterization of a mutated, ADCC-enhanced human Fc fragment.
  • We report here the three-dimensional structure of a human Fc fragment engineered for enhanced antibody dependent cell mediated cytotoxicity (ADCC).

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  • (PMID = 18078997.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 2QL1
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carbohydrates; 0 / Immunoglobulin Fc Fragments; 0 / Immunoglobulin G; 0 / Ligands; 0 / Metals; 0 / Mutant Proteins; 0 / Receptors, IgG
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32. Herbet M, Feige JJ, Thomas M: Insights into the role of genetic alterations in adrenocortical tumorigenesis. Mol Cell Endocrinol; 2009 Mar 5;300(1-2):169-74

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Insights into the role of genetic alterations in adrenocortical tumorigenesis.
  • Whereas benign adrenocortical tumors are frequent in the population, adrenocortical carcinoma (ACC) is a rare cancer.
  • Significant advances in the understanding of the pathogenesis of sporadic ACCs have been possible through the study of hereditary syndromes responsible for ACCs.
  • Progressive transformation of a normal tissue into a benign tumor and ultimately into a carcinoma occurs via accumulation of genetic and epigenetic alterations.
  • This review summarizes the molecular alterations likely involved in the multistage tumorigenesis and describes a mouse model which allows us to evaluate the effect of individual genes or combination of genes in the development of adrenocortical tumors.

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  • (PMID = 19007854.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Number-of-references] 64
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33. Clémenceau B, Gallot G, Vivien R, Gaschet J, Campone M, Vié H: Long-term preservation of antibody-dependent cellular cytotoxicity (ADCC) of natural killer cells amplified in vitro from the peripheral blood of breast cancer patients after chemotherapy. J Immunother; 2006 Jan-Feb;29(1):53-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term preservation of antibody-dependent cellular cytotoxicity (ADCC) of natural killer cells amplified in vitro from the peripheral blood of breast cancer patients after chemotherapy.
  • Results from clinical studies suggest that antibody-dependent cellular cytotoxicity (ADCC) is involved in the clinical response of Herceptin-treated patients.
  • The purpose of the current study was to evaluate the possibility of amplifying in vitro the CD3-/CD16+ natural killer (NK) cell subset that mediates ADCC from breast cancer patients after chemotherapy.
  • These LCL + IL2 activated cultures (ACs) were tested for ADCC potential, and their CD3/CD16 NK proportion was quantified.
  • Control and patient ACs displayed ADCC activity (tested in the presence of Rituximab against the autologous LCL to take into account any possible effect of inhibitory NK receptors) as well as against the MCF-7(Her2/neu) breast cancer cell line in the presence of Herceptin.
  • This ADCC activity was maintained during the entire culture period.
  • In conclusion, chemotherapy in breast cancer patients does not obviate the possibility of amplifying in vitro the NK cell subset that mediates ADCC.
  • Consequently, adoptive transfer of lymphocytes mediating ADCC can be considered using this protocol to test its benefit in patients under Herceptin treatment.

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  • (PMID = 16365600.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Interleukin-2; P188ANX8CK / Trastuzumab
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34. Ito A, Ishida T, Yano H, Inagaki A, Suzuki S, Sato F, Takino H, Mori F, Ri M, Kusumoto S, Komatsu H, Iida S, Inagaki H, Ueda R: Defucosylated anti-CCR4 monoclonal antibody exercises potent ADCC-mediated antitumor effect in the novel tumor-bearing humanized NOD/Shi-scid, IL-2Rgamma(null) mouse model. Cancer Immunol Immunother; 2009 Aug;58(8):1195-206
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Defucosylated anti-CCR4 monoclonal antibody exercises potent ADCC-mediated antitumor effect in the novel tumor-bearing humanized NOD/Shi-scid, IL-2Rgamma(null) mouse model.
  • PURPOSE: There are no suitable small animal models to evaluate human antibody-dependent cellular cytotoxicity (ADCC) in vivo, due to species incompatibilities.
  • Thus, the first aim of this study was to establish a human tumor-bearing mouse model in which human immune cells can engraft and mediate ADCC, but where the endogenous mouse immune cells cannot mediate ADCC.
  • The second aim was to evaluate ADCC mediated in these humanized mice by the defucosylated anti-CC chemokine receptor 4 (CCR4) monoclonal antibody (mAb) which we have developed and which is now in phase I clinical trials.
  • The chimeric defucosylated anti-CCR4 mAb KM2760 showed potent antitumor activity mediated by robust ADCC in these humanized mice bearing the HL or CTCL cell lines.
  • KM2760 significantly increased the number of tumor-infiltrating CD56-positive NK cells which mediate ADCC, and reduced the number of tumor-infiltrating FOXP3-positive regulatory T (Treg) cells in HL-bearing humanized mice.

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  • (PMID = 19048251.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm; 0 / Antigens, CD30; 0 / Receptors, CCR4
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35. Ito A, Ishida T, Utsunomiya A, Sato F, Mori F, Yano H, Inagaki A, Suzuki S, Takino H, Ri M, Kusumoto S, Komatsu H, Iida S, Inagaki H, Ueda R: Defucosylated anti-CCR4 monoclonal antibody exerts potent ADCC against primary ATLL cells mediated by autologous human immune cells in NOD/Shi-scid, IL-2R gamma(null) mice in vivo. J Immunol; 2009 Oct 1;183(7):4782-91

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Defucosylated anti-CCR4 monoclonal antibody exerts potent ADCC against primary ATLL cells mediated by autologous human immune cells in NOD/Shi-scid, IL-2R gamma(null) mice in vivo.
  • There is a lack of suitable small animal models to evaluate human Ab-dependent cellular cytotoxicity (ADCC) in vivo, because of the species incompatibility between humans and animals or due to nonspecific allogeneic immune reactions.
  • To overcome these problems, we established a human tumor-bearing mouse model, using NOD/Shi-scid, IL-2Rgamma(null) (NOG) mice as recipients, in which autologous human immune cells are engrafted and mediate ADCC but in which endogenous murine cells are unable to mediate ADCC.
  • In the present study, we used NOG mice bearing primary adult T cell leukemia/lymphoma (ATLL) cells and a therapeutic chimeric anti-CCR4 mAb, the Fc region of which is defucosylated to enhance ADCC.
  • We report significant antitumor activity in vivo associated with robust ADCC mediated by autologous effector cells from the same patients.
  • Human autologous ADCC in mice in vivo was confirmed by the depletion of human immune cells before ATLL PBMC inoculation.
  • Furthermore, the potent ADCC mediated by defucosylated anti-CCR4 mAb, observed here in vivo in humanized mice, will be exploited in clinical trials in the near future.

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  • (PMID = 19748990.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / CCR4 protein, human; 0 / Interleukin Receptor Common gamma Subunit; 0 / Receptors, CCR4; 3713-31-3 / Fucose
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36. Nattermann J, Schneiders AM, Leifeld L, Langhans B, Schulz M, Inchauspé G, Matz B, Brackmann HH, Houghton M, Sauerbruch T, Spengler U: Serum antibodies against the hepatitis C virus E2 protein mediate antibody-dependent cellular cytotoxicity (ADCC). J Hepatol; 2005 Apr;42(4):499-504
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum antibodies against the hepatitis C virus E2 protein mediate antibody-dependent cellular cytotoxicity (ADCC).
  • BACKGROUND/AIMS: The role of antibody dependent cellular cytotoxicity (ADCC) in HCV infection is unclear at present.
  • Antibodies mediating ADCC are usually directed against viral envelope proteins.
  • As cell surface expression of the HCV envelope E2 protein has been shown, the HCV E2 protein is an especially promising candidate target for ADCC.
  • E2-specific ADCC was observed in patients with acute (n=3/6), self-limited (n=5/11) and chronic (n=13/19) hepatitis C and was closely related to fluorescence intensity in the E2-binding assay (r=0.67, P<0.001).
  • CONCLUSIONS: We conclude that E2-antibodies from all stages of HCV infection can mediate ADCC.

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  • (PMID = 15763336.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hepatitis C Antibodies; 0 / Recombinant Proteins; 0 / Viral Envelope Proteins; 157184-61-7 / glycoprotein E2, Hepatitis C virus
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37. Schlaeth M, Berger S, Derer S, Klausz K, Lohse S, Dechant M, Lazar GA, Schneider-Merck T, Peipp M, Valerius T: Fc-engineered EGF-R antibodies mediate improved antibody-dependent cellular cytotoxicity (ADCC) against KRAS-mutated tumor cells. Cancer Sci; 2010 May;101(5):1080-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fc-engineered EGF-R antibodies mediate improved antibody-dependent cellular cytotoxicity (ADCC) against KRAS-mutated tumor cells.
  • We then investigated whether killing of tumor cells harboring mutated KRAS can be improved by enhancing antibody-dependent cellular cytotoxicity (ADCC).
  • Protein- and glyco-engineering of antibodies' Fc region are established technologies to enhance ADCC by increasing antibodies' affinity to activating Fcgamma receptors.
  • Additionally, cells transfected with mutated KRAS were killed as effectively by ADCC as vector-transfected control cells.
  • Together, these data demonstrate that KRAS mutations are not sufficient to render tumor cells resistant to ADCC.

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  • (PMID = 20331636.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / FCGR3A protein, human; 0 / Immunoglobulin Fc Fragments; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, IgG; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
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38. Kawai S, Koishihara Y, Iida S, Ozaki S, Matsumoto T, Kosaka M, Yamada-Okabe H: Construction of a conventional non-radioisotope method to quantify HM1.24 antigens: correlation of HM1.24 levels and ADCC activity of the humanized antibody against HM1.24. Leuk Res; 2006 Aug;30(8):949-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Construction of a conventional non-radioisotope method to quantify HM1.24 antigens: correlation of HM1.24 levels and ADCC activity of the humanized antibody against HM1.24.
  • A humanized monoclonal antibody (mAb) against HM1.24 (AHM) caused antibody-dependent cellular cytotoxicity (ADCC) against multiple myeloma (MM) cells.
  • More than 10(4) molecules/cell of HM1.24 were detected in 12 out of 14 patients' MM cells, and a linear correlation was found between ADCC by AHM and the amounts of HM1.24.

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  • (PMID = 16473407.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / BST2 protein, human; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; TPY09G7XIR / Fluorescein
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39. Kute TE, Savage L, Stehle JR Jr, Kim-Shapiro JW, Blanks MJ, Wood J, Vaughn JP: Breast tumor cells isolated from in vitro resistance to trastuzumab remain sensitive to trastuzumab anti-tumor effects in vivo and to ADCC killing. Cancer Immunol Immunother; 2009 Nov;58(11):1887-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Breast tumor cells isolated from in vitro resistance to trastuzumab remain sensitive to trastuzumab anti-tumor effects in vivo and to ADCC killing.
  • The observation that in vitro resistant cells are sensitive to trastuzumab in vivo could be explained by antibody dependent cellular cytotoxicity (ADCC).
  • Therefore, both parental and trastuzumab-resistant cells were assayed for ADCC in real time on electroplates with and without trastuzumab in the presence of a natural killer cell line (NK-92), and granulocyte or mononuclear cellular fractions isolated from human peripheral blood.
  • Both trastuzumab-resistant cells and trastuzumab-sensitive cells showed similar susceptibility to ADCC despite displaying divergent growth responses to trastuzumab.
  • These results support a model of trastuzumab tumor cell killing in vivo mediated primarily by ADCC from the mononuclear fraction of innate immune cells and suggest that in the clinical setting not only should changes in signaling transduction pathways be studied in acquired tumor resistance to trastuzumab, but also mechanisms by which tumors impede immune function should be evaluated.

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  • (PMID = 19340424.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab
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40. Kantakamalakul W, Pattanapanyasat K, Jongrakthaitae S, Assawadarachai V, Ampol S, Sutthent R: A novel EGFP-CEM-NKr flow cytometric method for measuring antibody dependent cell mediated-cytotoxicity (ADCC) activity in HIV-1 infected individuals. J Immunol Methods; 2006 Aug 31;315(1-2):1-10
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  • [Title] A novel EGFP-CEM-NKr flow cytometric method for measuring antibody dependent cell mediated-cytotoxicity (ADCC) activity in HIV-1 infected individuals.
  • The cells pulsed with HIV-1 gp120 were then used as target cells for the measurement of antibody dependent cell mediated-cytotoxicity (ADCC) by flow cytometry.
  • Kinetic studies demonstrated that the sum of ADCC activity measured at 1-h and again at 2-h incubations by this flow cytometric method was comparable to the activity at 6 h by the standard chromium (51Cr) release assay (CRA).
  • ADCC activity of HIV-1 seropositive sera measured by this new technique correlated strongly with that of CRA (Pearson's correlation coefficient of 0.832; p-value < 0.001 and intraclass correlation coefficient of 0.903; p-value < 0.001).
  • The EGFP-CEM-NKr stable cell line provides a novel method to measure ADCC activity to HIV-1 gp120 by flow cytometry without pre-staining or pre-labeling target cells.


41. Portnov BA, Barchana M, Dubnov J: Exploratory analysis of potential risk factors of a rare disease: spatial distribution of adrenocortical carcinoma in Israel as a case study. Sci Total Environ; 2009 Feb 15;407(5):1738-43
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  • [Title] Exploratory analysis of potential risk factors of a rare disease: spatial distribution of adrenocortical carcinoma in Israel as a case study.
  • In the present study, the performance of proposed approach is investigated by cross-examination of the spatial patterns of three widespread cancers--lung, larynx and colorectal (CRC)--with that of a rare malignant disease--Adrenocortical Carcinoma (ACC).
  • As the analysis indicates, the spatial distribution of ACC is more likely to be related to hereditary factors than to environmental causes, in accordance with current knowledge about this rare disease.
  • [MeSH-major] Adrenal Cortex Neoplasms / epidemiology. Adrenocortical Carcinoma / epidemiology. Colorectal Neoplasms / epidemiology. Laryngeal Neoplasms / epidemiology. Lung Neoplasms / epidemiology


42. Moreno M, Bontkes HJ, Scheper RJ, Kenemans P, Verheijen RH, von Mensdorff-Pouilly S: High level of MUC1 in serum of ovarian and breast cancer patients inhibits huHMFG-1 dependent cell-mediated cytotoxicity (ADCC). Cancer Lett; 2007 Nov 8;257(1):47-55
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  • [Title] High level of MUC1 in serum of ovarian and breast cancer patients inhibits huHMFG-1 dependent cell-mediated cytotoxicity (ADCC).
  • The huHMFG-1 (AS1402) antibody is a humanised IgG1 directed against MUC1 and is currently in clinical trials for the treatment of breast carcinoma.
  • Here, we have investigated the effects of MUC1 present in sera from breast and ovarian cancer patients and that of NK cells on in vitro huHMFG-1-mediated ADCC, performed with and without the addition of various cytokines.


43. Olivier S, Jacoby M, Brillon C, Bouletreau S, Mollet T, Nerriere O, Angel A, Danet S, Souttou B, Guehenneux F, Gauthier L, Berthomé M, Vié H, Beltraminelli N, Mehtali M: EB66 cell line, a duck embryonic stem cell-derived substrate for the industrial production of therapeutic monoclonal antibodies with enhanced ADCC activity. MAbs; 2010 Jul-Aug;2(4):405-15
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  • [Title] EB66 cell line, a duck embryonic stem cell-derived substrate for the industrial production of therapeutic monoclonal antibodies with enhanced ADCC activity.
  • The experimental control of IgG fucosylation to enhance antibody dependent cell cytotoxicity (ADCC) activity constitutes one of the promising strategies to improve the efficacy of monoclonal antibodies and to potentially reduce the therapeutic cost.
  • Furthermore, mAbs produced on EB66 cells display a naturally reduced fucose content resulting in strongly enhanced ADCC activity.

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  • (PMID = 20562528.001).
  • [ISSN] 1942-0870
  • [Journal-full-title] mAbs
  • [ISO-abbreviation] MAbs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 3713-31-3 / Fucose
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44. Imai-Nishiya H, Mori K, Inoue M, Wakitani M, Iida S, Shitara K, Satoh M: Double knockdown of alpha1,6-fucosyltransferase (FUT8) and GDP-mannose 4,6-dehydratase (GMD) in antibody-producing cells: a new strategy for generating fully non-fucosylated therapeutic antibodies with enhanced ADCC. BMC Biotechnol; 2007;7:84
The Lens. Cited by Patents in .

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  • [Title] Double knockdown of alpha1,6-fucosyltransferase (FUT8) and GDP-mannose 4,6-dehydratase (GMD) in antibody-producing cells: a new strategy for generating fully non-fucosylated therapeutic antibodies with enhanced ADCC.
  • BACKGROUND: Antibody-dependent cellular cytotoxicity (ADCC) is greatly enhanced by the absence of the core fucose of oligosaccharides attached to the Fc, and is closely related to the clinical efficacy of anticancer activity in humans in vivo.
  • Unfortunately, all licensed therapeutic antibodies and almost all currently-developed therapeutic antibodies are heavily fucosylated and fail to optimize ADCC, which leads to a large dose requirement at a very high cost for the administration of antibody therapy to cancer patients.
  • Finally, the stable manufacture of fully non-fucosylated antibodies with enhanced ADCC was confirmed using the converted cells in serum-free fed-batch culture.
  • We also demonstrated that double knockdown of FUT8 and GMD in antibody-producing cells could serve as a new strategy for producing next-generation therapeutic antibodies fully lacking core fucosylation and with enhanced ADCC.

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  • (PMID = 18047682.001).
  • [ISSN] 1472-6750
  • [Journal-full-title] BMC biotechnology
  • [ISO-abbreviation] BMC Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; EC 2.4.1.- / Fucosyltransferases; EC 2.4.1.68 / Glycoprotein 6-alpha-L-fucosyltransferase; EC 4.2.1.- / Hydro-Lyases; EC 4.2.1.47 / GDPmannose 4,6-dehydratase
  • [Other-IDs] NLM/ PMC2216013
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45. Correale P, Marra M, Remondo C, Migali C, Misso G, Arcuri FP, Del Vecchio MT, Carducci A, Loiacono L, Tassone P, Abbruzzese A, Tagliaferri P, Caraglia M: Cytotoxic drugs up-regulate epidermal growth factor receptor (EGFR) expression in colon cancer cells and enhance their susceptibility to EGFR-targeted antibody-dependent cell-mediated-cytotoxicity (ADCC). Eur J Cancer; 2010 Jun;46(9):1703-11
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  • [Title] Cytotoxic drugs up-regulate epidermal growth factor receptor (EGFR) expression in colon cancer cells and enhance their susceptibility to EGFR-targeted antibody-dependent cell-mediated-cytotoxicity (ADCC).
  • Here we have investigated whether the exposure to different cytotoxic drugs may affect the susceptibility of colon cancer cells in vitro to cetuximab immuno-targeting and related lymphokine-activated killer (LAK)-mediated antibody-dependent cell cytotoxicity (ADCC).
  • Five colon cancer cell lines expressing a different k-ras mutational status were evaluated for: (i) EGFR-expression, (ii) susceptibility to LAK cells and (iii) cetuximab-mediated ADCC, before and after exposure to 5-flurouracil (5-FU), gemcitabine (Gem), irinotecan (Iri) alone or in multiple two/three drug combinations.
  • Chemotherapy was able to greatly enhance the sensitivity to either LAK cells or cetuximab-mediated ADCC in all the colon cancer cell lines with a mechanism independent from k-ras status.
  • The results of our study suggest that chemotherapy may enhance cetuximab-mediated immuno-targeting and ADCC thus providing the rationale to design novel immuno-biochemotherapy regimens.

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20399639.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / panitumumab; 0W860991D6 / Deoxycytidine; 7673326042 / irinotecan; B76N6SBZ8R / gemcitabine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
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46. Hatjiharissi E, Xu L, Santos DD, Hunter ZR, Ciccarelli BT, Verselis S, Modica M, Cao Y, Manning RJ, Leleu X, Dimmock EA, Kortsaris A, Mitsiades C, Anderson KC, Fox EA, Treon SP: Increased natural killer cell expression of CD16, augmented binding and ADCC activity to rituximab among individuals expressing the Fc{gamma}RIIIa-158 V/V and V/F polymorphism. Blood; 2007 Oct 1;110(7):2561-4
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased natural killer cell expression of CD16, augmented binding and ADCC activity to rituximab among individuals expressing the Fc{gamma}RIIIa-158 V/V and V/F polymorphism.
  • We observed higher levels of FcgammaRIIIa transcripts among individuals with the FcgammaRIIIa-158 V/V versus V/F or F/F genotype (P < .001); increased cell surface CD16 expression by quantitative flow cytometry on NK cells from individuals expressing at least one valine at FcgammaRIIIa-158 versus F/F (P = .029); as well as augmented rituximab binding and rituximab-mediated, antibody-dependent cellular cytotoxicity (ADCC).
  • These results suggest that individuals expressing at least one valine at FcgammaRIIIa-158 might, in part, have better clinical outcomes due to increased CD16 expression, rituximab binding, and rituximab-mediated ADCC.

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  • (PMID = 17475906.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K23 CA087977; United States / NCI NIH HHS / CA / K23 CA087977-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / FCGR3A protein, human; 0 / Receptors, IgG; 4F4X42SYQ6 / Rituximab
  • [Other-IDs] NLM/ PMC1988936
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47. Rosati R, Cerrato F, Doghman M, Pianovski MA, Parise GA, Custódio G, Zambetti GP, Ribeiro RC, Riccio A, Figueiredo BC, Lalli E: High frequency of loss of heterozygosity at 11p15 and IGF2 overexpression are not related to clinical outcome in childhood adrenocortical tumors positive for the R337H TP53 mutation. Cancer Genet Cytogenet; 2008 Oct;186(1):19-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High frequency of loss of heterozygosity at 11p15 and IGF2 overexpression are not related to clinical outcome in childhood adrenocortical tumors positive for the R337H TP53 mutation.
  • A germline TP53 R337H mutation is present in childhood adrenocortical tumors (ACT) from southern Brazil.

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  • [Copyright] (c)2008 Elsevier Inc. All rights reserved.
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  • (PMID = 18786438.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA063230-13; United States / NCI NIH HHS / CA / R01 CA063230; United States / NCI NIH HHS / CA / CA63230; United States / NCI NIH HHS / CA / R01 CA063230-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 67763-97-7 / Insulin-Like Growth Factor II
  • [Other-IDs] NLM/ NIHMS70916; NLM/ PMC2603647
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48. Ragazzon B, Cazabat L, Rizk-Rabin M, Assie G, Groussin L, Fierrard H, Perlemoine K, Martinez A, Bertherat J: Inactivation of the Carney complex gene 1 (protein kinase A regulatory subunit 1A) inhibits SMAD3 expression and TGF beta-stimulated apoptosis in adrenocortical cells. Cancer Res; 2009 Sep 15;69(18):7278-84
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  • [Title] Inactivation of the Carney complex gene 1 (protein kinase A regulatory subunit 1A) inhibits SMAD3 expression and TGF beta-stimulated apoptosis in adrenocortical cells.
  • Carney complex (CNC) is a hereditary multiple neoplasia syndrome resulting from inactivating mutations of the gene encoding the PKA type I alpha regulatory subunit (PRKAR1A).
  • Primary pigmented nodular adrenocortical disease is the most frequent endocrine tumor of CNC.
  • We used an interference approach to test the effects of PRKAR1A inactivation on PKA and TGFbeta pathways and on apoptosis in adrenocortical cells.
  • Inactivating mutations of PRKAR1A observed in adrenocortical tumors alter SMAD3, leading to resistance to TGFbeta-induced apoptosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / enzymology. Adrenocortical Carcinoma / enzymology. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Smad3 Protein / biosynthesis. Transforming Growth Factor beta / metabolism

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  • (PMID = 19738044.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / SMAD3 protein, human; 0 / Smad3 Protein; 0 / Transforming Growth Factor beta; 1F7A44V6OU / Colforsin; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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49. Gómez-Román VR, Patterson LJ, Venzon D, Liewehr D, Aldrich K, Florese R, Robert-Guroff M: Vaccine-elicited antibodies mediate antibody-dependent cellular cytotoxicity correlated with significantly reduced acute viremia in rhesus macaques challenged with SIVmac251. J Immunol; 2005 Feb 15;174(4):2185-9
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  • Effector cells armed with Abs can eliminate virus-infected target cells by Ab-dependent cellular cytotoxicity (ADCC), an immune mechanism that has been largely overlooked in HIV vaccine development.
  • Here, we show that a prime/boost AIDS vaccine approach elicits potent ADCC activity correlating with protection against SIV in rhesus macaques (Macacca mulatta).
  • Priming with replicating adenovirus type 5 host range mutant-SIV recombinants, followed by boosting with SIV gp120, elicited Abs with ADCC activity against SIV(mac251)-infected cells.
  • In vitro ADCC activity correlated with in vivo reduced acute viremia after a mucosal challenge with pathogenic SIV.
  • Our findings expose ADCC activity as an immune correlate that may be relevant in the rational design of an efficacious vaccine against HIV.

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  • (PMID = 15699150.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Gene Products, env; 0 / Immunoglobulin G; 0 / SAIDS Vaccines; 0 / Vaccines, Synthetic
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50. Kawaguchi Y, Kono K, Mimura K, Sugai H, Akaike H, Fujii H: Cetuximab induce antibody-dependent cellular cytotoxicity against EGFR-expressing esophageal squamous cell carcinoma. Int J Cancer; 2007 Feb 15;120(4):781-7
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  • [Title] Cetuximab induce antibody-dependent cellular cytotoxicity against EGFR-expressing esophageal squamous cell carcinoma.
  • To evaluate the possibility of treatment with antiepidermal growth factor receptor (EGFR) mAb, Cetuximab against esophageal squamous cell carcinoma (SCC), we performed detail analysis of the antibody-dependent cellular cytotoxicity (ADCC) mediated by Cetuximab against esophageal SCC.
  • Esophageal SCC cell lines with various levels of EGFR (n = 8) were evaluated for their Cetuximab-mediated ADCC by (51)Cr-release assay.
  • As a result, Cetuximab was able to induce ADCC against EGFR-expressing esophageal SCC and the activities reflected the degree of EGFR expression on the esophageal SCC.
  • The activities of Cetuximab-mediated ADCC by patients' PBMC were impaired in comparison with those by healthy donors' PBMC.
  • Moreover, the inhibition of transforming growth factor (TGF)-beta could enhance Cetuximab-mediated ADCC against TGF-beta-producing SCC.
  • In conclusion, Cetuximab was able to induce ADCC against EGFR-expressing esophageal SCC.
  • Some modalities aiming at enhancing the Cetuximab-mediated ADCC may be necessary for successful Cetuximab treatment of patients with esophageal SCC.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antibody-Dependent Cell Cytotoxicity / drug effects. Antineoplastic Agents / pharmacology. Carcinoma, Squamous Cell / immunology. Esophageal Neoplasms / immunology. Receptor, Epidermal Growth Factor / immunology

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  • (PMID = 17096332.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Interleukin-2; 0 / TGFB2 protein, human; 0 / Transforming Growth Factor alpha; 0 / Transforming Growth Factor beta2; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
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51. Hara H, Oyama T, Suda K: New criterial for cytologic diagnosis of adenoid cystic carcinoma. Acta Cytol; 2005 Jan-Feb;49(1):43-50
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  • [Title] New criterial for cytologic diagnosis of adenoid cystic carcinoma.
  • OBJECTIVE: To formulate new criteria for adenoid cystic carcinoma (ADCC).
  • STUDY DESIGN: The usefulness of 17 items for a cytologically definitive diagnosis of ADCC was examined.
  • The frequency (- - +++) of the 17 items in 18 cases of ADCC and 10 non-ADCC cases (pleomorphic adenoma, basal cell adenoma, myoepithelioma and epithelial-myoepithelial carcinoma) that displayed mimicking cytology was examined cytologically.
  • The total score for cases of ADCC was compared with that for non-ADCC cases.
  • All cases with a total score of > 21 were ADCC (93.8%).
  • All cases with a total score of < 12 were non-ADCC (87.5%).
  • CONCLUSION: The 17 items appear to be useful as new criteria for ADCC.
  • [MeSH-major] Carcinoma, Adenoid Cystic / diagnosis. Carcinoma, Adenoid Cystic / pathology. Salivary Gland Neoplasms / diagnosis. Salivary Gland Neoplasms / pathology

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  • (PMID = 15717754.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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52. Laoprasopwattana K, Libraty DH, Endy TP, Nisalak A, Chunsuttiwat S, Ennis FA, Rothman AL, Green S: Antibody-dependent cellular cytotoxicity mediated by plasma obtained before secondary dengue virus infections: potential involvement in early control of viral replication. J Infect Dis; 2007 Apr 15;195(8):1108-16
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  • These antibodies may mediate protective effects by means of antibody-dependent cellular cytotoxicity (ADCC), in which virus-specific antibodies bind to the surface of heterologous DV-infected cells and mediate natural killer cell lysis.
  • In the present study, we examined the ability of plasma obtained before secondary DV infection to induce ADCC of DV-infected cells.
  • The ADCC activity in the plasma samples was measured by (51)Cr-release assay, using persistently DV2- or DV3-infected Raji cells as targets.
  • RESULTS: ADCC activity in plasma obtained before secondary infection directly correlated with neutralizing antibody titers, anti-DV immunoglobulin G1 levels, and a multitypic 50% plaque reduction neutralization test pattern.
  • ADCC activity in pre-secondary DV3 infection plasma samples inversely correlated with plasma viremia levels, but no such correlation was seen in pre-secondary DV2 infection plasma samples.
  • ADCC activity did not correlate with disease severity in subsequent secondary DV2 or DV3 infection but was lowest in plasma from patients with dengue hemorrhagic fever due to secondary DV3 infection.
  • CONCLUSIONS: ADCC may contribute to the early control of secondary DV3 viremia in vivo.

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  • (PMID = 17357046.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / K08 AI01729; United States / NIAID NIH HHS / AI / P01 AI34533; United States / NIAID NIH HHS / AI / U19 AI057319
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Immunoglobulin G
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53. Varchetta S, Gibelli N, Oliviero B, Nardini E, Gennari R, Gatti G, Silva LS, Villani L, Tagliabue E, Ménard S, Costa A, Fagnoni FF: Elements related to heterogeneity of antibody-dependent cell cytotoxicity in patients under trastuzumab therapy for primary operable breast cancer overexpressing Her2. Cancer Res; 2007 Dec 15;67(24):11991-9
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  • Preliminary results from a pilot trial on trastuzumab's mechanism of action against operable breast tumors overexpressing Her2 suggested a role for antibody-dependent cell cytotoxicity (ADCC).
  • To examine factors affecting ADCC intensity and variability, we extended this study to the phenotypic and functional analysis of circulating mononuclear cells in 18 patients.
  • ADCC was induced by trastuzumab therapy in 15 of 18 patients (83%).
  • Inability to develop ADCC in three patients did not depend on inadequate levels of trastuzumab because further increase in its concentration in vitro was ineffective.
  • Rather, susceptibility to develop ADCC was fairly predicted by test with trastuzumab before therapy and was correlated to the number of lymphocytes coexpressing CD16 and CD56.
  • Phenotypic analysis at the end of ADCC evaluating down-regulation of CD16, and up-regulation of CD69 and CD107a, confirmed that natural killer (NK) cells and CD56(+) T cells were involved in productive engagement of trastuzumab.
  • Also, the killing efficiency of CD16(+) lymphocytes was influenced by 158 V/F polymorphism of Fc gamma RIII (CD16), whereas variations of CD247 on NK cells were consistent with trends between ADCC before and after therapy.
  • Complete pathologic response was observed in one patient showing ADCC of outstanding intensity, whereas four cases of partial response showed intermediate ADCC; none of the three patients unable to mount ADCC had significant tumor regression.
  • These data indicate that quantity and lytic efficiency of CD16(+) lymphocytes are major factors for ADCC induction by trastuzumab, and confirm that breast cancer responses to short-term trastuzumab monotherapy may depend on involvement of the ADCC mechanism.

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  • (PMID = 18089830.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antineoplastic Agents; 0 / Receptors, IgG; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab
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54. Kim JS, Nag P, Landay AL, Alves M, Cohn MH, Bremer JW, Baum LL: Saliva can mediate HIV-1-specific antibody-dependent cell-mediated cytotoxicity. FEMS Immunol Med Microbiol; 2006 Nov;48(2):267-73
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  • Antiviral substances in saliva responsible for this may include HIV-1-specific antibody-dependent cell-mediated cytotoxicity (ADCC).
  • We evaluated saliva ADCC titers of 62 HIV-1-infected women from the Women's Interagency HIV Study (WIHS) and 55 uninfected individuals.
  • HIV-1-infected women were less likely to have ADCC activity in saliva than in serum or cervical lavage fluid (CVL).
  • 24% of HIV-1-positive women and a similar percentage of uninfected women had HIV-1-specific saliva ADCC activity.
  • A significant amount of saliva ADCC activity in infected women was HIV-gp120-specific.
  • These studies demonstrate that HIV-specific ADCC activity can be present in saliva.

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  • (PMID = 16978244.001).
  • [ISSN] 0928-8244
  • [Journal-full-title] FEMS immunology and medical microbiology
  • [ISO-abbreviation] FEMS Immunol. Med. Microbiol.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / P01 HD40539; United States / NIAID NIH HHS / AI / U01-AI-34993
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / HIV Antibodies; 0 / HIV Envelope Protein gp120; 0 / Immunoglobulin A
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55. García G, Arango M, Pérez AB, Fonte L, Sierra B, Rodríguez-Roche R, Aguirre E, Fiterre I, Guzmán MG: Antibodies from patients with dengue viral infection mediate cellular cytotoxicity. J Clin Virol; 2006 Sep;37(1):53-7
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  • Acute and late convalescent sera (collected at day 5 of disease onset and 1 year later) from dengue fever (DF) and dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS) laboratory confirmed cases, were tested for antibody-dependent cell-mediated cytotoxicity (ADCC) activity using dengue 1 (DENV-1) or dengue 2 (DENV-2) infected cells as target.
  • ADCC activity was detected in acute sera from DHF/DSS but not in sera from DF patients.
  • However, 1 year after illness, ADCC activity was observed in all cases.
  • This preliminary report represents one of the few studies of ADCC in dengue patients and suggests that ADCC could be implicated in dengue pathogenesis.

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  • (PMID = 16787760.001).
  • [ISSN] 1386-6532
  • [Journal-full-title] Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
  • [ISO-abbreviation] J. Clin. Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Viral
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56. Klein JS, Webster A, Gnanapragasam PN, Galimidi RP, Bjorkman PJ: A dimeric form of the HIV-1 antibody 2G12 elicits potent antibody-dependent cellular cytotoxicity. AIDS; 2010 Jul 17;24(11):1633-40
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  • OBJECTIVE: Increasing data support a role for antibody-dependent cellular cytotoxicity (ADCC) in controlling HIV-1 infection.
  • However, given the unusual structure of dimeric 2G12 with two Fc regions, it was not clear whether 2G12 dimer could bind to the CD16 Fc receptor on ADCC effector cells or trigger ADCC.
  • Here we compared the in-vitro ADCC activities of 2G12 monomer and dimer and investigated the effects of including ADCC-enhancing mutations in both forms of 2G12.
  • METHODS: An in-vitro ADCC assay using target cells stably expressing gp160 was developed to evaluate the activities of 2G12 monomer and dimer with and without ADCC-enhancing mutations that increase the CD16-binding affinity of the 2G12 Fc region.
  • RESULTS: Both 2G12 monomer and 2G12 dimer elicited ADCC, although the dimer showed increased potency [lower half-maximal concentration (EC(50))] in triggering ADCC, thus confirming its ability to bind CD16 and trigger ADCC.
  • The ADCC-enhancing mutations improved the ADCC activity of 2G12 monomer more than 2G12 dimer such that their EC(50) values were nearly equal.
  • However, no increase in nonspecific ADCC activity was observed using 2G12 IgGs with these mutations.
  • CONCLUSION: Given the likelihood that ADCC plays a role in protecting against initial infection and/or controlling chronic infection, these data suggest 2G12 dimers and/or addition of ADCC-enhancing mutations could augment the prophylactic and/or therapeutic potential of 2G12.

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  • (PMID = 20597163.001).
  • [ISSN] 1473-5571
  • [Journal-full-title] AIDS (London, England)
  • [ISO-abbreviation] AIDS
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / / ; United States / NIGMS NIH HHS / GM / T32 GM007616; United States / NIGMS NIH HHS / GM / 5 T32 GM07616
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2G12 monoclonal antibody; 0 / Antibodies, Monoclonal; 0 / Cell Adhesion Molecules; 0 / FCGBP protein, human; 0 / FCGR3B protein, human; 0 / GPI-Linked Proteins; 0 / HIV Antibodies; 0 / HIV Envelope Protein gp160; 0 / Immunoglobulin G; 0 / Receptors, IgG; 0 / gp160 protein, Human immunodeficiency virus 1
  • [Other-IDs] NLM/ HHMIMS203683; NLM/ PMC2898891
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57. Kimura H, Sakai K, Arao T, Shimoyama T, Tamura T, Nishio K: Antibody-dependent cellular cytotoxicity of cetuximab against tumor cells with wild-type or mutant epidermal growth factor receptor. Cancer Sci; 2007 Aug;98(8):1275-80
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  • To clarify the mode of antitumor action of cetuximab, we examined antibody-dependent cellular cytotoxicity (ADCC) activity against several tumor cell lines expressing wild-type or mutant EGFR.
  • ADCC activity and complement-dependent cytolysis activity were analyzed using the CytoTox 96 assay.
  • ADCC activities correlated with the EGFR expression value (R = 0.924).
  • ADCC activities were detected against all tumor cell lines, except K562 cells in a manner dependent on the cellular EGFR expression level, whereas complement-dependent cytolysis activity was not detected in any of the cell lines.
  • The ADCC activity mediated by cetuximab was examined in HEK293 cells transfected with wild-type EGFR (293W) and a deletional mutant of EGFR (293D) in comparison with the mock transfectant (293M).
  • ADCC activity was detected in 293W and 293D cells, in a cetuximab dose-dependent manner, but not in 293M cells (<10%).
  • These results indicate that ADCC-dependent antitumor activity results from the degree of affinity of cetuximab for the extracellular domain of EGFR, independent of EGFR mutation status.
  • These results suggest ADCC activity to be one of the modes of therapeutic action of cetuximab and to depend on EGFR expression on the tumor cell surface.

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  • (PMID = 17498200.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Quinazolines; 9007-36-7 / Complement System Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab; S65743JHBS / gefitinib
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58. Epivatianos A, Poulopoulos A, Dimitrakopoulos I, Andreadis D, Nomikos A, Vlahou S, Papazoglou G, Barbatis C: Application of alpha-smooth muscle actin and c-kit in the differential diagnosis of adenoid cystic carcinoma from polymorphous low-grade adenocarcinoma. Oral Oncol; 2007 Jan;43(1):67-76
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  • [Title] Application of alpha-smooth muscle actin and c-kit in the differential diagnosis of adenoid cystic carcinoma from polymorphous low-grade adenocarcinoma.
  • The expression of vimentin, alpha-smooth muscle actin (alpha-SMA) and c-kit in adenoid cystic carcinomas (AdCCs) and polymorphous low-grade adenocarcinomas (PLGAs) was investigated immunohistochemically to evaluate the application of these markers to distinguish AdCCs from PLGAs when the histological features are equivocal.
  • Tissue specimens of AdCCs and of PLGAs, formalin-fixed and paraffin-embedded were retrospectively studied using vimentin, alpha-SMA and c-kit.
  • Positive staining for alpha-SMA was identified in all AdCCs and 25% of PLGAs.
  • The immunoreactivity of c-kit in all positive cases of AdCCs (83%) and PLGAs (41%) was more than 50% and less than 50% of tumor cells respectively.
  • The expression pattern for both alpha-SMA and c-kit, in tubular structures of AdCCs was different of that seen in the same structures in PLGAs.
  • The results of this study support the potential application of alpha-SMA and c-kit as an adjunctive aid in the differential diagnosis of AdCCs from PLGAs.
  • [MeSH-major] Actins / analysis. Adenocarcinoma / diagnosis. Biomarkers, Tumor / analysis. Carcinoma, Adenoid Cystic / diagnosis. Proto-Oncogene Proteins c-kit / analysis. Vimentin / analysis

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  • (PMID = 16807072.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Biomarkers, Tumor; 0 / Cytoskeletal Proteins; 0 / Muscle Proteins; 0 / Smooth muscle protein, human; 0 / Vimentin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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59. Watanabe M, Kono K, Kawaguchi Y, Mizukami Y, Mimura K, Maruyama T, Fujii H: Interleukin-21 can efficiently restore impaired antibody-dependent cell-mediated cytotoxicity in patients with oesophageal squamous cell carcinoma. Br J Cancer; 2010 Feb 2;102(3):520-9
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  • [Title] Interleukin-21 can efficiently restore impaired antibody-dependent cell-mediated cytotoxicity in patients with oesophageal squamous cell carcinoma.
  • BACKGROUND: We previously reported that Trastuzumab- and Cetuximab-mediated antibody-dependent cell-mediated cytotoxicity (ADCC) in cancer patients was impaired in comparison with that in healthy donors because of NK-cell dysfunction.
  • In this study, we evaluated whether IL-21 could improve the impairment of ADCC in patients with oesophageal squamous cell carcinoma (ESCC), as IL-21 was reported to have the ability to activate NK cells.
  • METHODS: We examined Trastuzumab- and Cetuximab-mediated ADCC of peripheral blood mononuclear cells (PBMCs) or of enriched NK cells derived from ESCC patients (n=20) and healthy donors (n=16) in the presence of IL-21.
  • We further analysed ADCC-related molecules (perforin, granzyme-B, and CD247) on NK cells in response to IL-21.
  • RESULTS: Trastuzumab- and Cetuximab-mediated ADCC of PBMCs or of enriched NK cells was enhanced by the addition of IL-21 in a dose-dependent manner and the levels of ADCC enhanced by IL-21 in patients were high enough in comparison with those in healthy donors, paralleling the upregulation of CD247 on NK cells.
  • CONCLUSION: IL-21 could efficiently restore impaired ADCC in ESCC patients with the upregulation of CD247 molecules.
  • [MeSH-major] Antibody-Dependent Cell Cytotoxicity / drug effects. Carcinoma, Squamous Cell / drug therapy. Esophageal Neoplasms / drug therapy. Interleukins / pharmacology

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  • (PMID = 20029417.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Interleukins; 0 / Receptors, Interleukin-21; 0 / interleukin-21; PQX0D8J21J / Cetuximab
  • [Other-IDs] NLM/ PMC2822939
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60. Tang Y, Lou J, Alpaugh RK, Robinson MK, Marks JD, Weiner LM: Regulation of antibody-dependent cellular cytotoxicity by IgG intrinsic and apparent affinity for target antigen. J Immunol; 2007 Sep 1;179(5):2815-23
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  • Ab-dependent cellular cytotoxicity (ADCC) is believed to be a major antitumor mechanism of some anticancer Abs.
  • However, the factors that regulate the magnitude of ADCC are incompletely understood.
  • In this study, we described the relationship between Ab affinity and ADCC.
  • The IgG molecules were tested for their ability to elicit ADCC in vitro against three tumor cell lines with differing levels of HER2/neu expression using unactivated human PBMC from healthy donors as the effector cells.
  • The results demonstrated that both the apparent affinity and intrinsic affinity of the Abs studied regulate ADCC.
  • High-affinity tumor Ag binding by the IgGs led to the most efficient and powerful ADCC.
  • Tumor cells expressing high levels of HER2/neu are more susceptible to the ADCC triggered by Abs than the cells expressing lower amounts of HER2/neu.
  • These findings justify the examination of high affinity Abs for ADCC promotion.

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  • (PMID = 17709495.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 06927; United States / NCI NIH HHS / CA / CA 121033; United States / NCI NIH HHS / CA / CA 50633
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Immunoglobulin G; 0 / Immunoglobulin Variable Region; 0 / Receptors, IgG; EC 2.7.10.1 / Receptor, ErbB-2
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61. Mimura K, Kono K, Takahashi A, Kawaguchi Y, Mizukami Y, Fujii H: Vascular endothelial growth factor partially inhibits the trastuzumab-mediated antibody-dependent cellular cytotoxicity of human monocytes. Oncology; 2007;72(3-4):172-80
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  • In the present study, we investigated whether VEGF affects the antibody-dependent cell-mediated cytotoxicity (ADCC) of human monocytes mediated by trastuzumab.
  • METHODS: HER-2-expressing tumor cell lines (MKN-7, TE-4 and SKOV-3) were evaluated for trastuzumab-mediated ADCC of human monocytes in the presence of VEGF(165).
  • The trastuzumab-mediated, monocyte-derived ADCC were treated with the anti-human blocking VEGF R1 or VEGF R2 mAb.
  • RESULTS: VEGF partially inhibited the ADCC of human monocytes mediated by trastuzumab.
  • The VEGF-induced deficiency of human monocytes for ADCC was completely recovered by the anti-human blocking VEGF R1 mAb, while the anti-VEGF R2 blocking mAb did not have any effect.
  • CONCLUSION: VEGF partially inhibited the ADCC of human monocytes mediated by trastuzumab, and this inhibition was mainly mediated by VEGF R1 (Flt-1).

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  • [Copyright] (c) 2007 S. Karger AG, Basel
  • (PMID = 18097168.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; P188ANX8CK / Trastuzumab
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62. Shitara K: [Potelligent antibodies as next generation therapeutic antibodies]. Yakugaku Zasshi; 2009 Jan;129(1):3-9
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  • Antibody-dependent cellular cytotoxicity (ADCC), a lytic attack on antibody-targeted cells, is triggered upon binding of lymphocyte receptors (FcgammaRs) to the antibody constant region.
  • ADCC is considered to be a major therapeutic function of antibodies.
  • ADCC requires the presence of oligosaccharides in the Fc region and is sensitive to change in the oligosaccharide structure.
  • We have demonstrated that fucose is the most critical IgG1 oligosaccharide component, and the removal of fucose from IgG1 oligosaccharides results in a very significant enhancement of ADCC and anti-tumor activity in vivo.
  • Potelligent antibodies show potent ADCC upon target cells through the effective and antigen-specific activation of NK cells due to augmented binding to FcgammaRIIIa.
  • Moreover, Potelligent antibodies can evade the inhibitory effect of plasma IgG on ADCC through its high FcgammaRIIIa binding.

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  • (PMID = 19122430.001).
  • [ISSN] 0031-6903
  • [Journal-full-title] Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan
  • [ISO-abbreviation] Yakugaku Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies; 0 / FCGR3A protein, human; 0 / Immunoglobulin G; 0 / Oligosaccharides; 0 / Receptors, IgG; 3713-31-3 / Fucose
  • [Number-of-references] 19
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63. Singh I, McConnell I, Dalziel R, Blacklaws BA: Serum containing ovine IgG2 antibody specific for maedi visna virus envelope glycoprotein mediates antibody dependent cellular cytotoxicity. Vet Immunol Immunopathol; 2006 Oct 15;113(3-4):357-66

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Antibody-dependent cell-mediated cytotoxicity (ADCC) specific for maedi visna virus (MVV) has never been described.
  • To determine whether the isotypic restriction of the antibody response is responsible for the lack of ADCC, an ADCC assay was developed using polyclonal serum raised to recombinant MVV ENV protein.
  • The activity of this serum in an ADCC assay was compared to serum from persistently infected sheep.
  • Serum from immunised sheep mediated ADCC reactions whilst no activity was ever seen in persistently infected sheep serum.
  • IgG2 may therefore be the possible effector isotype for ADCC reactions against MVV.
  • Failure of the IgG2 dependent ADCC system in vivo may contribute to the persistence of MVV-infected macrophages in vivo.

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  • (PMID = 16876878.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / DNA, Viral; 0 / Immunoglobulin G; 0 / Recombinant Fusion Proteins; 0 / Viral Envelope Proteins
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64. Masuda K, Kubota T, Kaneko E, Iida S, Wakitani M, Kobayashi-Natsume Y, Kubota A, Shitara K, Nakamura K: Enhanced binding affinity for FcgammaRIIIa of fucose-negative antibody is sufficient to induce maximal antibody-dependent cellular cytotoxicity. Mol Immunol; 2007 May;44(12):3122-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Antibody-dependent cellular cytotoxicity (ADCC) is considered to be an important therapeutic function for clinical efficacy of monoclonal antibodies.
  • Recent studies have revealed two methods to increase binding affinity for FcgammaRIIIa and enhance ADCC more efficiently for antibodies: (i) fucose removal from antibody N-linked complex oligosaccharides and (ii) amino acid mutations in the antibody Fc region.
  • In this study, we compare the biological activities of the methods of generating high ADCC antibodies.
  • We used a fucose-negative antibody and two antibodies with sets of mutations, demonstrated previously to optimally enhance ADCC using the chimeric anti-CD20 antibody, rituximab, as the model.
  • Despite the differences manifested in binding for the FcgammaR, ADCCs were indistinguishable between methods and even when the methods were combined.
  • These results indicate that the affinity of binding to FcgammaRIIIa does not predict ADCC beyond a certain threshold and that each method alone is sufficient to induce maximal ADCC of the antibody.

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  • (PMID = 17379311.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / FCGR3A protein, human; 0 / Receptors, IgG; 3713-31-3 / Fucose
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65. Beum PV, Lindorfer MA, Taylor RP: Within peripheral blood mononuclear cells, antibody-dependent cellular cytotoxicity of rituximab-opsonized Daudi cells is promoted by NK cells and inhibited by monocytes due to shaving. J Immunol; 2008 Aug 15;181(4):2916-24
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  • THP-1 monocytes and PBMC promote shaving, but PBMC also kill antibody-opsonized cells by antibody-dependent cellular cytotoxicity (ADCC), a reaction generally considered to be due to NK cells.
  • We hypothesized that within PBMC, monocytes and NK cells would have substantially different and competing activities with respect ADCC or shaving, thereby either enhancing or inhibiting the therapeutic action of RTX.
  • We measured ADCC and RTX removal from RTX-opsonized Daudi cells promoted by PBMC, or mediated by NK cells and monocytes.
  • NK cells take up RTX and CD20 from RTX-opsonized B cells, and mediate ADCC.
  • PBMC depleted of NK cells show little ADCC activity, whereas PBMC depleted of monocytes have greater ADCC than the PBMC.
  • Pre-treatment of RTX-opsonized B cells with THP-1 cells or monocytes suppresses NK cell-mediated ADCC, and blockade of Fc gammaRI on monocytes or THP-1 cells abrogates their ability to suppress ADCC.
  • Our results indicate NK cells are the principal cells in PBMC that kill RTX-opsonized B cells, and that monocytes can suppress ADCC by promoting shaving.

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  • (PMID = 18684983.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Opsonin Proteins; 4F4X42SYQ6 / Rituximab
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66. Fischer L, Penack O, Gentilini C, Nogai A, Muessig A, Thiel E, Uharek L: The anti-lymphoma effect of antibody-mediated immunotherapy is based on an increased degranulation of peripheral blood natural killer (NK) cells. Exp Hematol; 2006 Jun;34(6):753-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: In patients treated with rituximab and alemtuzumab for lymphomas or CLL, antibody-dependent cellular cytotoxicity (ADCC) is a major mechanism of action.
  • Therefore, assessment of ADCC is mandatory to understand the complex mechanisms leading to the anti-lymphoma effects of monoclonal antibodies (mAb).
  • Due to methodical difficulties, little is yet known about the relevant cell subpopulations and effector mechanisms leading to tumor lysis in ADCC.
  • METHODS: We used a novel flow cytometric assay that detects CD107a as a marker for NK-cell degranulation to characterize and quantify peripheral blood natural killer (NK) cells mediating ADCC in vitro and in vivo.
  • We were able to quantify and characterize the peripheral blood NK cells mediating ADCC.
  • Furthermore, we found that the CD107a assay can also visualize ADCC under clinical conditions as we observed increased numbers of NK cells degranulating in response to CD20(+) lymphoma cell lines in patients with non-Hodgkin's lymphoma treated with rituximab.
  • CONCLUSIONS: We were able to quantify and characterize NK cells mediating ADCC with a new and feasible method.

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  • (PMID = 16728280.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, Differentiation; 0 / Antineoplastic Agents; 0 / Biomarkers; 0 / Lysosomal-Associated Membrane Protein 1; 4F4X42SYQ6 / Rituximab
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67. Chung AW, Rollman E, Center RJ, Kent SJ, Stratov I: Rapid degranulation of NK cells following activation by HIV-specific antibodies. J Immunol; 2009 Jan 15;182(2):1202-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ab-dependent cellular cytotoxicity (ADCC) Abs stimulate NK cell effector functions and play a role in protecting from and controlling viral infections.
  • We characterized ADCC Abs in a cross-sectional cohort of 80 HIV-infected subjects not on antiretroviral therapy.
  • We analyzed ADCC response by killing fluorescently labeled target cells, as well as expression of IFN-gamma and the degranulation marker CD107a from activated NK cells as measured by a novel intracellular cytokine assay.
  • HIV-specific ADCC directed toward Envelope proteins were present in the majority of 80 untreated HIV-infected individuals measured by killing function.
  • Interestingly, there was a poor correlation between ADCC-mediated killing of fluorescently labeled whole Envelope protein-pulsed cell lines and Ab-mediated expression of IFN-gamma by NK cells.
  • However, in contrast to healthy donor NK cells, autologous patient NK cells more effectively degranulated granzyme B in response to ADCC activation.
  • Our studies highlight the complexity of ab-mediated NK cell activation in HIV infection, and suggest new avenues toward studying the utility of ADCC in controlling HIV infection.

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  • (PMID = 19124764.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-(6)-carboxyfluorescein diacetate succinimidyl ester; 0 / Cytokines; 0 / Fluoresceins; 0 / Fluorescent Dyes; 0 / HIV Antibodies; 0 / HIV Antigens; 0 / Succinimides; 0 / env Gene Products, Human Immunodeficiency Virus; 0 / gp140 envelope protein, Human immunodeficiency virus 1
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68. Moga E, Alvarez E, Cantó E, Vidal S, Rodríguez-Sánchez JL, Sierra J, Briones J: NK cells stimulated with IL-15 or CpG ODN enhance rituximab-dependent cellular cytotoxicity against B-cell lymphoma. Exp Hematol; 2008 Jan;36(1):69-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Antibody-dependent cellular cytotoxicity (ADCC) is an important mechanism in the clinical activity of rituximab for treatment of B-cell malignancies.
  • Natural killer (NK) cells, through the activating receptor FcgammaRIIIa (CD16), play a major role in rituximab-mediated ADCC.
  • We have studied the in vitro effect of NK stimulators, such as interleukin-15 (IL-15) and CpG oligodeoxynucleotides A-Class (CpG ODN A), in the enhancement of rituximab-mediated ADCC against B-cell lymphoma.
  • RESULTS: The rituximab-mediated ADCC of IL-15-activated PBMC was twofold compared to unstimulated PBMC (73% +/- 7% vs 37% +/- 5% respectively, p < 0.001).
  • Similarly, rituximab-mediated ADCC was enhanced when PBMC were activated with CpG ODN A as compared to CpG ODN control (61% +/- 11% vs 36% +/- 8%, respectively, p = 0.02).
  • Nevertheless, the ADCC of purified NK cells was increased only with IL-15.
  • NK-depleted PBMC activated with either IL-15 or CpG ODN A showed no ADCC, suggesting that NK are the major effector cells.
  • CONCLUSIONS: IL-15 and CpG ODN A enhance rituximab-mediated ADCC against B-cell lymphoma.
  • Under these conditions, NK cells seem to be the main effector cells mediating ADCC.

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  • (PMID = 17959301.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / CpG ODN 2216; 0 / Interleukin-15; 0 / Oligodeoxyribonucleotides; 4F4X42SYQ6 / Rituximab; 82115-62-6 / Interferon-gamma
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69. Patel D, Guo X, Ng S, Melchior M, Balderes P, Burtrum D, Persaud K, Luna X, Ludwig DL, Kang X: IgG isotype, glycosylation, and EGFR expression determine the induction of antibody-dependent cellular cytotoxicity in vitro by cetuximab. Hum Antibodies; 2010;19(4):89-99
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  • PURPOSE: To evaluate the antibody-dependent cellular cytotoxicity (ADCC) of cetuximab, an anti-epidermal growth factor receptor (EGFR) IgG1 antibody, in vitro.
  • ADCC against a panel of tumor cell lines was evaluated using peripheral blood mononuclear cells or NK cells as effectors and lactate dehydrogenase release as a marker of cell killing.
  • RESULTS: Cetuximab bound with high affinity to FcγRI (EC50 = 0.13 nM) and FcγRIIIa (EC50 = 6 nM) and effectively induced ADCC across multiple tumor cell lines.
  • Panitumumab and aglycosylated cetuximab did not bind to FcγRI or FcγRIIIa nor have ADCC activity even at high effector-target cell ratios, even though the EGFR-binding affinity of cetuximab and panitumumab were shown to be comparable (KD = 87 pM and 83 pM, respectively).
  • The extent of cetuximab-elicited ADCC was associated with the level of EGFR expression on tumor cells.
  • CONCLUSIONS: Cetuximab elicits effective ADCC activity against a wide range of tumor cells in vitro.
  • These findings suggest that ADCC may contribute to the antitumor activity of cetuximab.

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  • (PMID = 21178280.001).
  • [ISSN] 1875-869X
  • [Journal-full-title] Human antibodies
  • [ISO-abbreviation] Hum Antibodies
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Immunoglobulin G; 0 / Immunoglobulin Isotypes; 0 / panitumumab; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
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70. Liu Q, Sun Y, Rihn S, Nolting A, Tsoukas PN, Jost S, Cohen K, Walker B, Alter G: Matrix metalloprotease inhibitors restore impaired NK cell-mediated antibody-dependent cellular cytotoxicity in human immunodeficiency virus type 1 infection. J Virol; 2009 Sep;83(17):8705-12
MedlinePlus Health Information. consumer health - HIV/AIDS in Women.

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  • NK cell cytolysis can be induced directly through diverse receptor families or can be induced indirectly through Fc receptors by antibodies mediating antibody-dependent cellular cytotoxicity (ADCC).
  • ADCC has been implicated in both protection from simian immunodeficiency virus infection and slower progression of HIV-1 disease.
  • ADCC activity declines with advancing infection, and yet the underlying mechanism for this dysfunction has not been defined, nor has it been determined whether the activity can be reconstituted.
  • Here we demonstrate that NK cell-mediated ADCC is severely compromised in chronic HIV infection.
  • The potency of ADCC function was directly correlated with baseline Fc gammaRIIIa receptor (CD16) expression on NK cells.
  • Inhibition of MMPs resulted in increased CD16 expression and augmented ADCC activity in response to antibody-coated target cells.
  • These data suggest that MMP inhibitors may improve NK cell-mediated ADCC, which may provide subjects with an opportunity to harness the cytolytic power of NK cells through naturally occurring nonneutralizing HIV-specific antibodies.

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  • (PMID = 19553339.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI080289; United States / NIAID NIH HHS / AI / R01AI080289-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FCGR3B protein, human; 0 / GPI-Linked Proteins; 0 / HIV Antibodies; 0 / Receptors, IgG; EC 3.4.24.- / Matrix Metalloproteinases
  • [Other-IDs] NLM/ PMC2738177
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71. Niwa R, Sakurada M, Kobayashi Y, Uehara A, Matsushima K, Ueda R, Nakamura K, Shitara K: Enhanced natural killer cell binding and activation by low-fucose IgG1 antibody results in potent antibody-dependent cellular cytotoxicity induction at lower antigen density. Clin Cancer Res; 2005 Mar 15;11(6):2327-36
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  • PURPOSE: Recent studies have revealed that fucose removal from the oligosaccharides of human IgG1 antibodies results in a significant enhancement of antibody-dependent cellular cytotoxicity (ADCC) via improved IgG1 binding to FcgammaRIIIa.
  • In this report, we investigated the relationship between enhanced ADCC and antigen density on target cells using IgG1 antibodies with reduced fucose.
  • EXPERIMENTAL DESIGN: Using EL4 cell-derived transfectants with differential expression levels of exogenous human CC chemokine receptor 4 or human CD20 as target cells, ADCC of fucose variants of chimeric IgG1 antibodies specific for these antigens were measured.
  • We further investigated IgG1 binding to natural killer (NK) cells and NK cell activation during ADCC induction to elucidate the mechanism by which low-fucose IgG1 induces ADCC upon target cells with low antigen expression.
  • RESULTS: Low-fucose IgG1s showed potent ADCC at low antigen densities at which their corresponding high-fucose counterparts could not induce measurable ADCC.
  • The quantitative analysis revealed that fucose depletion could reduce the antigen amount on target cells required for constant degrees of ADCC induction by 10-fold for CC chemokine receptor 4 and 3-fold for CD20.
  • CONCLUSIONS: Our data showed that fucose removal from IgG1 could reduce the antigen amount required for ADCC induction via efficient recruitment and activation of NK cells.

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  • (PMID = 15788684.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, CD56; 0 / CCR4 protein, human; 0 / Immunoglobulin G; 0 / Receptors, CCR4; 0 / Receptors, Chemokine; 3713-31-3 / Fucose
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72. Sun S, Wang Z: ALDH high adenoid cystic carcinoma cells display cancer stem cell properties and are responsible for mediating metastasis. Biochem Biophys Res Commun; 2010 Jun 11;396(4):843-8
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  • [Title] ALDH high adenoid cystic carcinoma cells display cancer stem cell properties and are responsible for mediating metastasis.
  • Here, we aimed to determine whether human adenoid cystic carcinoma (AdCC) also follows CSC model by exploring the CSC properties of AdCC cells expressing high level of ALDH activity.
  • Utilizing in-vivo series transplantation assays, we found ALDH(high) AdCC cells were capable of self-renewal and of generating tumors that recapitulate the heterogeneity of the parental tumor.
  • Utilizing in-vitro assay, we found only ALDH(high) AdCC cells have tumorsphere-forming ability in anchorage-independent cultures.
  • Finally, we showed ALDH(high) AdCC cells possess highly invasive capability and are responsible for mediating metastasis.
  • These findings suggest the existence of a developmental hierarchy within human AdCC and further elucidation of the unique survival mechanism of AdCC derived CSC population may provide novel therapeutic strategies to treat AdCC.
  • [MeSH-major] Aldehyde Dehydrogenase / metabolism. Biomarkers, Tumor / metabolism. Carcinoma, Adenoid Cystic / pathology. Neoplastic Stem Cells / pathology

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  • [Copyright] (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20450887.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 1.2.1.3 / Aldehyde Dehydrogenase
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73. Saghravanian N, Mohtasham N, Jafarzadeh H: Comparison of immunohistochemical markers between adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma. J Oral Sci; 2009 Dec;51(4):509-14
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  • [Title] Comparison of immunohistochemical markers between adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma.
  • Adenoid cystic carcinoma (AdCC) and polymorphous low-grade adenocarcinoma (PLGA) have several common histological and clinicopathological features that may create diagnostic difficulties.
  • In this study, 10 AdCCs, 8 PLGAs, and 5 normal minor salivary glands as a control group were selected.
  • Data analysis showed high expression of CEA, MSA and Ki-67 in AdCCs compared with PLGAs, although CEA expression was limited to luminal cells.
  • The immunoreactivities of EMA and P53 were not helpful for distinguishing between the two tumors, although the EMA expression pattern in AdCCs was limited to luminal cells, whereas it was present in both luminal and non-luminal cells in PLGAs.
  • Thus, immunohistochemistry can be helpful for differential diagnosis of AdCC and PLGA, particularly that for CEA, vimentin, and Ki-67.
  • [MeSH-major] Adenocarcinoma / chemistry. Biomarkers, Tumor. Carcinoma, Adenoid Cystic / chemistry. Salivary Gland Neoplasms / chemistry


74. Tanaka N, Urabe K, Hashitani S, Sakurai K, Urade M: Establishment and characterization of a human adenoid cystic carcinoma cell line forming colonies cultured in collagen gel and transplantable in nude mice. Oncol Rep; 2007 Feb;17(2):335-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment and characterization of a human adenoid cystic carcinoma cell line forming colonies cultured in collagen gel and transplantable in nude mice.
  • We established a new cell line (ACCNS) from human adenoid cystic carcinoma (AdCC) of the maxilla, using tissue culture techniques and it has been successfully subcultured for more than 100 passages during 2 years.
  • Immunohistochemically, ACCNS cells demonstrated expressions of keratin, alpha-smooth muscle actin, vimentin and S-100 protein, similar to those of original AdCC.
  • These findings indicate that ACCNS cells possess the characteristics of AdCC.
  • In addition, inoculation of 4.0x10(6) cells into nude mice developed tumors that were histologically confirmed as undifferentiated carcinoma.
  • Therefore, ACCNS is the first AdCC cell line with tumorigenicity in nude mice.
  • Based on these results, ACCNS provides a useful culture model of AdCC to analyze the biological characteristics and behavior of this tumor.
  • [MeSH-major] Carcinoma, Adenoid Cystic / genetics. Carcinoma, Adenoid Cystic / pathology. Collagen / metabolism. Gene Expression Regulation, Neoplastic. Jaw Neoplasms / genetics

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  • (PMID = 17203170.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 9007-34-5 / Collagen
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75. Opocher G, Schiavi F, Cicala MV, Patalano A, Mariniello B, Boaretto F, Zovato S, Pignataro V, Macino B, Negro I, Mantero F: Genetics of adrenal tumors. Minerva Endocrinol; 2009 Jun;34(2):107-21
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  • Less well understood is the genetics of adrenal cortex tumors, in particular adrenocortical carcinoma, a rare and particularly aggressive disease.
  • There are only a few examples of hereditary transmission of adrenocortical carcinoma, but the analysis of low penetrance genes by genome wide association study may enable us to discover new genetic mechanisms responsible for adrenocortical-derived tumors.
  • [MeSH-minor] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Genetic Predisposition to Disease. Genomics. Humans. Neoplasm Proteins / genetics. Paraganglioma / genetics

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  • (PMID = 19471236.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Number-of-references] 81
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76. Qu YH, Li Y: [Progress of study on antitumor effects of antibody dependent cell mediated cytotoxicity--review]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Oct;18(5):1370-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In recent years, as increasing of monoclonal antibody application in clinic, the antitumor effect of antibody dependent cell-mediated cytotoxicity (ADCC) get increasing attention.
  • The natural killer (NK) cells are the most important effector cells mediating specific antitumor of ADCC; the phagocytes, T-cells and granulocytes have the definite effect on antitumor of ADCC.
  • ADCC is confirmed as the important mechanism and means for clinically treating the cancers with monoclonal antibodies.
  • The IgG antibody firstly combines with target cells (tumor cells) through antigen-binding sites, and then FcγR on effector cells identifies its Fc fragment and mediates ADCC.
  • Today many kinds of monoclonal antibodies have been put into clinical application such as rituximab and other new anti-CD20 monoclonal antibodies including trastuzumab, erbitux, cetuximab, edrecolomab, nimotuzumab, gemtuzumab ozogamicin and so on, which all can mediate ADCC.
  • The antitumor effects of ADCC mediated by monoclonal antibody can be influenced by IgG Fc receptor gene polymorphism, tumor cell antigen, serum antibody levels, cytokines and drugs etc.
  • As to peripheral blood mononuclear cells, ADCC efficacies of FcγRIIIa-158V/V and FcγRIIa-131H/H are higher than that of other genotypes, while increasing the level of tumor antigen and decreasing the level of serum antibody or adding some cytokines (IL-2, IL-21, IL-15, etc) may elevate the ADCC effect mediated by monoclonal antibodies.
  • Avoiding use of certain drugs (dexamethasone, TNF antagonist) or appropriately using of ondansetron and clemastine also can enhance the anti-tumor effect of ADCC mediated by monoclonal antibodies.
  • In short, ADCC is very important in clinical application for anti-tumor treatment, but its efficacy may be impacted by multiple factors.In this article, the killing mechanisms of ADCC, the clinical use of monoclonal antibodies with antitumor effect of ADCC, the factors influencing anti-tumor efficacy of ADCC, and the antitumor effects of ADCC by other cells are reviewed.

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  • (PMID = 21129296.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
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77. Wang SY, Racila E, Taylor RP, Weiner GJ: NK-cell activation and antibody-dependent cellular cytotoxicity induced by rituximab-coated target cells is inhibited by the C3b component of complement. Blood; 2008 Feb 01;111(3):1456-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Antibody-dependent cellular cytotoxicity (ADCC) and complement fixation both appear to play a role in mediating antitumor effects of monoclonal antibodies (mAbs), including rituximab.
  • We evaluated the relationship between rituximab-induced complement fixation, natural killer (NK)-cell activation, and NK cell-mediated ADCC.
  • C5-depleted serum blocked NK cell-mediated ADCC.
  • These data suggest that C3b deposition induced by rituximab-coated target cells inhibits the interaction between the rituximab Fc and NK-cell CD16, thereby limiting the ability of rituximab-coated target cells to induce NK activation and ADCC.
  • Further studies are needed to define in more detail the impact of complement fixation on ADCC, and whether mAbs that fail to fix complement will be more effective at mediating ADCC.

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  • [Cites] Cancer Sci. 2006 Jan;97(1):80-3 [16367925.001]
  • [Cites] J Clin Invest. 2006 Feb;116(2):512-20 [16453025.001]
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  • (PMID = 18024795.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097274; United States / NCI NIH HHS / CA / P50 CA97274
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, Protozoan; 0 / Antigens, Surface; 0 / C5 phagosomal antigen, Paramecium multimicronucleatum; 0 / Macrophage-1 Antigen; 0 / Receptors, IgG; 126547-89-5 / Intercellular Adhesion Molecule-1; 4F4X42SYQ6 / Rituximab; 80295-33-6 / Complement C1q; 80295-43-8 / Complement C3b
  • [Other-IDs] NLM/ PMC2214766
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78. Binyamin L, Alpaugh RK, Hughes TL, Lutz CT, Campbell KS, Weiner LM: Blocking NK cell inhibitory self-recognition promotes antibody-dependent cellular cytotoxicity in a model of anti-lymphoma therapy. J Immunol; 2008 May 1;180(9):6392-401
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  • Human NK cells lyse Ab-coated target cells through the process of Ab-dependent cellular cytotoxicity (ADCC).
  • Improving ADCC responses is desirable because it is thought to be an important antitumor mechanism for some Abs.
  • Accordingly, we enhanced ADCC responses by blocking NK cell inhibitory receptors, thus perturbing induction of the self-recognition signal.
  • The results show, for the first time, that disruption of inhibitory self-recognition can efficiently promote ADCC in a human model, applying an autologous system in which physiologic checkpoints are in place.
  • This method provides an alternative approach to potentiate the therapeutic benefit of antitumor Abs that mediate ADCC.

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  • (PMID = 18424763.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 06927; United States / NCI NIH HHS / CA / CA 50633; United States / NCI NIH HHS / CA / R01 CA050633; United States / NCI NIH HHS / CA / CA050633-19A1; United States / NIAID NIH HHS / AI / R01 AI050656; United States / NCI NIH HHS / CA / R01 CA050633-19A1; United States / NCI NIH HHS / CA / R01 CA083859; United States / NCI NIH HHS / CA / CA 083859; United States / NIAID NIH HHS / AI / AI 050656; United States / NCI NIH HHS / CA / P30 CA006927
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Receptors, KIR; 4F4X42SYQ6 / Rituximab
  • [Other-IDs] NLM/ NIHMS163662; NLM/ PMC2810560
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79. van Meerten T, van Rijn RS, Hol S, Hagenbeek A, Ebeling SB: Complement-induced cell death by rituximab depends on CD20 expression level and acts complementary to antibody-dependent cellular cytotoxicity. Clin Cancer Res; 2006 Jul 1;12(13):4027-35
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  • Complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) are thought to be important effector mechanisms, but the exact mechanism of rituximab-mediated cell kill is still unknown.
  • Importantly, no data have been reported on the combined contribution of CDC and ADCC.
  • This set of cells, with the CD20 molecule as the only variable, was used to study the importance of CD20 expression level on rituximab-mediated CDC, ADCC, and the combination.
  • RESULTS: We show a sigmoidal correlation of CD20 expression level and rituximab-mediated killing via CDC but not ADCC.
  • Furthermore, CDC and ADCC act simultaneously and CDC-resistant cells are sensitive to ADCC and vice versa.
  • CONCLUSIONS: These findings suggest that CDC depends on CD20 expression level and that both CDC and ADCC act complementary.

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  • (PMID = 16818702.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigen-Antibody Complex; 0 / Antigens, CD20; 4F4X42SYQ6 / Rituximab
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80. Iida S, Misaka H, Inoue M, Shibata M, Nakano R, Yamane-Ohnuki N, Wakitani M, Yano K, Shitara K, Satoh M: Nonfucosylated therapeutic IgG1 antibody can evade the inhibitory effect of serum immunoglobulin G on antibody-dependent cellular cytotoxicity through its high binding to FcgammaRIIIa. Clin Cancer Res; 2006 May 1;12(9):2879-87
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  • PURPOSE: Recent studies have revealed that fucosylated therapeutic IgG1s need high concentrations to compensate for FcgammaRIIIa-competitive inhibition of antibody-dependent cellular cytotoxicity (ADCC) by endogenous human plasma IgG.
  • Here, we investigated whether ADCC of nonfucosylated therapeutic IgG1 is also influenced by plasma IgG in the same way as fucosylated IgG1s.
  • EXPERIMENTAL DESIGN: Ex vivo ADCC upon CD20+ human B cells was induced by incubation of human whole blood with nonfucosylated and/or fucosylated anti-CD20 IgG1s rituximab, and quantified by measuring the remaining CD19+ human B cells using flow cytometry.
  • In contrast, nonfucosylated anti-CD20 reached saturated ADCC at lower concentrations (0.01-0.1 microg/mL) with much higher efficacy than fucosylated anti-CD20 in all nine donors through improved FcgammaRIIIa binding.
  • CONCLUSIONS: Our data showed that nonfucosylated IgG1, not including fucosylated counterparts, can evade the inhibitory effect of plasma IgG on ADCC through its high FcgammaRIIIa binding.
  • Hence, nonfucosylated IgG1 exhibits strong therapeutic potential through dramatically enhanced ADCC at low doses in humans in vivo.

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  • (PMID = 16675584.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 0 / FCGR3A protein, human; 0 / Immunoglobulin G; 0 / Receptors, IgG; 3713-31-3 / Fucose; 4F4X42SYQ6 / Rituximab; EC 2.7.10.1 / Receptor, ErbB-2
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81. Marchiò C, Weigelt B, Reis-Filho JS: Adenoid cystic carcinomas of the breast and salivary glands (or 'The strange case of Dr Jekyll and Mr Hyde' of exocrine gland carcinomas). J Clin Pathol; 2010 Mar;63(3):220-8
MedlinePlus Health Information. consumer health - Salivary Gland Cancer.

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  • Adenoid cystic carcinoma (AdCC) is a tumour with myoepithelial differentiation and characterised by the presence of a dual population of basaloid and luminal cells arranged in specific growth patterns.
  • However, the clinical behaviour of salivary gland and breast AdCC differs; while salivary gland lesions have a relatively high proclivity to metastasise, patients with breast AdCCs have an excellent outcome.
  • Here the clinical, morphological and molecular features, and potential therapeutic targets of salivary gland and breast AdCCs are reviewed.
  • [MeSH-major] Breast Neoplasms / diagnosis. Carcinoma, Adenoid Cystic / diagnosis. Salivary Gland Neoplasms / diagnosis

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  • (PMID = 20203221.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 113
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82. Triozzi PL, Shah JJ, Wang WQ, Aldrich W, Edberg JC, Su K, Carlisle R, Conry R, LoBuglio AF, Forero A: Anti-GD3 monoclonal antibody effects on lymphocytes and antibody-dependent cellular cytotoxicity. Cancer Biother Radiopharm; 2006 Dec;21(6):553-60
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  • DESIGN: Anti-GD3 complement-mediated (CMC) and antibody-dependent cellular cytotoxicity (ADCC) were tested against cell line Mel-624.
  • The effect of antibody and antibody-treated lymphocyte supernates on effector cell ADCC and Fc receptor expression were evaluated.
  • RESULTS: R24 and KW-2871 antibodies mediated CMC and ADCC to the Mel-624 cell line.
  • Preincubation of effector cells with either antibody inhibited ADCC and reduced monocyte expression of FcgammaRI and II.
  • Supernates of effector cells preincubated with either antibody were able to inhibit ADCC.
  • CONCLUSIONS: R24 and KW-2871 antibody differ in their lymphocyte proliferation and lymphokine release activity but have similar inhibition of lymphocyte ADCC and FcgammaR expression in vitro.

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  • (PMID = 17257070.001).
  • [ISSN] 1084-9785
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cytokines; 0 / Gangliosides; 0 / RNA, Messenger; 0 / Receptors, Fc; 62010-37-1 / ganglioside, GD3
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83. Flieger D, Varvenne M, Kleinschmidt R, Schmidt-Wolf IG: Influence of immunomodulatory drugs on the cytotoxicity induced by monoclonal antibody 17-1A and interleukin-2. Cell Immunol; 2007 Mar;246(1):26-33

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Therefore, we investigated with a flowcytometric cytotoxicity assay the effect of several immunomodulatory drugs on antibody dependent cellular cytotoxicity (ADCC), interleukin-2 (IL-2) induced cytotoxicity and IL-2-induced-ADCC.
  • We found that dexamethasone markedly inhibited the IL-2 induced cytotoxicity and the IL-2-induced-ADCC.
  • Ondansetron, a 5-HT-3 serotonin receptor antagonist augmented significantly ADCC.
  • Clemastine, a histamine type-2 receptor antagonist augmented the IL-2-induced-ADCC.
  • The TNF antagonist thalidomide suppressed ADCC whereas pentoxifylline proved to be ineffective.
  • According to our in vitro data the other drugs tested did not have a negative impact on cellular cytotoxicity and ADCC.

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  • (PMID = 17562330.001).
  • [ISSN] 0008-8749
  • [Journal-full-title] Cellular immunology
  • [ISO-abbreviation] Cell. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Edrecolomab; 0 / Immunologic Factors; 0 / Interleukin-2
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84. Kurai J, Chikumi H, Hashimoto K, Yamaguchi K, Yamasaki A, Sako T, Touge H, Makino H, Takata M, Miyata M, Nakamoto M, Burioka N, Shimizu E: Antibody-dependent cellular cytotoxicity mediated by cetuximab against lung cancer cell lines. Clin Cancer Res; 2007 Mar 1;13(5):1552-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, we investigated the antibody-dependent cellular cytotoxicity (ADCC) activity of cetuximab against lung cancer cell lines.
  • EXPERIMENTAL DESIGN: We studied the correlation between EGFR expression in lung cancer cell lines and the ADCC activity of cetuximab as well as the influence of interleukin-2 and chemotherapy on the ADCC activity.
  • The ADCC activity was assessed by a 4-h (51)Cr release assay.
  • RESULTS: Fresh peripheral blood mononuclear cells exhibited cetuximab-mediated ADCC activity against lung cancer cell lines at a low concentration of cetuximab (0.25 microg/mL).
  • A logarithmic correlation was observed between the number of EGFRs and ADCC activity.
  • Even low EGFR expression, which was weakly detectable by immunohistochemistry, was sufficient for maximum ADCC activity, and further increases in EGFR expression on the target cells had no further effect on the ADCC activity.
  • In addition, ADCC activity was enhanced by interleukin-2 mainly through activation of NK cells and was less susceptible to immunosuppression by chemotherapy than NK activity in lung cancer patients.
  • CONCLUSIONS: These observations suggest the importance of ADCC activity as an immunologic mechanism of cetuximab in biological therapy for lung cancer patients.

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  • (PMID = 17332301.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
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85. Ide F, Mishima K, Yamada H, Saito I: Adenoid cystic carcinoma ex pleomorphic adenoma of the parotid gland. Head Neck Pathol; 2009 Jun;3(2):159-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenoid cystic carcinoma ex pleomorphic adenoma of the parotid gland.
  • There is a considerable variation in the histologic subtype of epithelial malignancies among carcinoma ex pleomorphic adenomas (CXPA) and virtually any known carcinoma entity can develop.
  • To our knowledge, adenoid cystic carcinoma (AdCC) ex PA is quite rare despite the fact that de novo AdCC is the fourth most common salivary gland malignancy.
  • We describe a new case of AdCC ex PA in the parotid gland of a 62 year-old woman.
  • Although most of the reported cases are considered low-grade, evidence is presented here that AdCC can take the form of a high-grade malignancy in PA.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Carcinoma, Adenoid Cystic / pathology. Parotid Neoplasms / pathology

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  • (PMID = 19644550.001).
  • [ISSN] 1936-0568
  • [Journal-full-title] Head and neck pathology
  • [ISO-abbreviation] Head Neck Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Adenoid cystic carcinoma / Carcinoma ex pleomorphic adenoma / High-grade malignancy / Parotid gland
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86. Horner H, Frank C, Dechant C, Repp R, Glennie M, Herrmann M, Stockmeyer B: Intimate cell conjugate formation and exchange of membrane lipids precede apoptosis induction in target cells during antibody-dependent, granulocyte-mediated cytotoxicity. J Immunol; 2007 Jul 1;179(1):337-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The production of reactive oxygen intermediates (ROI) has been observed to occur during Ab-dependent, cell-mediated cytotoxicity (ADCC).
  • However, PMN from a patient with chronic granulomatous disease demonstrated strong ADCC against malignant lymphoma cells.
  • Furthermore, the inhibition of ROI production in PMN from healthy donors had no significant effect on ADCC.
  • Therefore, ROI production by the NADPH oxidase of PMN does not appear to be mandatory for PMN-mediated ADCC.
  • However, in our assays concanamycin A, an inhibitor of perforin-mediated ADCC by mononuclear cells, had no inhibitory effect on PMN-mediated ADCC.
  • The presence of transient PMN-tumor cell aggregates and the accumulation of PMN with tumor cell-derived membrane lipids and vice versa were associated with effective ADCC as measured by chromium-release or apoptosis induction.

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  • (PMID = 17579054.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / HLA-D Antigens; 0 / Macrolides; 0 / Membrane Glycoproteins; 0 / Membrane Lipids; 0 / Pore Forming Cytotoxic Proteins; 0 / Reactive Oxygen Species; 126465-35-8 / Perforin; 80890-47-7 / concanamycin A; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
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87. Borgerding A, Hasenkamp J, Engelke M, Burkhart N, Trümper L, Wienands J, Glass B: B-lymphoma cells escape rituximab-triggered elimination by NK cells through increased HLA class I expression. Exp Hematol; 2010 Mar;38(3):213-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Antibody-dependent cellular cytotoxicity (ADCC) by natural killer (NK) cells is a major effector mechanism of the monoclonal anti-CD20 antibody rituximab in eliminating B-cell lymphomas.
  • MATERIALS AND METHODS: A model of ADCC was established by stimulating human bulk NK cells and inhibitory killer immunoglobulin receptor (KIR)-defined NK cells from human leukocyte antigen (HLA)-typed donors.
  • The effect of KIR ligation by anti-KIR antibodies and HLA, the HLA expression density and rituximab concentrations on the efficacy of ADCC were analyzed in granzyme B ELISPOT measuring NK-cell activation and fluorescein-activated cell sorting cytotoxicity assay.
  • ADCC was increased or decreased following HLA shielding or KIR activation by anti-KIR antibodies, respectively.
  • Herein we show that rituximab-induced ADCC is attenuated upon ligation of KIR by HLA molecules expressed on human B-lymphoma target cells.
  • An explanation for the failure of rituximab treatment may be the protection of the tumor cells from ADCC by inhibiting NK-cell function with their surface HLA.

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  • [Copyright] Copyright 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20056126.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 0 / HLA-C Antigens; 0 / Histocompatibility Antigens Class I; 0 / KIR2DL1 protein, human; 0 / KIR2DL2 protein, human; 0 / KIR2DL3 protein, human; 0 / Receptors, KIR; 0 / Receptors, KIR2DL1; 0 / Receptors, KIR2DL2; 0 / Receptors, KIR2DL3; 4F4X42SYQ6 / Rituximab
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88. Rebuffat SA, Nguyen B, Robert B, Castex F, Peraldi-Roux S: Antithyroperoxidase antibody-dependent cytotoxicity in autoimmune thyroid disease. J Clin Endocrinol Metab; 2008 Mar;93(3):929-34

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Indeed, the role of thyroperoxidase (TPO) autoantibodies (aAbs) in complement-mediated damage by binding to TPO expressed on the surface of human thyroid cells was demonstrated, whereas their activity in antibody-dependent cell cytotoxicity (ADCC) is not well established.
  • RESULTS: The relative capability of anti-TPO aAbs to mediate ADCC using human thyroid cells in culture varies from 11 to 74.5%, depending on the effectors cells used.
  • It seems obvious that the mechanism of ADCC is mediated quite exclusively by FcgammaRI.
  • In addition to ADCC, the anti-TPO aAbs mediate the destruction of thyrocytes by CDC (56%).
  • CONCLUSIONS: These results demonstrate that anti-TPO aAbs can damage cultured thyroid cells by ADCC and CDC mechanisms.
  • The monocytes, via their FcgammaRI, are important effector cells in ADCC mediated by anti-TPO aAbs and may contribute with T cells to the destruction of thyroid gland in AITD.

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  • (PMID = 18073303.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 80295-33-6 / Complement C1q; EC 1.11.1.8 / Iodide Peroxidase
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89. Peipp M, Lammerts van Bueren JJ, Schneider-Merck T, Bleeker WW, Dechant M, Beyer T, Repp R, van Berkel PH, Vink T, van de Winkel JG, Parren PW, Valerius T: Antibody fucosylation differentially impacts cytotoxicity mediated by NK and PMN effector cells. Blood; 2008 Sep 15;112(6):2390-9
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  • Our results confirmed that low fucose levels enhance mononuclear cell-mediated antibody-mediated cellular cytotoxicity (ADCC).
  • Whole blood ADCC assays, containing both types of effector cells, revealed little differences in tumor cell killing between both batches.
  • Significantly, however, high-fucose antibody induced superior ADCC in blood from granulocyte colony-stimulating factor-primed donors containing higher numbers of activated polymorphonuclear cells.
  • In conclusion, our data demonstrated for the first time that lack of fucose does not generally increase the ADCC activity of therapeutic antibodies and that the impact of Fc glycosylation on ADCC is critically dependent on the recruited effector cell type.

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  • (PMID = 18566325.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Immunoglobulin Fc Fragments; 3713-31-3 / Fucose
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90. Scallon BJ, Tam SH, McCarthy SG, Cai AN, Raju TS: Higher levels of sialylated Fc glycans in immunoglobulin G molecules can adversely impact functionality. Mol Immunol; 2007 Mar;44(7):1524-34
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  • We report that in vitro analyses of pairs of monoclonal human IgG Abs that differ in the amount of sialic acid in their Fc glycans revealed that, for each of the three Ab pairs we examined, higher levels of sialylation were associated with reduced activity in Ab-dependent cellular cytotoxicity (ADCC) assays.
  • This relationship between sialylation and ADCC activity was observed regardless of whether the differences in the extent of sialylation were derived by different Ab production processes, use of a lectin column to separate monoclonal Ab preparations into differentially sialylated fractions, or use of direct in vitro glycoengineering methods to convert a lesser sialylated Ab into a highly sialylated Ab.
  • Subsequent investigations revealed that, depending on the individual Ab and how the differences in sialylation were derived, the lower ADCC potency of the more sialylated variants was apparently due to lower-affinity binding to FcgammaRIIIa on natural killer (NK) cells and/or, more interestingly, lower-affinity binding to cell-surface antigen.
  • Our data provide the first example of an Fc glycan structure impacting antigen binding and suggest that avoiding Fc glycan sialylation can offer another means of optimizing ADCC activity of Abs.

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  • (PMID = 17045339.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens; 0 / FCGR3A protein, human; 0 / Immunoglobulin Fc Fragments; 0 / Immunoglobulin G; 0 / Polysaccharides; 0 / Receptors, IgG; GZP2782OP0 / N-Acetylneuraminic Acid
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91. Wang W, Nishioka Y, Ozaki S, Jalili A, Verma VK, Hanibuchi M, Abe S, Minakuchi K, Matsumoto T, Sone S: Chimeric and humanized anti-HM1.24 antibodies mediate antibody-dependent cellular cytotoxicity against lung cancer cells. Lung Cancer; 2009 Jan;63(1):23-31
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  • Antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) of chimeric and humanized anti-HM1.24 mAbs against lung cancer cells were determined by chromium-release assay.
  • Chimeric and humanized anti-HM1.24 mAbs effectively induced ADCC against lung cancer cells mediated more efficiently by lymphocytes than monocytes.
  • Natural killer cells were identified as the major effector cells in ADCC mediated by the anti-HM1.24 mAb.
  • The treatment of lymphocytes or monocytes with IL-2, IL-12, IL-15, M-CSF, or IFN-gamma significantly increased the ADCC activity.
  • Moreover, the culture of lung cancer cells with IFN-beta or IFN-gamma augmented their susceptibility to ADCC and CDC.
  • PBMCs from patients with lung cancer induced a level of ADCC comparable to that induced by PBMCs from healthy donors.
  • Chimeric or humanized anti-HM1.24 mAbs have potential as a new therapeutic tool in lung cancer, and in combination with interleukins and interferons, could be useful for enhancing ADCC.

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  • (PMID = 18524412.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / BST2 protein, human; 0 / Cytokines; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Recombinant Fusion Proteins; 77238-31-4 / Interferon-beta; 82115-62-6 / Interferon-gamma
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92. Ishiguro T, Kawai S, Habu K, Sugimoto M, Shiraiwa H, Iijima S, Ozaki S, Matsumoto T, Yamada-Okabe H: A defucosylated anti-CD317 antibody exhibited enhanced antibody-dependent cellular cytotoxicity against primary myeloma cells in the presence of effectors from patients. Cancer Sci; 2010 Oct;101(10):2227-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The humanized monoclonal antibody (mAb) against CD317 antigen (anti-HM1.24 antibody; AHM), which is highly expressed on multiple myeloma (MM), induces antibody-dependent cellular cytotoxicity (ADCC).
  • In this study, we produced defucosylated AHM and evaluated its potency for clinical application by performing autologous ADCC assays against primary MM cells from patients.
  • Defucosylated AHM that was produced in rat myeloma YB2/0 cells expressing a low level of fucosyltransferase (FUT8) showed significant ADCC activity against three out of six primary MM cells in the presence of autologous PBMC, whereas conventional AHM did not.
  • The results indicate that the potency of AHM to induce ADCC against primary MM cells was insufficient, but was significantly augmented by defucosylation.

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  • [Copyright] © 2010 Japanese Cancer Association.
  • (PMID = 20701608.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / BST2 protein, human; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Monosaccharide Transport Proteins; 0 / SLC35C1 protein, human; EC 2.4.1.- / Glucosyltransferases
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93. Epivatianos A, Iordanides S, Zaraboukas T, Antoniades D: Adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma of minor salivary glands: a comparative immunohistochemical study using the epithelial membrane and carcinoembryonic antibodies. Oral Dis; 2005 May;11(3):175-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma of minor salivary glands: a comparative immunohistochemical study using the epithelial membrane and carcinoembryonic antibodies.
  • OBJECTIVE: The purpose of this study was to investigate immunohistochemically the expression of epithelial membrane antigen (EMA) and carcinoembryonic antigen (CEA) in adenoid cystic carcinoma (AdCC) and polymorphous low-grade adenocarcinoma (PLGA) in an attempt to assess the ability of these markers to distinguish AdCC from PLGA when the histological features on routine hematoxylin and eosin are equivocal.
  • MATERIALS AND METHODS: Fourteen specimens of AdCC, 10 PLGA, and five normal minor salivary glands fixed in 10% formalin and embedded in paraffin, were retrieved from the files of our department and were retrospectively studied with the streptavidin-biotin complex method using the epithelial membrane and carcinoembryonic antibodies.
  • RESULTS: The immunoreactivities and the expression patterns of EMA and CEA in AdCC and PLGA were similar.
  • CONCLUSIONS: The results of this study suggest that the immunostaining of AdCC and PLGA with EMA and CEA could not offer an adjunctive aid in differential diagnosis between these two tumors.
  • [MeSH-major] Adenocarcinoma / diagnosis. Carcinoma, Adenoid Cystic / diagnosis. Salivary Gland Neoplasms / diagnosis


94. Prokopovich ME, Varakin IuIa, Oshchepkova EV, Rebrova OIu: [Acute disorders of cerebral circulation: prognostic factors in essential hypertension]. Ter Arkh; 2006;78(10):14-8
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  • AIM: To study subclinical signs of cerebrovascular pathology as prognostic factors of development of acute disorders of cerebral circulation (ADCC) in essential hypertension (EH).
  • MATERIAL AND METHODS: A prospective (10-13 years) cohort trial of prognostic significance of subclinical forms of cerebral pathology in EH in relation to ADCC development covered 111 men aged 45-55 years who had undergone a unified neurological and cardiological examination in 1992-1993.
  • RESULTS: Such factors as disordered circulation along major arteries of the head (a relative risk 3.1 [1.2; 10.3]), thick intima-media complex of the common carotid artery (a relative risk: 5.2 [2.1; 14.3]), the presence of asymptomatic lacunar brain infarctions (a relative risk: 6.6 [2.3; 13.5]) were revealed to be of unfavourable prognostic significance in respect to development of ADCC in EH.
  • CONCLUSION: Some subclinical risk factors may have prognostic value in relation to development of ADCC in EH.

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  • (PMID = 17180930.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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95. Mimura K, Kono K, Hanawa M, Kanzaki M, Nakao A, Ooi A, Fujii H: Trastuzumab-mediated antibody-dependent cellular cytotoxicity against esophageal squamous cell carcinoma. Clin Cancer Res; 2005 Jul 1;11(13):4898-904
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trastuzumab-mediated antibody-dependent cellular cytotoxicity against esophageal squamous cell carcinoma.
  • PURPOSE: In the present study, we investigated the degree of protein expression and gene amplification of HER-2 in esophageal squamous cell carcinoma (SCC) cell lines and freshly isolated tumors, and trastuzumab-mediated biological activity, in particular antibody-dependent cellular cytotoxicity (ADCC) against HER-2-expressing esophageal SCC cell lines.
  • EXPERIMENTAL DESIGN: Ten different SCC cell lines with various levels of HER-2 status evaluated by flow cytometry, immunocytochemistry (HercepTest), and fluorescence in situ hybridization were evaluated for ADCC, growth inhibitory, or apoptosis-inducing activities mediated by trastuzumab.
  • RESULTS: Trastuzumab induced ADCC against HER-2-expressing esophageal SCC and the activities reflected the degree of HER-2 expression analyzed by flow cytometric analysis, but not by HercepTest nor fluorescence in situ hybridization analysis.
  • Furthermore, trastuzumab-mediated ADCC against transforming growth factor-beta-producing SCC was enhanced by the treatment with SB-431542, which is a selective inhibitor of the phosphorylation induced by transforming growth factor-beta.
  • CONCLUSION: HER-2-expressing esophageal SCC cells could be killed by trastuzumab-mediated ADCC and the activity reflected the degree of HER-2 expression detected by flow cytometry.
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antineoplastic Agents / pharmacology. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Cell Line, Tumor. Esophageal Neoplasms / genetics. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Flow Cytometry. Gene Amplification / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunoblotting. Immunohistochemistry. In Situ Hybridization, Fluorescence. Receptor, ErbB-2 / biosynthesis. Receptor, ErbB-2 / genetics. Receptor, ErbB-2 / immunology. Transforming Growth Factor beta / immunology. Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta2. Trastuzumab

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  • (PMID = 16000588.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / TGFB2 protein, human; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta2; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab
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96. Karakas Z, Tugcu D, Unuvar A, Atay D, Akcay A, Gedik H, Kayserili H, Dogan O, Anak S, Devecioglu O: Li-Fraumeni syndrome in a Turkish family. Pediatr Hematol Oncol; 2010 May;27(4):297-305
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  • Li-Fraumeni syndrome (LFS) is one of the familial cancers characterized by different tumors and hereditary TP53 mutations.
  • The adrenocortical carcinoma (ACC) association with acute leukemia is unusual in childhood, even in LFS.
  • The authors here present a family with pR337P mutation in TP53 gene who had a child with acute lymphoblastic leukemia (ALL) and associated adrenocortical carcinoma as a case 1 and his cousin with brain tumor as a case 2.
  • A hereditary TP53 mutation supported the diagnosis of LFS in this family.
  • [MeSH-major] Adrenocortical Carcinoma / genetics. Brain Neoplasms / genetics. Li-Fraumeni Syndrome / genetics. Mutation, Missense. Neoplasms, Second Primary / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 20426520.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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97. Karnasuta C, Paris RM, Cox JH, Nitayaphan S, Pitisuttithum P, Thongcharoen P, Brown AE, Gurunathan S, Tartaglia J, Heyward WL, McNeil JG, Birx DL, de Souza MS, Thai AIDS Vaccine Evaluation Group, Thailand: Antibody-dependent cell-mediated cytotoxic responses in participants enrolled in a phase I/II ALVAC-HIV/AIDSVAX B/E prime-boost HIV-1 vaccine trial in Thailand. Vaccine; 2005 Mar 31;23(19):2522-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Antibody-dependent cell-mediated cytotoxicity (ADCC) was assessed in volunteers participating in an ALVAC-HIV (vCP1521)/AIDSVAX B/E gp120 prime-boost vaccine trial in Thailand.
  • ADCC activity was measured using chromium release from gp120 subtype B- and CRF01_AE-coated targets in 95 vaccinees and 28 placebo recipients.
  • There was a significant difference in the magnitude of the ADCC response to both targets between vaccinees and placebo recipients.
  • The results demonstrate that this HIV vaccine is a potent inducer of ADCC activity and may be an additional protection of this prime-boost vaccine in preventing HIV disease.

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  • (PMID = 15752839.001).
  • [ISSN] 0264-410X
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AIDS Vaccines; 0 / AIDSVAX; 0 / Chromium Radioisotopes; 0 / HIV Antibodies; 0 / HIV Envelope Protein gp120; 0 / Vaccines, Subunit
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98. Nechansky A, Schuster M, Jost W, Siegl P, Wiederkum S, Gorr G, Kircheis R: Compensation of endogenous IgG mediated inhibition of antibody-dependent cellular cytotoxicity by glyco-engineering of therapeutic antibodies. Mol Immunol; 2007 Mar;44(7):1815-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recently, Preithner et al. showed that the high amount of endogenous serum IgG impairs the antibody-dependent cellular cytotoxicity effector function (ADCC) of therapeutic Abs in vivo by competing for binding to Fcgamma-RIII on the effector cells.
  • Modification of the glycosylation moieties attached to the Fc part of the Ab, e.g. de-fucosylation, has been shown to increase ADCC activity.
  • We here show that the ADCC activity of a fucose-deficient, moss-produced therapeutic IgG is not impaired by normal human serum.
  • The increased ADCC activity of the fucose-deficient Ab variant even in the presence of high endogenous IgG indicates that glyco-engineering of Abs may translate into improved clinical efficacy.

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  • [CommentOn] Mol Immunol. 2006 Mar;43(8):1183-93 [16102830.001]
  • (PMID = 17011625.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / FCGR3A protein, human; 0 / IGN 311; 0 / Immunoglobulin G; 0 / Receptors, IgG
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99. Niwa R, Natsume A, Uehara A, Wakitani M, Iida S, Uchida K, Satoh M, Shitara K: IgG subclass-independent improvement of antibody-dependent cellular cytotoxicity by fucose removal from Asn297-linked oligosaccharides. J Immunol Methods; 2005 Nov 30;306(1-2):151-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Fucose depletion from oligosaccharides of human IgG1-type antibodies results in a great enhancement of antibody-dependent cellular cytotoxicity (ADCC).
  • As found previously for IgG1, fucose-negative variant of IgG2, IgG3, and IgG4 exhibited enhanced ADCC and FcgammaRIIIa binding compared with their highly fucosylated counterparts.
  • Consequently, fucose removal from IgG2 and IgG4 resulted in a unique effector function profile; they had potent ADCC and no CDC.
  • In conclusion fucose depletion can provide a panel of IgGs with enhanced ADCC without an impact on other inherent properties specific for each IgG subclass, such as CDC.

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  • (PMID = 16219319.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / FCGR3A protein, human; 0 / Immunoglobulin G; 0 / Oligosaccharides; 0 / Receptors, IgG; 0 / Recombinant Fusion Proteins; 3713-31-3 / Fucose; 4F4X42SYQ6 / Rituximab; 7006-34-0 / Asparagine
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100. Mitroviç Z, Aurer I, Radman I, Ajdukoviç R, Sertiç J, Labar B: FCgammaRIIIA and FCgammaRIIA polymorphisms are not associated with response to rituximab and CHOP in patients with diffuse large B-cell lymphoma. Haematologica; 2007 Jul;92(7):998-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These results suggest that ADCC via FcgammaRIIIa and FcgammaRIIa may not be the major mechanism of activity of the R-CHOP combination in DLBCL.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 17606457.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD; 0 / FCGR3A protein, human; 0 / Fc gamma receptor IIA; 0 / Receptors, IgG; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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