Non-Hodgkin’s Lymphoma

Our study demonstrates that our local population has similar clinicopathological and prognostic characteristics of DLBCL as compared to global findings. It also highlights the limitations of R-CHOP(-like) regimens in contemporary DLBCL management and therefore an ongoing need for improved therapeutic strategies.

The patient was treated with six cycles of the R-CHOP regimen (rituximab, cyclophosphamide, vincristine, doxorubicin, prednisone), achieving complete metabolic remission as confirmed by positron emission tomography-computed tomography. Through our literature review of additional six cases of primary seminal vesicle lymphoma, we aim to elucidate the typical clinical presentations, imaging features, pathological characteristics, genetic mutations, and therapeutic strategies, aiming to contribute to better detection and management of this rare malignancy. This case underscores the diagnostic challenges and emphasizes the necessity for heightened clinical suspicion and definitive pathological examination in the management of primary seminal vesicle lymphoma.

This case underscores the importance of early biopsy and molecular testing when standard treatments fail. Early recognition and routine examinations, including lymph node assessments and skin biopsies, are critical for improving patient outcomes, as timely diagnosis leads to more effective treatment options and potential remission.

Complete remission was achieved with a reduced immunomodulatory drug dosage and rituximab therapy. She has been alive for 8 months postoperatively without recurrence. This case suggests that PTLD should be considered in assessing patients presenting with abdominal symptoms following organ transplantation.

Pediatric SPTCL in Thailand frequently involves germline HAVCR2 mutations and/or HLH/HLH-like systemic illnesses. With comparable response and modest therapy-related toxicity, IST-based regimens may alternatively be considered as first-line treatment for pediatric SPTCL.

Our results provide the first lipid metabolism-based gene signature for predicting the survival of patients with DLBCL. Furthermore, by determining novel subtypes with our lipid metabolism prognostic model we illustrated that drugs that compromising MYC target genes rather than immune checkpoint inhibitors may be beneficial to DLBCL patients with certain lipid metabolism profiles.

M2-polarized TAMs and low infiltration of CD8+ TILs were more strongly correlated with poor clinical pathological indicators and worse prognosis, and MVD values may serve as an aiding means for the diagnosis and prognostic prediction of LBCL-IP disease.

We applied targeted next-generation sequencing for detection of recurrent single nucleotide variants, copy number alterations and zygosity abnormalities in diagnostic specimens from 78 PCNSL patients treated with a standard methotrexate-based regimen, to identify prognostically significant molecular subgroups...These genomic aberrations identify a high-risk molecular subgroup that may inform risk stratification in PCNSL. Further elucidation of the mechanisms of therapeutic resistance associated with the high-risk genetic phenotype is requisite to facilitate precision medicine and progress in therapy.

In summary, our research over the past three decades identified cHL as the first lymphoid malignancy driven by a disturbed telomere/shelterin/lamin AC interaction, generating the diagnostic RS. Our findings may act as trailblazer for tailored therapies in refractory cHL.

The ABC subtype was also associated with lower white blood cell counts and more frequent chemotherapy courses than the GCB subtype. These findings suggest that nuclear Nrf2 could be a biomarker for DLBCL clinical diagnosis.

Additionally, there was increased immunohistochemically detected expression of colonic B-cell lymphoma-1 (Bcl-2) and cytokeratins AE1/AE3, but reduced expression of mucin 1 (MUC1) and carcinoembryonic antigen (CEA) in NaAsO2 + GSO and GSO treated rats when compared with the NaAsO2 group. These results suggest that GSO promoted anti-inflammatory processes in the liver, stomach and colon, as well as opposing apoptosis in the colon, resulting in significant attenuation of damage to these tissues.

The antiproliferative activity of MH was determined using MTT and colony formation assays against drug-sensitive (A549 and H1299) and Taxol-resistant lung cancer cells (A549-TR)...In vivo, MH (25 mg/kg b. wt.) significantly (p < 0.001) inhibited the growth of A549 lung cancer orthotopic xenografts in NOD Scid mice by 70%. Our study provides new mechanistic insights into MH's therapeutic potential against NSCLC.

Data further indicate that antiviral T cells may play a role in antitumor efficacy in the case of CPMV immunotherapy, however this may not be the case for PVX. Regardless of the mechanism of action, both CPMV and PVX elicited a durable antitumor response against a B-cell lymphoma tumor model and thus are intratumoral immunotherapy candidates for clinical development.

P1, N=18, Active, not recruiting, Novartis Pharmaceuticals | Recruiting --> Active, not recruiting | N=40 --> 18

P2, N=37, Recruiting, David Bond, MD | Trial primary completion date: Dec 2024 --> Dec 2025

P1/2, N=27, Recruiting, Instituto de Investigación Biomédica de Salamanca | Trial completion date: Oct 2028 --> Jul 2030 | Trial primary completion date: Apr 2027 --> Jul 2028

In addition, longitudinal 18F-fluorodeoxyglucose positron-emission tomography (18F-FDG PET) of one MCM successfully detected lymphoproliferative disease in the adrenal glands prior to clinical signs of disease. These data demonstrate successful induction of lymphocryptovirus-associated PTLD-like disease in 4 of 5 MCMs, and thus support the use of MCMs as a preclinical NHP model of EBV-associated lymphoproliferative disease that could be employed to test novel diagnostic and therapeutic modalities.

P1, N=30, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Recruiting --> Active, not recruiting

P=N/A, N=20, Not yet recruiting, Tongji Hospital

The promising clinical efficacy observed warrants further investigation, and development of acimtamig for patients with R/R CD30+ lymphomas continues in combination with allogeneic natural killer cells.

Together, our study identified HBX's role in inhibiting MALAT1 expression, promoting SFPQ-mediated splicing of SLC7A11 pre-mRNA, and reducing the GCB-type DLBCL sensitivity to Erastin-induced ferroptosis. Combined with the recent studies that ferroptosis may be involved in the occurrence and development of DLBCL, these findings explain our clinical data analysis that DLBCL patients with low expression of MALAT1 have poorer prognosis and shorter overall survival, and provide a valuable therapeutic target for the HBV-infected GCB-type DLBCL patients.

The CHOP regimen induces male reproductive toxicity, potentially mediated through alterations in hormone levels and increased expression of inflammatory cytokines and oxidative stress. Using E2 as the sole predictor in the model accurately predicts the extent of reproductive damage, offering a non-invasive method for detecting reproductive system damage.

Here, we review FoxO1's roles across B cell and myeloid malignancies, namely acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), follicular lymphoma (FL), diffuse large B cell lymphoma (DLBCL), mantle cell lymphoma (MCL), Burkitt lymphoma (BL), Hodgkin lymphoma (HL), and multiple myeloma (MM). We also discuss preclinical evidence for FoxO1 targeting by currently available inhibitors (AS1708727, AS1842856, cpd10).

P1, N=16, Completed, Beijing Boren Hospital | Recruiting --> Completed

P2, N=36, Not yet recruiting, Washington University School of Medicine

P1, N=154, Completed, Xencor, Inc. | Active, not recruiting --> Completed | N=270 --> 154 | Trial completion date: Jan 2025 --> Apr 2024 | Trial primary completion date: Oct 2024 --> Apr 2024

IDH1/2 mutations are identified in a small subset of NSCLCs. Our findings suggest that >25% of these mutations are hematopoietic in origin with important implications for diagnosis and management of these patients. Among those with mutations arising from the lung neoplasm, IDH1/2 mutations were primarily seen in conjunction with another driver and were subclonal in nature, suggesting patterns of clonal heterogeneity and evolution.

In this study, 3 pre-analytical components were assessed for the VENTANA Kappa and Lambda Dual ISH mRNA Probe Cocktail Assay. There are many acceptable tissue thickness, fixation, and decalcification options that are compatible with this assay.

Six weeks later, while receiving the CD20-directed immunotherapies glofitamab and obinutuzumab, another bone marrow biopsy revealed eradication of the B-ALL and new involvement by pure erythroid leukemia (PEL). This patient's B-ALL lacked an IGH::BCL2 fusion resulting from t(14; 18), suggesting it did not arise through transformation of his prior FL/DLBCL. Instead, the B-ALL was likely caused by his extensive exposure to genotoxic chemotherapy drugs – including alkylating agents – for his preceding lymphomas. The shared cytogenetic and molecular features between this patient's B-ALL and PEL imply they are clonally related.

Based on our experience, SHM status can be achieved by routine NGS testing. Our first-year mutated-versus-unmutated test results are reasonably close to what is reported in the literature, supporting the effectiveness of this assay. The majority (66.6%) of QNS samples were due to lack of evidence of clonality in CLL samples.

Our NGS testing found tier 1 or 2 variants in the majority of cases, supporting its use in the clinical setting. Additionally, a subset of variants identified with the pan-Heme list likely represents mutations of clonal hematopoiesis of indeterminate potential, which could be removed with a more lymphoma-specific gene list. Given these findings, and a growing number of targets in indolent B cell lymphomas, future studies focusing on evaluation of a lymphoma-specific gene list is of interest for clinical validation and implementation.

P3, N=847, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Sep 2024 --> Sep 2025

P2, N=59, Recruiting, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine

P2, N=9, Active, not recruiting, Mayo Clinic | Trial completion date: Oct 2024 --> Oct 2025 | Trial primary completion date: Oct 2024 --> Oct 2025

P1, N=35, Recruiting, Sana Biotechnology | Initiation date: Oct 2024 --> Apr 2024

P1, N=16, Active, not recruiting, Sana Biotechnology | Recruiting --> Active, not recruiting | N=57 --> 16 | Trial completion date: Dec 2027 --> Nov 2038 | Trial primary completion date: Dec 2026 --> Nov 2025

P2, N=51, Recruiting, Fudan University | Trial completion date: Sep 2025 --> Dec 2026 | Trial primary completion date: Dec 2023 --> Dec 2026

P2, N=40, Recruiting, The First Affiliated Hospital of Soochow University

P=N/A, N=30, Active, not recruiting, University of Chicago | Recruiting --> Active, not recruiting

P=N/A, N=25, Not yet recruiting, The second hospital of Dalian Medical University; The second hospital of Dalian Medical University

P=N/A, N=30, Not yet recruiting, ganzhou people's hospital; ganzhou people's hospital

P=N/A, N=45, Not yet recruiting, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine; Ruijin Hospital, Shanghai Jiao Tong University School of Medicine