Journal of Leukemia
Open Access

A Brief Note on Follicular Lymphoma

Stella Brambilla^{* *}Correspondence: Dr. Stella Brambilla, Department of Medicine, Surgery and Neuroscience, University of Naples, Corso Umberto ,Napoli , NA, Italy, Email:

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About the Study

Follicular Lymphoma (FL) is a malignancy that affects lymphocytes, which are white blood cells. The malignancy is caused by the unregulated division of centrocytes and centroblasts, two types of B-cells. These cells generally reside in the germinal centres of lymphoid tissues such as lymph nodes, where they form follicles (nodular swirls of several types of lymphocytes). The malignant cells in FL generally develop follicular or follicle-like structures in the tissues they invade. These structures are frequently the cancer's most prominent histological feature. CB/CC lymphoma (centroblastic and centrocytic lymphoma), nodular lymphoma, Brill-Symmers Disease, and the subtype name, follicular large-cell lymphoma are all synonyms and obsolete designations for FL. This disease is the second most prevalent type of non-lymphoma Hodgkin's in the United States and Europe, trailing only diffuse large B-cell lymphoma. FL accounts for 10%-20% of non-lymphomas, Hodgkin's with around 15,000 new cases identified each year in the United States and Europe.

According to recent studies, FL is also frequent in Japan. FL is a wide-ranging and exceedingly complicated clinical entity with a variety of manifestation that has yet to be fully systematized. It is frequently preceded by a benign precancerous condition characterized by the accumulation of aberrant Centro blast and/or Centro blasts in lymphoid tissue. They may then circulate in the bloodstream, causing in situ lymphoid neoplasia of the follicular lymphoma type, which is asymptomatic (i.e. ISFL). Only a fraction of these cases advance to FL. The swelling of lymph nodes in the neck, armpits, and/or groyne is the most prevalent symptom of FL. It appears as a gastrointestinal tract cancer, a malignancy in children involving lymphoid tissues of the head and neck (e.g. tonsils), or one or more tumours in nonlymphoid tissues such as the testes less frequently. FL is a slowmoving disease that can last for years with no change in its course. However, 2-3 percent of FL cases advance to a very aggressive form known as stage 3B FL, aggressive diffuse large Bcell lymphoma, or another type of aggressive B-cell malignancy every year. Transformed follicular lymphomas (t-FL) are almost always fatal. However, recent breakthroughs in the treatment of t-FL (for example, the inclusion of medicines like rituximab to conventional chemotherapy) have increased overall survival times. These newer regimens may also help to postpone the transition from FL to t-FL. Further developments in our understanding of FL may lead to improvements in the disease's treatment. The accumulation of increasing numbers of genomic changes (i.e. chromosome abnormalities and gene mutations) in the formative B-cell progenitors to both illnesses appears to be involved in the serial progressions of in situ FL to FL and FL to t-FL. At least some of these changes appear to result in the overor under-expression of gene products that control these cells' ability to survive, proliferate, and disseminate to other tissues, as well as their vulnerability to develop further genomic abnormalities. As a result, the condition is populated by many Bcell clones with growing genomic abnormalities and malignant characteristics. There does not appear to be a single genetic mutation that causes all of the FL illnesses. This serial progression appears to be driven by interactions between numerous genetic changes. An aggregation of monoclonal B cells (i.e. cells descended from a single ancestor cell) in the germinal centers of lymphoid tissue is known as in situ follicular lymphoma. A translocation between position 32 on chromosome 14's long arm and position 21 on chromosome 18's q arm is a common pathogenic genetic aberration in these cells.

Conclusion

The B-cell lymphoma 2 (BCL2) genes on chromosome 18 at position q21·33 is close to the immunoglobulin heavy chain locus (IGH@) on chromosome 14 at position q21 in this translocation. BCL2 overexpresses its product, BCL2 apoptotic regulator, as a result (i.e. Bcl2). Bcl2 prevents cells from dying due to programmed cell death, allowing them to live longer. Overexpression of Bcl2 in ISFL B-cells is thought to play a key role in their abnormal accumulation and eventual malignant development.