Transcriptional co-regulation of sets of adjacent genes at the chromosomal domain level has been demonstrated recently in eukaryotes, supporting the idea that genomes are divided into regions of clustered expression of groups of adjacent genes. The mechanism underlying this phenomenon and its significance for human pathology is not yet known. Systematic analysis of the chromosomal positions of cancer-associated transcripts for prostate, breast, ovarian, and colon tumors identified short segments of human chromosomes that appear to represent a common target for transcriptional activation in major epithelial malignancies in human (1q21–q23 [140–160 Mbp]; 11q12–q13 [62–69 Mbp]; 12q13 [49–58 Mbp]; 17q21 [37–50 Mbp]; 17q23–q25 [70–81 Mbp]; 19p13 [0.2–19 Mbp]; Xq28 [147–153 Mbp]). At least some of these cancer-associated MARTAs correspond well to the regions of recurrent amplification in human cancer and seemed to be targets for DNA amplifications in established cancer cell lines.