Tumor-specific chromosomal translocations in lymphoid malignancy frequently involve the fusion of immunoglobulin (Ig) or T-cell receptor (TCR) gene loci with oncogenes, thereby activating the latter to contribute to the malignant phenotype. The preponderance of chromosomal translocations involving Ig or TCR genes suggests that the enzymatic machinery, the lymphocyte recombinase, is used in the formation of abnormal chromosomes. However, the role of ectopic recombination signals for recombinase in chromosomal translocations has been controversial. In this paper, molecular studies of genes adjacent to the breakpoints of these chromosomal translocation are reviewed, and the mechanism of chromosomal translocation and clinical characteristics of the tumor with specific chromosomal translocation are discussed.