Abstract
In chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) the Ph1 chromosome (22q-) is the most frequent chromosomal aberration encountered. At the molecular level the c-abl gene from chr. 9 is translocated to the bcr gene on chr. 22. As a result, a chimeric bcr-abl gene is generated, which encodes chimeric proteins. Since these proteins are only expressed in Ph1 positive cells, they are per definition tumor-specific. In this report we describe the reactivity of polyvalent antisera raised against synthetic peptides corresponding to the tumor-specific bcr-abl junctions. Native chimeric proteins were specifically recognized by these junction-specific antisera. Therefore we conclude that the bcr-abl junctions are antigenically exposed on the chimeric proteins. We discuss the relevance of these antisera for CML and ALL diagnosis.
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