Abstract
HEAVY-CHAIN diseases in humans, which have been described for the three main classes of immunoglobulins, are B-cell disorders in which proliferating cells produce truncated monoclonal heavy chains that lack associated light chains.1 The abnormal proteins have deletions of part or all of the variable region and of one or two constant domains, usually CH1. The normal sequence resumes at a position corresponding to the beginning of an exon.2 The heavy chains are synthesized as abnormally short chains.3 , 4 Recent studies in a few cases of μ–heavy-chain and γ-heavy-chain diseases have shown that the messenger RNA (mRNA) was short and . . .
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