This amplification is achieved via two distinct mechanisms. These gene copies often distort the normal karyotypic banding pattern of the chromosome in which they are lodged. As a consequence, a homogeneous staining region is observed at a specific site along the chromosome. The second mechanism of gene amplification is when a chromosomal segment is cut loose from its normal site in the chromosome and begins to replicate as an extrachromosomal particle, often called a double minute. Because the replication of these double minutes is not closely coupled with that of the chromosomes from which they originate, the double minutes may accumulate in large numbers in the cells, yielding small extrachromosomal particles that may also be karyotypically visible.
Chromosomal translocation is a mechanism that is often observed in hematopoietic tumors.
Translocations result from an inappropriate crossing-over of two unrelated chromosomal arms. As a consequence, at the fusion point between two joined chromosomal segments, a DNA segment from one chromosomal region becomes juxtaposed with a segment from another. This juxtaposition often yields a hybrid gene that acquires functions that were not exhibited previously by either of the two parent genes. Alternatively, the gene fusion resulting from a translocation may place one gene under the transcriptional control of another. In Burkitt's lymphoma, the myc gene becomes closely juxtaposed with transcription-regulating segments from one of the genome's three immunoglobulin gene clusters.