We report the case of a 66-year-old woman who was diagnosed with localized tracheal amyloid light-chain (AL) amyloidosis caused by an underlying B-cell neoplasm. The diagnosis was confirmed through subsequent bronchoscopy and biopsies; however, she experienced a challenging episode of hypoxic respiratory failure that required intervention. Repeat bronchoscopies showed persistent subglottic stenosis and tracheobronchomalacia, which led to tracheal debulking surgery and additional interventions. The patient\'s treatment began with rituximab, zanubrutinib, and dexamethasone with outpatient follow-up. The rarity of tracheobronchial amyloidosis and its connection to B-cell malignancies are highlighted, emphasizing the challenges in diagnosis and the importance of tailored treatment strategies. The patient\'s clinical course, characterized by atypical respiratory symptoms, delayed diagnosis, and an evolving treatment approach, underscores the complexities of managing such a rare and intricate case.

Primary drug resistance and minimal residual disease are major challenges in the treatment of B cell neoplasms. Therefore, this study aimed to identify a novel treatment capable of eradicating malignant B cells and drug-resistant disease. Oncolytic viruses eradicate malignant cells by direct oncolysis and activation of anti-tumor immunity, have proven anti-cancer efficacy, and are safe and well tolerated in clinical use. Here, we demonstrate that the oncolytic virus coxsackievirus A21 can kill a range of B cell neoplasms, irrespective of an anti-viral interferon response. Moreover, CVA21 retained its capacity to kill drug-resistant B cell neoplasms, where drug resistance was induced by co-culture with tumor microenvironment support. In some cases, CVA21 efficacy was actually enhanced, in accordance with increased expression of the viral entry receptor ICAM-1. Importantly, the data confirmed preferential killing of malignant B cells and CVA21 dependence on oncogenic B cell signaling pathways. Significantly, CVA21 also activated natural killer (NK) cells to kill neoplastic B cells and drug-resistant B cells remained susceptible to NK cell-mediated lysis. Overall, these data reveal a dual mode of action of CVA21 against drug-resistant B cells and support the development of CVA21 for the treatment of B cell neoplasms.

Non-Hodgkin lymphoma is made from the B-cell lineage and includes extra-nodal marginal lymphomas, follicular lymphomas, mantle cell lymphoma, diffuse large B-cell lymphoma, and Burkitt lymphoma. Burkitt lymphoma is associated with Epstein Barr Virus and Human Immunodeficiency Virus. Although it is common for other B-cell lymphomas to develop in the stomach, it is less common for Burkitt lymphoma tumors to manifest there. Additionally, primary and/or secondary involvement of the duodenum, pancreas, and intestines is very rare in Burkitt lymphoma. Herein, we present a male diagnosed with extensive Burkitt lymphoma of the bone, lymph nodes, pancreas, small intestine, duodenum, and stomach.

Plasmablastic lymphoma (PBL) is considered an aggressive rare variant of diffuse large B-cell lymphoma that has a predilection to develop in immunocompromised patients, particularly HIV-positive individuals. This report highlights the development of such a rare and aggressive malignancy in a 55-year-old immunocompetent male. It outlines the atypical clinical presentation and pathological features of this disease entity. Overall prognosis and response to chemotherapy differ in the absence or presence of immunosuppression. This report includes a summary of the epidemiologic, clinical, and immunohistochemical characteristics of PBL based on a comprehensive review of the reported cases occurring in immunocompetent individuals.

Heavy chain diseases (HCDs) are rare B cell lymphoplasma cell proliferative disorders that are characterized by the production of incomplete monoclonal immunoglobulin (Ig) heavy chains without the associated light chains. γ-HCD (IgG subtype) is a rare subtype, with ~150 cases reported in the literature to date; however, to the best of our knowledge, no reports of T cell receptor (TCR) gene rearrangement in γ-HCD exist in the literature. The present study reports the case of an 81-year-old man with γ-heavy chain disease associated with TCR gene rearrangement, identified in lymph node biopsy and bone marrow aspirate specimens. The present case revealed an alternative manifestation of γ-HCD, which may provide additional biological insights into this rare B cell disorder.