Behind the paper: Mantle cell lymphoma is more dynamic than we thought
Mantle cell lymphoma is often viewed as biologically stable over time. By following patients longitudinally with whole-exome sequencing, we found that the disease evolves more than expected, with treatment shaping the accumulation of genetic alterations.
Gasdermin E mediating lysosome-pore formation curbs pancreatic ductal adenocarcinoma via IFN-γ/IFN-β/TGF-β cocktail mRNA-LNP
Our study is the first to identify GSDME-mediated, lysosome-dependent cell death, revealing a novel lysosome-targeted killing mechanism co-regulated by three cytokines. Combined with the LNP system for PDAC targeting provide a new therapeutic direction.
Published in Cellular & Molecular Immunology
First clinical proof-of-concept of CAR T-cell combination therapy: The phase 2, single-arm ZUMA-14 trial of axicabtagene ciloleucel in combination with rituximab for refractory large B-cell lymphoma
In this study, researchers looked at how safe and well axi-cel and rituximab worked to treat people with refractory large B-cell lymphoma. These therapies target 2 different markers on the surface of the cancer cell. The study showed that this dual-targeting strategy is feasible and generally safe.
STING Agonism and B Cells in Liver Cancer: How Immune Activation Can Drive Both Tumor Control and Metastasis—and Why Targeting Regulatory B Cells Can Unlock Durable Anti-Tumor Immunity
Immunotherapy can potently activate anti-cancer immunity, yet liver cancer often resists it. Our new research reveals one reason why: STING agonism or PD1/VEGFR2 blockade increases regulatory B cells that suppress T cells. Targeting these B cells can restore the immune balance and block metastasis.
Hearing Loss and Chronic Myeloid Leukemia: A Decade-long Review
Although hearing loss is associated with acute leukemia and is less common in patients with late-stage CML, increasing evidence suggests sudden hearing loss in patients with CML.
USP43 promotes gemcitabine resistance in bladder cancer by stabilizing E2F1 to regulate cholesterol homeostasis
Gemcitabine (GEM) resistance remains a critical barrier in the treatment of bladder cancer (BLCA). Based on the observation that metabolic reprogramming drives chemoresistance, we identified USP43 as a promoter of GEM resistance via an E2F1-driven mechanism that modulates cholesterol metabolism.
YKT6 drives bladder cancer progression by stabilizing β-catenin via a USP7-mediated mechanism
Bladder cancer (BLCA) remains a highly lethal malignancy with limited therapeutic strategies. In our latest study, we investigated the oncogenic role of YKT6, a conserved SNARE protein, in BLCA progression.
