Gastrointestinal Symptom-Free Multiple Lymphomatous Polyposis: An Atypical Case Presentation of Mantle Cell Lymphoma.

Introduction: Mantle cell lymphoma (MCL), a rare non-Hodgkin's lymphoma, exhibits a genetic translocation causing CCND1 gene overexpression, affecting 5% of NHL cases, predominantly in males aged 60-70. Typically diagnosed with advanced symptoms, MCL involves widespread disease and organ spread, being aggressive and incurable with a 1.8-9.4-year average survival. Optimal treatment depends on disease aggressiveness and age. Multiple lymphomatous polyposis (MLP), a rare MCL subtype in the GI tract, is usually present with GI symptoms. Case Presentation: A 71-year-old woman was diagnosed with asymptomatic MLP during MCL staging who underwent thoracentesis due to large right pleural effusion and significant axillary lymphadenopathy and was treated with a chemotherapy regimen of rituximab/cytarabine and later transitioned to bendamustine/rituximab. This patient eventually underwent a bone marrow biopsy and later a bone marrow transplant. Conclusion: We present a unique case of asymptomatic MLP, emphasizing the importance of early detection for the poor prognosis of MLP with a mean survival of less than 3 years.

Patient-derived organoids recapitulate glioma-intrinsic immune program and progenitor populations of glioblastoma.

Glioblastoma multiforme (GBM) is a highly lethal human cancer thought to originate from a self-renewing and therapeutically-resistant population of glioblastoma stem cells (GSCs). The intrinsic mechanisms enacted by GSCs during 3D tumor formation, however, remain unclear, especially in the stages prior to angiogenic/immunological infiltration. In this study, we performed a deep characterization of the genetic, immune, and metabolic profiles of GBM organoids from several patient-derived GSCs (GBMO). Despite being devoid of immune cells, transcriptomic analysis across GBMO revealed a surprising immune-like molecular program, enriched in cytokine, antigen presentation and processing, T-cell receptor inhibitors, and interferon genes. We find two important cell populations thought to drive GBM progression, Special AT-rich sequence-binding protein 2 (SATB2+) and homeodomain-only protein homeobox (HOPX+) progenitors, contribute to this immune landscape in GBMO and GBM in vivo. These progenitors, but not other cell types in GBMO, are resistant to conventional GBM therapies, temozolomide and irradiation. Our work defines a novel intrinsic immune-like landscape in GBMO driven, in part, by SATB2+ and HOPX+ progenitors and deepens our understanding of the intrinsic mechanisms utilized by GSCs in early GBM formation.