1. B lineage lymphoblastic lymphoma and acute myeloid leukemia are histologically indistinguishable, but the former is positive for PAX5, CD19, CD79a, or CD22, while the latter is positive for CD13, CD33, and myeloperoxidase. CD10, CD38, CD43, CD71 and bcl-6 are also expressed. TdT is almost always present in the nucleus of lymphoblastic lymphoma cells (although it may also be found in biphenotypic and some myeloid leukemias). By evaluating the patterns of CDs present on the cells, it is possible to classify the cells. Other T cell lymphomas are often lumped together as peripheral T cell lymphomas. Some oncologists and pathologists feel LL is acute lymphoblastic leukemia in an extramedullarly site. The protein has no known natural ligand[8] and its function is to enable optimal B-cell immune response, specifically against T-independent antigens. Cytochemistry: PAX-5 (B cell marker), Ki-67 (proliferation marker) is expected to be strongly positive. Here is a list of commonly-used markers. Neuroendocrine carcinomas, including carcinoids and small cell carcinoma, can mimic T-LBL, although immunophenotypic studies readily show the correct diagnosis. On small biopsies, extensive crush artifact and encrustation of vessel walls by basophilic debris (the Azzopardi phenomenon) can also be observed. Lymphoblastic lymphoma and acute lymphoblastic leukemia are morphologically and immunophenotypically the same disease and are distinguished on clinical grounds. The remaining LL patients have a precursor B-cell phenotype more commonly presenting as disease localized in skin and bone rather than T-cell LL. Distinguishing populations of cells can be relatively straightforward for cell lines where there is only one type of cell, but it can be more complex for samples where there are multiple cell types. Surface expression of CD3 may be slight to absent, so the cells may appear to be negative on flow cytometry, although immunohistochemical stains show cytoplasmic positivity. Tumor cells are positive for CD45, the B cell markers CD19, CD22 and CD79a with a monoclonal light chain expression of kappa or lambda. Cancer 6: 35. doi:10.1186/1476-4598-6-35. [3], Burkitt lymphoma can be divided into three main clinical variants: the endemic, the sporadic, and the immunodeficiency-associated variants.[3]. PathologyOutlines.com website. Diffuse Large B-cell lymphoma (DLBCL) the single largest category of lymphoma, is a heterogeneous group of malignant lymphomas with several morphologic features. Fifty percent to 70 percent of patients with lymphoblastic lymphoma (T cell) present with an intrathoracic tumor. The median age is 70-80 years of age; however, can be seen in children. The blast markers CD34 and TdT are negative. An anterior mediastinal mass is commonplace (up to 80% of patients) and can induce clinical symptoms mimicking bronchial asthma (resulting from tracheal compression) or the superior vena cava syndrome. Actually, Burkitt lymphoma can be the initial manifestation of AIDS. CD11c, CD25, CD103, CD123: Hairy cell leukemia cells. CYTOMORPHOLOGY OF LYMPHOBLASTIC LYMPHOMA: Smears are nearly always cellular and contain monotonous lymphoblasts to the near exclusion of any other cell type. Copyright © 2020 Elsevier B.V. or its licensors or contributors. Currently you have JavaScript disabled. [5], In humans CD20 is encoded by the MS4A1 gene. Debris and dead cells often have a lower level of forward scatter and are found at the bottom left corner of the density plot. About 90% of cases are of T-cell derivation, the remainder derives from B-cells. It might be a good idea to know some of these markers. Click here for instructions on how to download the free FCS Express Reader to view and manipulate the sample cases. In a large study by Nathwani and colleagues,232 78% of patients died of the disease, with a median survival of 17 months. Forward and side scatter gating is often used to remove dead cells which have increased autofluorescence and non-specific binding of antibodies, however, including a viability dye is a much more reliable method. Although a convoluted nuclear configuration is very helpful for diagnosis, that feature may be absent in up to 50% of cases.232 The key to diagnosis lies in recognizing the immature appearance of the nuclei, which are characterized by their finely distributed chromatin and inconspicuous nucleoli. Today there are more than 320 CD clusters described in humans. The protection afforded by anti-CD-20 lasted approximately forty days—the time it takes the body to replenish its supply of B cells—after which repetition was necessary to restore it. https://www.pathologystudent.com/a-short-list-of-cd-markers/, F.M. Immunodeficiency-associated Burkitt lymphoma may demonstrate more plasmacytic appearance or more pleomorphism, but these features are not specific. [25] Epstein-Barr virus infection is strongly correlated with this cancer. 2-Light is used to illuminate the cells in the channel. The lower incidence was possibly the result of more intensive systemic treatment and incorporation of intrathecal chemoprophylaxis for LBL. When the DNA of tumor cells is analyzed using electrophoresis, a clonal band can be demonstrated, since identical IgH genes will move to the same position. Jejunal ulceration and perforation often supervene. Burkitt lymphoma is a cancer of the lymphatic system, particularly B lymphocytes found in the germinal center.It is named after Denis Parsons Burkitt, the Irish surgeon who first described the disease in 1958 while working in equatorial Africa. In a trial of patients with DLBCL to whom intrathecal methotrexate (MTX) was given as CNS prophylaxis, the incidence was only 1.6%. You already know a few: CD3, for example, is a CD marker that’s on the surface of all mature T cells, CD4 is on helper T cells and CD8 is on cytotoxic T cells. similar in size and morphology) population of medium size lymphoid cells with highproliferative activity and apoptotic activity. The cells are unusually large, have a variable display of T cell antigens, and often involve nodal sinuses and extranodal sites. It will always remain difficult to assemble sufficiently large cohorts of particular subgroups, especially some rare ones, that are treated with the same or closely comparable regimens, to solve these questions. This gene encodes a B-lymphocyte surface molecule that plays a role in the development and differentiation of B-cells into plasma cells. Pleural effusions are often observed, and patients may complain of dyspnea, chest pain, or dysphagia. Translocation of the bcl-2 gene (generally associated with FCL) can occur in 20-30% of cases of DLBCL. DLBCL would fall in the large lymphocyte region as shown below. Consists of sheets of monotonous (i.e. CD23 and CD5 : Chronic lymphocytic leukemia/small lymphocytic lymphoma CD23 negative and CD5 positive: Mantle cell lymphoma cells CD30 and CD15: Reed-Sternberg cells CD30 positive and CD15 negative: Anaplastic large cell lymphoma cells CD31: Endothelial cells (positive in angiosarcoma) CD33: Myeloid cells and precursors The forward scatter threshold can be increased to avoid collecting these events, or they can be removed by gating on the populations of interest (Figure A). Independent risk factors in a multivariable analysis were increased LDH concentration and the involvement of more than one extranodal site at presentation. Antibodies to CD43 are often thought of as T-cell markers, but their specificity is quite broad. The distinction between these two conditions is made mainly on clinical grounds. The tumor cells have a similar appearance to the cancer cells of classical African or endemic Burkitt lymphoma. Immunologic markers in non-Hodgkin's lymphoma. The EBV genome is found in the majority  of neoplastic BL cells. This gene encodes a member of the membrane-spanning 4A gene family. It accounts for 30-50% of childhood lymphoma. Precursor T-cell ALLs are much less common than precursor B-cell ALLs, but they compose greater than 80% of cases that present as lymphoblastic lymphoma. tumor nuclei size similar to that of histiocytes or endothelial cells). these can be stratified as large and small lymphocytes (CD45 positive). For more information and a comprehensive list of CD markers please visit this link. All types of Burkitt lymphoma are characterized by dysregulation of the c-myc gene by one of three chromosomal translocations. The tumor cells of lymphoblastic lymphoma are histologically indistinguishable from those of acute lymphoblastic leukemia. A recent large study of adult patients with aggressive NHL registered CNS disease in only 2.2% (Boehme et al., 2007). Normal B cells of a germinal center possess rearranged immunoglobulin heavy and light chain genes, and each isolated B cell possesses a unique IgH gene rearrangement. Neoplasms may be benign (non-cancerous), malignant (cancerous), or precancerous, but, like any other cell, have CD markers that scientists can use to identify them. Lymphoblastic lymphoma affects predominantly children and adolescents, although it may occur at any age, with a second peak after 40 years of age. Other treatments for Burkitt lymphoma include immunotherapy, bone marrow transplants, stem cell transplant, surgery to remove the tumor, and radiotherapy. Rein Willemze M.D., in The Lymphomas (Second Edition), 2006, B-lymphoblastic lymphoma is a malignant proliferation of precursor B lymphocytes. CD20 and LCA may be negative in precursor B-cell lymphoblastic lymphoma/leukemia.