Non-Hodgkin’s lymphoma (NHL) is a group of malignancies that develop in lymphoid tissues, mainly in the lymph nodes. These tumors can be caused by chromosomal translocations, toxins, chronic inflammation, and infections.
Non-Hodgkin’s lymphoma (NHL) is a group of heterogeneous lymphoproliferative malignancies that are much less predictable than Hodgkin’s lymphoma and have a much greater tendency to spread to extranodal sites. About 25% of NHL cases occur in the extranodal site, and most occur in both the nodular and extranodal sites1.
In developed countries, the most common NHL subtypes are large B-cell lymphoma (about 30%) and follicular lymphoma (about 20%). The incidence of all other NHL subtypes is less than 10%2. NHL is the sixth leading cause of cancer-related death in the United States, after lung, prostate, breast, bladder, and colorectal cancers.
Etiology of non-Hodgkin’s lymphoma
Central etiological mechanisms include
- loss of control of T-cell function, and
- stimulation of chronic antigens associated with latent EBV infection.
B and T lymphocytes are important cells of the immune system, primarily protecting against infectious agents. Normally, B cells produce antibodies that have the ability to bind to antigens, while T cells recognize antigens presented by other cells.
Immunosuppression due to various medical conditions increases the risk of NHL. The best-known risk factors for malignant lymphoma are dysfunction or inhibition of T cell function (HIV/AIDS, organ transplantation), resulting in B cell proliferation and transformation by Epstein–Barr virus (EBV)3.
Chronic antigen stimulation increases B cell proliferation, increasing the risk of accidental genetic errors, particularly those caused by rearrangements of immunoglobulin genes. Therefore, factors contributing to the prevalence could potentially lead to more errors.
When a virus acts as an external stimulus, the virus itself can infect normal cells and integrate the viral DNA into the host’s genome, turning the cells into self-replicating malignant cells. In any case, stimulation of the antigen can result in a compensatory reduction in the T cell response, an immunosuppressive state.
Lymphoma tumor cells are a malignant form of these progenitor lymphocytes, the growth of which stopped at certain stages of differentiation.
Chromosomal translocations, usually recombination, are a genetic feature of lymphoid malignancies. Their presence is confirmed in 90% of NHL cases. At the molecular level, these transfers with or without additional chromosomal deletions and mutations can lead to activation or inactivation of tumor suppressor genes4.
- 1.Bowzyk AN, Ajithkumar T, Behan S, Hodson D. Non-Hodgkin lymphoma. BMJ. 2018;362:k3204. doi:10.1136/bmj.k3204
- 2.Ekström-Smedby K. Epidemiology and etiology of non-Hodgkin lymphoma–a review. Acta Oncol. 2006;45(3):258-271. doi:10.1080/02841860500531682
- 3.Meena JP, Gupta AK, Parihar M, Seth R. Clinical profile and outcomes of Non-Hodgkin’s lymphoma in children: A report from a tertiary care hospital from India. Indian Journal of Medical and Paediatric Oncology. Published online January 2019:41-47. doi:10.4103/ijmpo.ijmpo_70_18
- 4.Fisher S, Fisher R. The epidemiology of non-Hodgkin’s lymphoma. Oncogene. 2004;23(38):6524-6534. doi:10.1038/sj.onc.1207843