Non-Hodgkin’s Lymphoma

Summary

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.

Introduction

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 sites^​1​.

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

• immunosuppression,
• 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 genes^​4​.

References