![]() ![]() ![]() Elevated levels of LDH and uric acid suggest high cell turnover and release of degradation products into the bloodstream. Systemic symptoms (B-symptoms) are due to increased cytokine production. Lymphadenopathy occurs due to the proliferation of B cells in or around the germinal center. B cell lymphomas are categorized based on the stage of B cell development that has resulted in malignancy (i.e., mantle cell vs. Pathophysiology of non-Hodgkin B cell lymphomas is dependent on the type of lymphoma. DLBCL commonly involves extranodal sites, which include the brain, bones, kidneys, adrenal glands, and other soft tissues. The t(14:18) is seen in more than 90% of FL and about 30% of DLBCL patients. A triple hit lymphoma has rearrangements in BCL2, BCL6, and MYC. The (14 18) translocation is related to disseminated and nodal disease and does not imply a poor prognosis. Double hit lymphoma presents like DLBCL but has MYC along with BCL2 and/or BCL6. More than 50% of the DLBCL expresses surface or cytoplasmic immunoglobulin IgM. Very rarely, they can express CD5, which has a poor prognosis. CD30 can be seen in 25% and carries a favorable prognosis. The flow cytometry reveals CD19, CD20, CD22, CD45 and CD79a. Some of them also express abnormalities in the gene MYC. About 80% of DLBCL expresses B cell leukemia or lymphoma 2 (BCL2) protein, and 70% expresses B cell lymphoma 6 (BCL6) protein. To better understand the molecular diversity among morphologically similar variants of DLBCL, high throughput technology such as gene expression profiling (GEP) could classify DLBCL into germinal center B-cells (GCB) and activated B-cells (ABC). Most of the patients with DLBCL show gene rearrangements in the heavy and light chains of the immunoglobulin. ![]() Non-Hodgkin lymphoma (NHL) is more common in obese and patients with an underlying history of autoimmune diseases. Chemical agents such as dyes and pesticides can also increase the risk for lymphoma. Other risk factors for the development of B-cell lymphomas include family or personal history of lymphoma, history of radiation, and chemotherapy. Also, the transformation from different kinds of lymphomas, including splenic marginal zone lymphoma, marginal zone (MALT) lymphoma, chronic lymphocytic leukemia (Ritcher transformation), can result in DLBCL. Likewise, an immunosuppressive medication used in transplant patients is a risk factor for the development of B-cell lymphomas. HIV is a risk factor for neoplasm development, as it decreases the hosts' ability to regulate malignant cells. Certain infectious agents can directly manipulate the DNA, as seen in Burkitt's lymphoma, where the Epstein Barr virus DNA is transported into the B cell nucleus, thus altering the B cell growth and development. Chronic immunodeficiency of T cells and B cell stimulation can be the possible cause for NHL in human immunodeficiency virus (HIV) infected patients. Genetic alterations in the BCL6 gene can be seen in 20% to 40% of the patients. Like any other malignancy, B cell lymphomas can result from the genetic mutations affecting the proto-oncogenes and tumor suppressor genes however, the environment within the lymph nodes can also promote lymphomagenesis. Most of the B- cell lymphomas are derived from the germinal center. ![]() The development of B cells can be categorized into 3 stages- pre-germinal, germinal, and post-germinal center. Depending on the morphology, genetics, and immunophenotype of the neoplastic cells, a cell of origin (COO) is proposed. The B cell lymphomas result from the malignant proliferation of B cells during their various stages of development. ![]()
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