Final answer:
In Burkitt's lymphoma patients, B cells exhibit chromosomal breakage and rejoining at characteristic locations due to reciprocal translocations, often involving the MYC oncogene. While DNA recombinase normally contributes to antibody diversity through V(D)J recombination, the translocations in lymphoma are abnormal and can lead to cancer progression.
Step-by-step explanation:
In transformed B cells of Burkitt's lymphoma patients, the chromosomal sites of breakage and rejoining are characteristic locations known as reciprocal translocations. This particular genetic alteration involves the translocation between two nonhomologous chromosomes, which generally does not result in the loss or duplication of genetic information. However, this structural chromosomal rearrangement can lead to the development of certain cancers, such as Burkitt's lymphoma, by moving oncogenes to new loci which may lead to their overexpression or by placing them under the control of different regulatory elements.
A well-known example of a chromosomal translocation that occurs in another type of cancer is the Philadelphia chromosome, a translocation between chromosomes 9 and 22, which is often observed in chronic myelogenous leukemia. This translocation results in the formation of the BCR-abl fusion protein, an oncogenic tyrosine kinase. Similarly, in Burkitt's lymphoma, a translocation often occurs that involves the MYC oncogene being placed next to one of the immunoglobulin heavy chain loci, leading to its deregulation.
During normal B cell development, genetic recombination events occur that contribute to the antibody diversity needed for immune responses. An enzyme called DNA recombinase randomly excises segments from the immunoglobulin genes in what is known as V(D)J recombination, but these normal biological processes are distinct from the aberrant translocations seen in cancers like Burkitt's lymphoma.