MYC rearrangement + BCL6 rearrangement

The most frequent type of lymphoma is DLBCL with a GCB immunophenotype. In this cohort, most patients received chemotherapy and had a favourable prognosis.

He then received dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-EPOCH) followed by high-dose methotrexate and initially responded but relapsed several months later. As the patient was not a candidate for transplant, subsequent treatment rounds included rituximab, gemcitabine, dexamethasone, and cisplatin (R-GDP) and CD19 CAR T-cell therapy; tafasitamab-cxix and lenalidomide; and polatuzumab vedotin plus bendamustine and rituximab (pola-BR)...Within approximately 1 month, he could resume treatment, achieving a Deauville score of 1 approximately 3 months after beginning epcoritamab, and continues follow-up nearly 2 years later. T-cell engager therapies, such as epcoritamab, can play a role in managing patients with refractory DLBCL, including those refractory to CAR T-cell therapy.

P2, N=50, Recruiting, Fujian Medical University Union Hospital; Fujian Medical University Union Hospital

Patient is still in complete remission at 21 months from infusion. This report represents a case of a correct referral and a full collaboration between centers.

Following induction with R-CHOP chemotherapy, BCL6-DHL patients demonstrated a poor OS similar to BCL2-DHL patients and worse than that of DLBCL patients (p = 0.024)...The data also suggest that BCL6-DHL as currently defined, is heterogeneous and that neoplasms with a GCB immunophenotype are more likely to have DH-like signature and behave more aggressively. Lastly, we suggest that BCL6-DHL cases deserve to be recognized separately in a lymphoma classification to facilitate further understanding of these neoplasms and for optimal patient management.

High-grade B-cell lymphomas are subclassified based on morphologic and genetic features. There are differences in the nomenclature and definition of these lymphomas in the WHO-5 and ICC classifications. Distinguishing HGBLs from other mature B-cell lymphomas and B-LBL/ALL is critical so that patients receive appropriate treatment.

In this review, we provide an update of HGBL and its subgroups, focusing on their clinicopathologic features, diagnosis, molecular genetic features, and pathogenesis. Our diagnostic approach and caveats for differential diagnosis are also discussed with an emphasis on the differential diagnosis with B lymphoblastic leukemia/lymphoma.

The patient was assigned Stage IEA, IPI = 0 and received chemotherapy. This case depicts a very uncommon occurrence of fully localized LBL in a patient of an unusually young age and clinical presentation for this type of lymphoma.

Furthermore, because one IGH allele is already disrupted by the existing BCL2 rearrangement, the MYC rearrangement architecture in HGBCL-DH-BCL2 likely reflects selective pressure to preserve both BCL2 and B cell receptor expression. These data provide new mechanistic explanations for the distinct patterns of MYC rearrangements observed across different lymphoma entities.

She was treated with dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin and rituximab chemotherapy. Rituximab was discontinued owing to largely absent CD20 expression. Interim positron emission tomography-CT after three cycles revealed a complete response, and the patient completed six cycles of therapy.

Our virtual MTB approach identified potential molecularly targeted treatment options alongside targetable genomic signatures for both prDLBCL/HGBL-MYC/BCL2 and prHGBL, NOS-MYC/BCL6. These results underline the potential of MTB consultations in difficult-to-treat lymphomas early in the treatment sequence.