Genetic Abnormalities in Lymphoma
Like all cancers, lymphoma begins with damage to the cell’s deoxyribonucleic acid (DNA), the molecules containing all the information that determines the structure and function of cells. Within each cell, DNA is housed in structures known as chromosomes, which are made up of sections called genes.
The development of lymphoma begins with damage to the DNA of T-cells and B-cells (lymphocytes), immune cells that protect the body from infections (Coffey J et al 2003; Kuppers R et al 2002). DNA damage that can start cancer development occurs in genes called oncogenes or tumor-suppressor genes, which play important roles in maintaining a balance between cell death and cell growth.
Excessive cell growth occurs in lymphoma as a result of malfunction of the proteins that control cell growth (leading to permanent cell division) and cell death (making the cell insensitive to normal signals to die). Numerous genetic abnormalities have been implicated in the malfunction of cell controls. Two critical proteins involved in lymphoma development are bcl-2 and bcl-6.
The identification of these genetic irregularities has important implications for treating lymphoma, as it indicates potential targets for manipulation with pharmaceutical drugs or nutritional supplements. For example, pharmacological agents capable of inactivating bcl-6 can cause increased cell death (apoptosis) in lymphoma cells (Pasqualucci L et al 2003). Furthermore, in clinical studies, an agent that targets bcl-2 has also been shown to have efficacy in non-Hodgkin’s lymphoma patients (Chanan-Khan A 2004).