caa a22 4500 469073764 CHVBK 20180323132929.0 cr unu---uuuuu 170328e19920501xx s 000 0 eng 10.1007/BF01756182 doi (NATIONALLICENCE)springer-10.1007/BF01756182 Cytotoxic functions of blood mononuclear cells in patients with colorectal carcinoma treated with mAb 17-1A and granulocyte/macrophage-colony-stimulating factor [Elektronische Daten] [P. Ragnhammar, G. Masucci, J Frödin, A Hjelm, H. Mellstedt] Summary: Unconjugated monoclonal antibodies (mAb) may induce tumour regression in patients. The mechanisms of action are complex. Antibody-dependent cellular cytotoxicity (ADCC) is considered one of the effector functions. Augmentation of the killing capacity of cytotoxic cells may thus be a way to increase the therapeutic potential of mAb. Granulocyte/macrophage-colony-stimulating factor (GM-CSF) has been shown to enhance this function in vitro. Eighteen patients with metastatic colorectal carcinoma received GM-CSF (250 µg m−2 day−1 s.c.) for 10 days and a single infusion of the anti-(colon carcinoma) mAb 17-1A (mouse IgG2A) (400 mg) on day 3 of the cycle. The cycles were repeated once a month four times. Neutrophils, eosinophils, monocytes and lymphocytes increased significantly in a biphasic way. However, at the fourth cycle the rise in white blood cells was significantly lower compared to the preceding courses. ADCC (SW948, a human CRC cell line, + mAb 17-1A) or peripheral blood mononuclear cells (PBMC) was significantly (P <0.05) augmented by day 6 of a cycle and then declined gradually and, at the end of a cycle, the ADCC activity had returned to the pretreatment level. The spontaneous cytotoxicity of PBMC against the natural-killer-resistant cell line, SW948, varied in a similar way. During GM-CSF treatment there was also a significant increase in FcRI+ (CD64), FcRII+ (CD32), FcRIII+ (CD16) and CD14+ cells but not of CD56+ cells. Springer-Verlag, 1992 Monoclonal antibodies nationallicence GM-CSF nationallicence Colorcetal carcinoma nationallicence Ragnhammar P. Department of Oncology (Radiumhemmet) and Immunologic Research Laboratory, Karolinska Hospital, S-104 01, Stockholm, Sweden aut Masucci G. Department of Oncology (Radiumhemmet) and Immunologic Research Laboratory, Karolinska Hospital, S-104 01, Stockholm, Sweden aut Frödin J. Department of Oncology (Radiumhemmet) and Immunologic Research Laboratory, Karolinska Hospital, S-104 01, Stockholm, Sweden aut Hjelm A. Department of Oncology (Radiumhemmet) and Immunologic Research Laboratory, Karolinska Hospital, S-104 01, Stockholm, Sweden aut Mellstedt H. Department of Oncology (Radiumhemmet) and Immunologic Research Laboratory, Karolinska Hospital, S-104 01, Stockholm, Sweden aut Cancer Immunology, Immunotherapy Springer-Verlag 35/3(1992-05-01), 158-164 0340-7004 35:3<158 1992 35 262 https://doi.org/10.1007/BF01756182 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF01756182 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Ragnhammar P. Department of Oncology (Radiumhemmet) and Immunologic Research Laboratory, Karolinska Hospital, S-104 01, Stockholm, Sweden aut NATIONALLICENCE 700 1- Masucci G. Department of Oncology (Radiumhemmet) and Immunologic Research Laboratory, Karolinska Hospital, S-104 01, Stockholm, Sweden aut NATIONALLICENCE 700 1- Frödin J. Department of Oncology (Radiumhemmet) and Immunologic Research Laboratory, Karolinska Hospital, S-104 01, Stockholm, Sweden aut NATIONALLICENCE 700 1- Hjelm A. Department of Oncology (Radiumhemmet) and Immunologic Research Laboratory, Karolinska Hospital, S-104 01, Stockholm, Sweden aut NATIONALLICENCE 700 1- Mellstedt H. Department of Oncology (Radiumhemmet) and Immunologic Research Laboratory, Karolinska Hospital, S-104 01, Stockholm, Sweden aut NATIONALLICENCE 773 0- Cancer Immunology, Immunotherapy Springer-Verlag 35/3(1992-05-01), 158-164 0340-7004 35:3<158 1992 35 262 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer