Structural changes or chromosomal aberrations include deletions, duplications, inversions, isochromosome and translocations. Deletion is a consequence of a break and lost of chromosomal segment. Duplication of chromosomal segment occurs after irregular crossing-over or shift of chromosomal segment to a new location, and pairing and crossing-over. Inversion include two breaks, rotation of 180º and reconnection. Isochromosome causes the formation of metacentric chromosome and isochromosome the long arm of the loss shows a short-tail, a short arm shows a loss of long arms of chromosomes. There are reciprocal and Robertsonian translocation and translocation of chromosome segments are formed by changing nehomologous chromosomes. Although the t(14:18) translocation is found in B-cell lymphomas and leukemias, something else must contribute to creating the cancer because over 50% of us have small numbers of B-cells with translocation that never progress to cancer. The antibody gene loci are dangerous places for proto-oncogenes to take up residence. Translocation of the proto-oncogene c-myc close to the enhancer of the antibody heavy chain genes also produces cancerous B cells resulting in Burkitt´s lymphoma. The translocation of the Bcl-2 locus is just one of many mutations that can give rise to a chronic lymphocytic leukemia. The p53 tumor suppressor gene product, and the bcr/abl, bcl-2 and c-myc gene products all appear to influence the susceptibility of cells to apoptosis (Canman and Kastan, 1995). In addition to the role p53 protein plays in mediating a cell cycle arrest in G1 following DNA damage, p53 also performs functions critical for removal of damaged cells by initiating apoptosis in certian physiological situations. Cells which express deregulated c-myc are sensitized to apoptosis. An escape from apoptosis is often a hallmark of cancer cells, and is associated to chemotherapy resistance (Johnstone et al., 2002). Proteins from the Bcl-2 family are the key regulators of the intrinsic pathway of apoptosis, controlling the point-of no-return and setting the threshold to engage the death machinery in response to a chemical damage. Therefore, Bcl-2 proteins have emerged as an attractive target to develop novel anticancer drugs.