CD79B (CD79b Molecule)

Nonetheless, some patients experienced high-grade AEs or symptom recurrence and stopped BV/PV therapy. Future studies may provide clarification and guide clinical practice.

CD20-negative large B-cell lymphomas exhibit aggressive behavior and are ineligible for rituximab-containing therapy...In conclusion, CD79B and CD19 were variably expressed in CD20-negative large B-cell lymphomas, but lower in de novo DLBCL, and especially in plasmablastic lymphoma. Programmed cell death protein 1/programmed death-ligand one inhibitors may represent a treatment option.

Polatuzumab vedotin, an antibody-drug conjugate (ADC) targeting the B cell receptor (BCR) signaling subunit CD79B, has recently entered frontline therapy for diffuse large B cell lymphoma (DLBCL) and high-grade B cell lymphoma (HGBCL), achieving encouraging clinical results...Overall, our results uncover targetable vulnerabilities in MYC-driven B cell lymphomas, possibly extending to other aggressive B cell tumors silencing BCR expression. The data provide a rational basis for integrating CD79B-directed ADCs with mTOR or CDK4/6 inhibitors to prevent or overcome treatment resistance of aggressive B cell lymphomas.

Recently, ADCs have expanded the DLBCL therapeutic landscape, with the approvals of CD79b-targeted polatuzumab vedotin and CD19-directed loncastuximab tesirine for R/R and even frontline disease. However, the clinical application of ADCs is accompanied by challenges, including the management of characteristic toxicities, understanding and overcoming mechanisms of resistance. This review systematically synthesizes the mechanisms of action, updated clinical evidence, toxicity profiles, and resistance mechanisms of ADCs in DLBCL, while also discusses management strategies and provides perspectives on future directions.

The avidity of both 68Ga- and 177Lu- cyclic pentapeptide radiotracers was noted in the mesenteric mass at the L4 level. Dosimetry study using 177Lu-cyclic pentapeptide indicated kidneys as the critical organ with max residence time of 5.39 h. Theragnostic complex of radiolabelled 68Ga/177Lu- cyclic pentapeptides have the potential to in-vivo target the CXCR4 receptor expression.

These exploratory data suggest that CD79B downregulation is a recurrent feature of MDS and AML and that CD79B may influence leukemic cell behavior and immune microenvironmental signals. The findings generate hypotheses for future mechanistic studies and evaluation of CD79B as a potential biomarker in myeloid malignancies.

P2, N=22, Recruiting, Zulfa Omer | Not yet recruiting --> Recruiting

P2, N=62, Recruiting, Zulfa Omer | Not yet recruiting --> Recruiting | Initiation date: Jun 2025 --> Dec 2025

Across the entire upper airway cohort (n = 111), MCD-like status consistently correlated with site-specific relapse and adverse clinical outcomes. These findings support expanding the utility of simplified MCD-like classification as a practical tool for prognostic prediction, relapse site estimation, and therapeutic guidance in upper airway DLBCL, with potential for broader application to anatomically diverse DLBCL-NOS cases.

PHH and NMDARE revealed distinct neuroinflammatory proteomic signatures compared to our control samples. PHH was marked by a broad increase in detection of the majority of inflammation-related proteins, with highest representation among the alternative complement and coagulation-related pathways. The persistent detection of these proteins for weeks after the initial hemorrhage may be indicative of chronic neuroinflammation, even at the time of permanent CSF diversion. Conversely, NMDARE induced a narrower lymphocyte-driven profile, more consistent with an antibody-mediated autoimmune disease. Furthermore, suppression of NELL2 and up-regulation of immunoglobulin-related markers (IGLC2, MZB1, CD79B) are potential candidates for biomarkers in PHH and NMDARE, respectively.

TP53 mutation showed an association with poorer overall survival in a secondary analysis, consistent with prior reports, while survival by CD79B/MYD88 mutation status and the differentially expressed genes showed no significant differences in this cohort. In conclusion, the current study identified novel up-regulated genes in CD79B-mutated DLBCLs beyond NF-κB pathway signaling, which may contribute to a better definition of potential therapeutic targets and further improves the characterization of this distinct and aggressive DLBCL subgroup.