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Biodistribution of a monoclonal antibody (RNL‐1) against the neural cell adhesion molecule (NCAM) in athymic mice bearing human small‐cell lung‐cancer xenografts
Author(s) -
Boerman O. C.,
Mijnheere E. P.,
Broers J. L. V.,
Vooijs G. P.,
Ramaekers F. C. S.
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910480325
Subject(s) - monoclonal antibody , neural cell adhesion molecule , biodistribution , microbiology and biotechnology , antigen , cell adhesion molecule , cancer research , chemistry , pathology , antibody , biology , cell adhesion , cell , immunology , in vitro , medicine , biochemistry
The purpose of this investigation was to determine the targeting potential of the murine monoclonal antibody (MAb) RNL‐1 for human small‐cell lung cancer (SCLC) in a nude mouse model. RNL‐1 is preferentially reactive with SCLC and lung carcinoids, and was classified as a cluster‐1 MAb as defined by the International Workshop on Small‐Cell Lung‐Cancer Antigens. From the intercellular location of the target antigen and Its reactivity with 3T3 cells transfected with nucleic acid sequences encoding for the neural cell adhesion molecule (NCAM), it was concluded that RNL‐1 is directed against NCAM. RNL‐1 was radiolabelled with either 125 iodine or 111 indium and injected into nude mice bearing NCI‐H82 SCLC xenografts. The biodistribution of the radiolabels was determined up to 120 hr post injection. Maximum tumour accretion for 111 In‐RNL‐1 was 11.6% ID/g and 6.5% ID/g for 125 I‐RNL‐1. The accumulation of 111 In‐RNL‐1 could be visualized clearly by gamma scintigraphy without background subtraction techniques. Autoradiographs of whole‐body sections from animals injected with 125 I‐RNL‐1 showed that activity in the SCLC xenografts was mainly peripheral, suggesting that tumour uptake is dependent on the vascularization of the tumour tissue.