Non-Hodgkin’s Lymphoma

P2, N=68, Recruiting, Fred Hutchinson Cancer Center | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2027

P2, N=76, Not yet recruiting, University Health Network, Toronto | Trial primary completion date: Dec 2025 --> Apr 2026

P2, N=59, Suspended, Henan Cancer Hospital | Recruiting --> Suspended | Trial primary completion date: Dec 2023 --> Nov 2024

P1, N=114, Recruiting, Kite, A Gilead Company | Trial primary completion date: Jul 2026 --> May 2027 | Trial completion date: Jul 2026 --> May 2027

P2, N=30, Recruiting, Henan Cancer Hospital | Trial primary completion date: Jan 2024 --> Jun 2025

P2, N=92, Recruiting, Kyorin University

P=N/A, N=20, Not yet recruiting, Affiliated Hospital of Guangdong Medical University

P2, N=60, Completed, Henan Cancer Hospital | Active, not recruiting --> Completed | Trial completion date: Jan 2025 --> Apr 2025

P1/2, N=100, Recruiting, Werewolf Therapeutics, Inc.

P2, N=46, Completed, Memorial Sloan Kettering Cancer Center | Active, not recruiting --> Completed | Trial completion date: Feb 2026 --> Apr 2025 | Trial primary completion date: Feb 2026 --> Apr 2025

P3, N=904, Active, not recruiting, Regeneron Pharmaceuticals | Recruiting --> Active, not recruiting | Trial completion date: Sep 2028 --> Apr 2029 | Trial primary completion date: Sep 2028 --> Mar 2028

These findings suggest that the BTG1/BECN1/ATG5 signaling axis plays a critical role in enhancing autophagy and reversing Rituximab resistance. The combination of Chidamide and Rituximab presents a promising therapeutic strategy, offering new insights into overcoming drug resistance in DLBCL.

We compared these findings with Coilin expression in diffuse large B-cell lymphomas (DLBCL), where the marker was also negative. This finding represents the first data on coilin in lymphomas and prompts further studies to explore this downregulation.

Accuracy is better compared with the IPI and NCCN-IPI prediction models. We also developed a web server to facilitate using our model.

P1, N=50, Active, not recruiting, Emory University | Recruiting --> Active, not recruiting

P=N/A, N=120, Recruiting, University of Miami | Trial completion date: Apr 2025 --> Jan 2026 | Trial primary completion date: Apr 2025 --> Jan 2026

P1/2, N=11, Active, not recruiting, AIDS Malignancy Consortium | Trial completion date: Jun 2025 --> Mar 2036

P=N/A, N=60, Not yet recruiting, Ruijin Hospital

P1, N=30, Recruiting, National Cancer Institute (NCI) | Trial primary completion date: Dec 2025 --> Jun 2027 | Trial completion date: Dec 2025 --> Jun 2027

For CD5 strong positive cases, a wild pattern of p53 likely indicates MCD subtype, while a mutant p53 pattern may suggest TP53Mut subtype. CD5 and p53 may potentially offer initial molecular subtyping for CD5-positive DLBCLs. We suggest incorporating these two markers into the routine pathological diagnosis of DLBCL to assist in guiding preliminary classification and influencing treatment decisions.

P3, N=241, Active, not recruiting, Seagen, a wholly owned subsidiary of Pfizer | Trial completion date: Apr 2027 --> Nov 2025 | Trial primary completion date: May 2025 --> Nov 2025

These findings indicate that targeting FGFR4 can be a promising novel strategy to overcome paclitaxel resistance and improve the outcomes of EOC patients.

P3, N=150, Recruiting, Corvus Pharmaceuticals, Inc. | Trial completion date: Sep 2027 --> Jul 2028 | Trial primary completion date: Feb 2026 --> Nov 2026

P2, N=60, Not yet recruiting, The Lymphoma Academic Research Organisation

P=N/A, N=40, Recruiting, Dana-Farber Cancer Institute | Trial completion date: May 2025 --> May 2026 | Trial primary completion date: Jan 2025 --> Jan 2026

P1, N=29, Completed, Pacylex Pharmaceuticals | Recruiting --> Completed | N=60 --> 29

Additionally, in the cell lines where activity was observed, some compounds demonstrated an In vitro inhibitory effect superior to that of the control, paclitaxel...In Gb-d1 cells, compounds 4l and 4p exhibited favorable interactions with mitogen-activated protein kinase (MEK) protein, similar to those observed with the known inhibitor selumetinib. In HeLa cells, compounds 4h and 4g showed activity against dihydrofolate reductase (DHFR) protein, driven by hydrogen bonding interactions and favorable aromatic ring orientations. On the other hand, compounds 4b and 4t exhibited no activity, likely due to unfavorable interactions related to halogen substitutions in the aromatic rings.

Common treatments following surgical resection include PD-1-targeting checkpoint inhibitors (pembrolizumab), as 20% of tumors are PD-L1 positive with or without systemic chemotherapy. Over the last several years, our laboratory has developed nano-immune conjugates (NIC) in which hydrophobic chemotherapy drugs like paclitaxel (PTX) and SN38, the active metabolite of irinotecan, are made water soluble by formulating them into albumin-based nanoparticles (nab) that are hydrophobically linked to various IgG1 monoclonal antibodies, creating an antigen-targetable nano-immune conjugate...In vitro testing suggests that the chemotherapy drug and antibody retain their toxicity and ligand binding capability in the context of the NIC. Furthermore, both the PTX and SN-38 NIC demonstrate superior anti-tumor efficacy relative to antibody and chemotherapy drugs alone in a PD-L1 + MDA-MB-231 human TNBC xenograft model, which could translate clinically to patients with TNBC.

An inactivating somatic mutation in the TREX1 gene (p.T49fs) has not been previously described in patients with non-Hodgkin lymphomas. Additionally, our analysis uncovered a key cancer hallmark: tumor genomic instability, manifested as a high tumor mutational burden, which likely contributed to the aggressive disease course.

The present study demonstrates that MG132 can induce AID accumulation, which in turn restores dysfunctional CSR in ABC-DLBCL. Using MG132 as a tool, the present study elucidates the anti-lymphoma effect of proteasome inhibitors on ABC-DLBCL by rescuing the abnormal AID-induced CSR.

P1/2, N=424, Recruiting, Genmab | N=304 --> 424

P2, N=248, Recruiting, Miltenyi Biomedicine GmbH | N=110 --> 248 | Trial completion date: Dec 2026 --> Dec 2028 | Trial primary completion date: Dec 2024 --> Dec 2026

This genetic anomaly frequently coexists with trisomy 12. Preliminary data suggest that these cases may have a shorter TTFT, though larger cohorts are needed for validation.

This study identifies two distinct DLBCL subtypes based on PCD-related gene expression, with the C2 subtype characterized as high-risk due to enhanced DNA repair and cell cycle pathways. Five key biomarkers (CTSB, DPYD, SCARB2, STOM, GBP1) may improve risk stratification and understanding of DLBCL heterogeneity. These findings lay the groundwork for further exploration of DLBCL progression and potential prognostic improvements.

The inducible ablation of PDL1 on macrophages was sufficient to improve immune control of MYC-expressing lymphoma in a syngeneic immunocompetent model. These results implicate the macrophage/CD8+ T-cell axis as a key pathogenetic determinant and immunotherapeutic target in a subset of DLBCL patients with poor prognosis.

it is the first study to indicate that PARK-2 rs1801474 and rs1801334 SNPs carrying significant risk factors of NHL and it is correlated to some clinical pathological parameters may be due to down regulation of PARK-2 gene expression.

Together, our findings are the first to identify the central role of FDX1 in synergizing with ES to activate IFN-β signaling and induce PANoptosis. This study enables us to re-explore the clinical anticancer potential of ES as a novel therapeutic strategy for DLBCL.

Conversely, specific inhibition of p-S6 suppressed DLBCL cell proliferation and exhibited synergistic effects with chemotherapy in vivo. In summary, our findings elucidated the specific tumor microenvironment in DE DLBCL tissues and identified p-S6 as a promising therapeutic target to enhance the efficacy of chemotherapy.

In this issue of Blood Cancer Discovery, Iyer and colleagues employ a CRISPR interference screen targeted at open chromatin regions to unveil enhancers critical for MYC overexpression in lymphoma, including a novel regulatory element in the MYC locus that controls germinal center reentry and is recurrently amplified in diffuse large B-cell lymphomas (germinal center B-cell diffuse large B-cell lymphoma). See related article by Iyer et al., p. XX.

Novel targets in patients with B-cell lymphoma are BCL2, the NF-κB pathway, components of the BCR activator of RhoGEF and GTPase signalling pathway and the PI3K-mTOR pathway. In this review, information is provided on the common types of B-cell lymphoma in CTD, the pathogenic factors implicated in lymphoma development and recent advancements in therapies effective for both autoimmune conditions and malignant lymphoproliferative diseases.

P2, N=40, Recruiting, University of Washington | Trial completion date: Jul 2026 --> Jul 2027 | Trial primary completion date: Dec 2025 --> Dec 2026

P1, N=7, Completed, Otsuka Beijing Research Institute | Unknown status --> Completed | N=42 --> 7