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Whether a large B-cell lymphoma resembles a germinal-centre B cell or an activated B cell; the activated type does worse and depends on different pathways.
Cell of origin classifies diffuse large B-cell lymphoma by whether it resembles a germinal-centre B cell (GCB) or an activated B cell (ABC); the activated type does worse and depends on different pathways. It is determined by gene expression with the Lymph2Cx assay or approximated by the Hans immunohistochemistry algorithm. ABC or non-GCB lymphomas depend on NF-kappaB and B-cell receptor signalling through BTK, IRAK4 and MYD88 L265P, while GCB lymphomas depend on BCL-2 and EZH2; the CD79b target entry also links here. Newer genetic classifications such as LymphGen, with its MCD, BN2, N1, EZB, ST2 and A53 clusters, refine the split but are not yet clinically routine. The concept also appears in primary CNS lymphoma and HIV-associated lymphomas.
In plain words · A protein that stops cells from self-destructing. Venetoclax removes that protection and has transformed leukaemia treatment.
Showing the target this term concerns: BCL-2.
The glossary entry explains the word; the readout page carries the scoring rule, the thresholds approvals use, the companion diagnostics and the tests.
The piece that turns a research classification into something a trial can use on one person's biopsy, with a probability attached rather than a flat label. It is the reason genetics-directed lymphoma trials became possible at all.
A failure worth reading: the drug worked where patients could tolerate the regimen it was added to, and harmed where they could not. It is the strongest argument in lymphoma for designing first-line combinations around what an older patient can finish.
The genetic nosology that precision-medicine trials in diffuse large B-cell lymphoma now use to pick patients. It gives a mechanism, not just a label: two of the four subtypes point at a drug class that already exists.
One of the two foundational genetic classifications of diffuse large B-cell lymphoma. Neither has yet changed what a patient receives outside a trial, but together they are the reason precision-medicine trials in this disease now select by genetics rather than by cell of origin.
Rituximab remains the CD20 antibody used in first-line diffuse large B-cell lymphoma. The result is a warning against assuming an antibody improvement carries from one B-cell malignancy to another: the same substitution improved progression-free survival in chronic lymphocytic leukaemia and in follicular lymphoma.
The paper that established lymphoma as the solid-tumour field where circulating tumour DNA works best, because the mutations are many and the tumour sheds. It underpins the response-adapted trial designs now being built on molecular rather than radiographic response.
The practical form of cell-of-origin classification, used in pathology laboratories worldwide. When a report says germinal-centre or non-germinal-centre, this is almost always the algorithm behind it.
The reason a pathology report on diffuse large B-cell lymphoma says germinal-centre or non-germinal-centre, and the origin of every attempt since to treat the two differently. It also made the case that microarray profiling could do something the clinical index could not, which is what pulled genomics into haematology.
Shares Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray, Cell of origin in practice: Hans against expression profiling, and what it changes, The use of molecular profiling to predict survival after chemotherapy for diffuse large-B-cell lymphoma, Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes.
Shares Cell of origin in practice: Hans against expression profiling, and what it changes, CD79B ITAM mutation, ARCHED, MYD88 L265P and CXCR4 mutations.
Shares The germinal centre reaction, LymphGen and the genetic clusters of large B-cell lymphoma, The germinal centre: why lymphoma starts where antibodies are made, EZH2.
Shares Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes, LymphGen and the genetic clusters of large B-cell lymphoma, A probabilistic classification tool for genetic subtypes of diffuse large B cell lymphoma with therapeutic implications, Genetics and pathogenesis of diffuse large B-cell lymphoma.
Shares Double expressor: MYC and BCL2 protein together by immunohistochemistry, The germinal centre reaction, The germinal centre: why lymphoma starts where antibodies are made, BCL-2.
Shares The use of molecular profiling to predict survival after chemotherapy for diffuse large-B-cell lymphoma, A probabilistic classification tool for genetic subtypes of diffuse large B cell lymphoma with therapeutic implications, Genetics and pathogenesis of diffuse large B-cell lymphoma, Lymphoma roadmap: from a jaw tumour in Uganda and the first human cancer virus to gene-expression subtypes, PET-adapted chemotherapy, CAR-T cells, bispecific antibodies and the genetics-directed trials now recruiting.
Shares Double expressor: MYC and BCL2 protein together by immunohistochemistry, The germinal centre reaction, The germinal centre: why lymphoma starts where antibodies are made, BCL-2.
Shares Obinutuzumab or rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone in previously untreated diffuse large B-cell lymphoma, GOYA, Randomized phase III trial of ibrutinib and R-CHOP in non-germinal centre B-cell diffuse large B-cell lymphoma (PHOENIX), Lymphoma roadmap: from a jaw tumour in Uganda and the first human cancer virus to gene-expression subtypes, PET-adapted chemotherapy, CAR-T cells, bispecific antibodies and the genetics-directed trials now recruiting.