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Blood, Vol. 95 No. 8 (April 15), 2000:
pp. 2666-2671
MUC1 is activated in a B-cell lymphoma by the
t(1;14)(q21;q32) translocation and is rearranged and amplified in
B-cell lymphoma subsets
Vadim G. Dyomin,
Nallasivam Palanisamy,
Kenneth O. Lloyd,
Katerina Dyomina,
Suresh C. Jhanwar,
Jane Houldsworth, and
R. S. K. Chaganti
From the Cell Biology Program, the Immunology Program, and the
Department of Human Genetics, Memorial Sloan-Kettering Cancer
Center, New York, NY.
The band 1q21 is among the most common sites affected by chromosomal
translocations in lymphoid, myeloid, epithelial, and sarcomatous
lesions. In non-Hodgkin's lymphoma (NHL), translocations and
duplications affecting this chromosomal site are frequently, but not
exclusively, seen in association with primary abnormalities such as the
t(14;18)(q32;q21) and t(8;14)(q24;q32) translocations, suggesting a
role for 1q21 rearrangements in tumor progression. We report here the
characterization and cloning of breakpoints in a case of extranodal
ascitic B-cell lymphoma with a t(1;14)(q21;q32) translocation. The
breakpoints on the der(1) and der(14) chromosomes were mapped by
fluorescence in situ hybridization and Southern blot analysis and
cloned using an IGHG (C ) probe. The translocation linked the
IGHG4 switch (S4) sequences of the productively rearranged allele to chromosome 1 sequences downstream of MUC1, leaving
the MUC1 transcriptional unit intact. MUC1 was markedly
overexpressed in the tumor at the mRNA and protein levels relative to
lymphoma cell lines lacking a 1q21 rearrangement. Presumably,
MUC1 transcription is aberrantly regulated by the IGHA
(C ) 3' enhancer element retained on the same chromosome.
Screening of a panel of B-cell lymphomas by Southern blot analysis
identified a subset with a 3' MUC1 breakpoint and another
with low-level amplification of MUC1. MUC-1 mucin has
previously been shown to be frequently overexpressed in human epithelial cancers and to be associated with tumor progression and poor
clinical outcome. Thus, MUC1 activation by chromosomal translocation, rearrangement, and amplification, identified here for
the first time in NHL, is consistent with its suggested role in tumorigenesis.
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