The antigen defined by MAb 17-1A, raised against colorectal cancer cells and currently used in immunotherapy trials, is a 37 kDa protein containing N-linked glycans as demonstrated by inhibition of glycosylation with tunicamycin. The 17-1A antigen (17-1A Ag) is broadly distributed in normal epithelial tissues and is also found in various types of carcinoma. Quantitative differences in expression between normal and malignant tissues were only apparent in gastric carcinomas. After immunizing mice with fresh colon carcinoma tissue, 4 MAbs were obtained that showed the same tissue reaction pattern as MAb 17-1A and recognized the 17-1A Ag as judged from precipitation and immunoblotting experiments. MAbs M72 and M74 reacted with an anti-idiotypic serum directed against the original MAb 17-1A and were able to block 17-1A binding. In contrast, M77 and M79 are directed against a different epitope. This makes them potentially interesting for passive immunotherapy in regimens involving a combination of MAbs.
Low amplitude of the P300 evoked potential waves has been linked to substance abuse. Defects in opioidergic genes regulating reward pathways have been implicated as risk factors in substance abuse. Since the rate of degradation of enkephalins regulates their CNS level, we focused on the MME gene for metallo-membrane endopeptidase (neutral endopeptidase, enkephalinase). We identified a GT repeat polymorphism 5' to the gene and examined its potential association with P300 wave amplitude in 25 male subjects with substance abuse. There was significant association of low mol. wt alleles with low amplitude of the P300 wave at the parietal (p = 0.0087) and coronal (p = 0.009) leads. These results support a role of endogenous opioids in the regulation of P300 wave amplitude.
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