MAD and MXI1, two recently described members of the basic helix-loop-h
elix (bHLH) gene family, encode proteins that dimerize with and modula
te the DNA binding of max. In turn, mad-max or mxi1-max heterodimers o
r max homodimers can compete for DNA binding sites with dimers formed
between max and myc oncoproteins and antagonize the transcriptional ac
tivities of this latter class of proteins. Using a combination of soma
tic cell mapping and fluorescence in situ hybridization techniques, we
have determined the chromosomal locations of the MAD and MXI1 genes.
The MAD gene maps to chromosome 2p12-p13, a region involved in translo
cations and deletions in acute and chronic lymphocytic leukemias as we
ll as nonlymphocytic leukemias and Hodgkin disease. The MXI1 gene loca
lizes to chromosome 10q24-q25, a region involved in translocations and
deletions in acute and chronic lymphocytic leukemias and prostatic ca
rcinomas. The availability of genomic clones of MAD and MXI1 will perm
it an assessment of their involvement in these diseases at the molecul
ar level. (C) 1994 Academic Press, Inc.