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Gene Rearrangement in Leukemias and Lymphomas
Published in John T. Kemshead, Pediatric Tumors: Immunological and Molecular Markers, 2020
The monoclonal nature of B-PLL (B cell prolymphocytic leukemia) has been demonstrated by immunological and molecular methods.5,34 In 5/5 cases, both alleles of the IgH gene were rearranged. Immunological analysis of one case demonstrated that the neoplastic clone expressed both K and X light chains.5 However, only K gene rearrangement was detected by Southern blotting, probably because the proportion of the population expressing λ chains (8%) was below the threshold of sensitivity of the technique.
Mature B-Cell Neoplasms
Published in Dongyou Liu, Tumors and Cancers, 2017
Accounting for about 85% of NHL cases, mature B-cell neoplasms are subdivided into at least 45 types (i.e., chronic lymphocytic leukemia/small lymphocytic lymphoma [CLL/SLL], monoclonal B-cell lymphocytosis, B-cell prolymphocytic leukemia, splenic marginal zone lymphoma, hairy cell leukemia [splenic B-cell lymphoma/leukemia unclassifiable—splenic diffuse red pulp small B-cell lymphoma/hairy cell leukemia-variant], lymphoplasmacytic lymphoma [LPL], Waldenström macroglobulinemia, monoclonal gammopathy of undetermined significance [MGUS] IgM, μ heavy-chain disease, γ heavy-chain disease, α heavy-chain disease, monoclonal gammopathy of undetermined significance [MGUS] IgG/A, plasma cell myeloma, solitary plasmacytoma of bone, extraosseous plasmacytoma, monoclonal immunoglobulin deposition diseases, extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue [MALT lymphoma], nodal marginal zone lymphoma—pediatric nodal marginal zone lymphoma, follicular lymphoma [FL], in situ follicular neoplasia, duodenal-type follicular lymphoma, pediatric-type follicular lymphoma—large B-cell lymphoma with IRF4 rearrangement, primary cutaneous follicle center lymphoma, mantle cell lymphoma [MCL], in situ mantle cell neoplasia, diffuse large B-cell lymphoma not otherwise specified [DLBCL NOS], germinal center B-cell type, activated B-cell type, T-cell/histiocyte-rich large B-cell lymphoma, primary DLBCL of the central nervous system [CNS], primary cutaneous DLBCL leg type, EBV+ DLBCL NOS—EBV+ mucocutaneous ulcer, DLBCL associated with chronic inflammation, lymphomatoid granulomatosis, primary mediastinal [thymic] large B-cell lymphoma, intravascular large B-cell lymphoma, ALK+ large B-cell lymphoma, plasmablastic lymphoma, primary effusion lymphoma—HHV8+ DLBCL NOS, Burkitt lymphoma—Burkitt-like lymphoma with 11q aberration, high-grade B-cell lymphoma with MYC and BCL2 and/or BCL6 rearrangements, high-grade B-cell lymphoma NOS, and B-cell lymphoma unclassifiable with features intermediate between DLBCL and classical Hodgkin lymphoma) [2].
Diagnostic and therapeutic challenges in hairy cell leukemia-variant: where are we in 2021?
Published in Expert Review of Hematology, 2021
There is no recurrent chromosomal abnormality identified by conventional cytogenetics in HCL-V. Complex karyotypes including numerical and structural abnormalities are common [6,11,16]. Translocations may involve the 8q24 breakpoint but 17p deletions encompassing the tumor suppressor TP53 gene are more common than 8q abnormalities. Deletion of ATM has also been reported in close to a quarter of HCL-V cases [11]. A number of genetic lesions have been identified by high-resolution genomic profiling in both typical HCL and HCL-V but any of them are specific to a disease [8]. Copy number aberrations (CNA) were documented in both diseases with chromosome losses predominating over gains and a much higher complexity and instability in HCL-V compared to typical HCL. Common to both disease included gains on chromosome 5 and losses on 7q with a minimal deleted region at 7q31-32 as in SMZL. By contrast deletions of 17p, encompassing the TP53 gene were only found in HCL-V confirming previous reports that this abnormality is exceedingly rare in typical HCL [22]. Cases with 17p deletion had frequently a TP53 mutation in the other non-deleted allele. The frequency of 17p deletion in HCL-v is similar to that of B-cell prolymphocytic leukemia (B-PLL) and higher than that seen in CLL, SMZL, and SDRPL.
Polatuzumab vedotin: an investigational anti-CD79b antibody drug conjugate for the treatment of diffuse large B-cell lymphoma
Published in Expert Opinion on Investigational Drugs, 2020
Estelle Bourbon, Gilles Salles
Since its discovery in 1992 [25–27], CD79 has been considered as an interesting therapeutic target for antibody as it is physiologically and exclusively expressed on mature B-cell and in the vast majority of B-cell NHLs, including DLBCLs (from 90% to 100%) [28,29], but also B acute lymphoblastic leukemia (B-ALL), chronic lymphocytic leukemia (CLL), B-cell prolymphocytic leukemia (PLL), splenic lymphoma with villous lymphocytes (SLVL), hairy cell leukemia (HCL), follicular lymphoma (FL), and mantle-cell (MCL) lymphoma [21–23].