In chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (AL
L) the Ph1 chromosome (22q-) is the most frequent chromosomal aberrati
on encountered. At the molecular level the c-abl gene from chr. 9 is t
ranslocated to the bcr gene on chr. 22. As a result, a chimeric bcr-ab
l gene is generated, which encodes chimeric proteins. Since these prot
eins are only expressed in Ph1 positive cells, they are per definition
tumor-specific. In this report we describe the reactivity of polyvale
nt antisera raised against synthetic peptides corresponding to the tum
or-specific bcr-abl junctions. Native chimeric proteins were specifica
lly recognized by these junction-specific antisera. Therefore we concl
ude that the bcr-abl junctions are antigenically exposed on the chimer
ic proteins. We discuss the relevance of these antisera for CML and AL
L diagnosis.