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Journal Articles
Journal: Blood
Blood blood.2024026599.
Published: 2025
Includes: Supplemental data
Journal Articles
Journal Articles
Journal: Blood
Blood (2025) 146 (2): 140–141.
Published: 2025
Journal Articles
Clinical Trials & Observations
Journal: Blood
Blood (2025) 146 (2): 131–133.
Published: 2025
Journal Articles
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Journal Articles
Journal: Blood
Blood (2025) 146 (2): 135–136.
Published: 2025
Journal Articles
Clinical Trials & Observations
Journal: Blood
Blood (2025) 146 (2): 129–131.
Published: 2025
Journal Articles
Journal Articles
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Images
Mechanisms of GPRC5D loss mediating resistance to anti-GPRC5D CAR T therapy. In the T-cell therapy–naive setting, GPRC5D is highly expressed on multiple myeloma (MM) tumor cells, enabling effective targeting by anti-GPRC5D CAR T cells (arrows hitting the bullseye). After relapse, tumor cells evade immune recognition through loss of GPRC5D, making anti-GPRC5D CAR T therapy ineffective. Mechanisms of GPRC5D antigen escape include genomic deletion of the GPRC5D locus and epigenetic silencing via promoter/enhancer methylation. CAR, chimeric antigen receptor. Figure generated using BioRender.
Published: 2025
Mechanisms of GPRC5D loss mediating resistance to anti-GPRC5D CAR T therapy. In the T-cell therapy–naive setting, GPRC5D is highly expressed on multiple myeloma (MM) tumor cells, enabling effective targeting by anti-GPRC5D CAR T cells (arrows hitting the bullseye). After relapse, tumor cells eva... More about this image found in Mechanisms of GPRC5D loss mediating resistance to anti-GPRC5D CAR T thera...
Images
Evolution of prognostic systems in LCH. (Left) Traditional risk-organ–based prognostication categorizes patients based on the presence or absence of risk-organ involvement, affecting overall survival. Patients with risk-organ involvement exhibit poorer survival compared with those without. (Right) Molecular-based prognostication highlights the role of PBMC-BRAFV600E mutation status incorporated in the LangIndex in predicting event-free survival and the development of LCH-ND. The evolution of LCH over time is illustrated as a transition from a high-mortality disease to a chronic, incurable condition with associated morbidity. Professional illustration by Somersault18:24.
Published: 2025
Evolution of prognostic systems in LCH. (Left) Traditional risk-organ–based prognostication categorizes patients based on the presence or absence of risk-organ involvement, affecting overall survival. Patients with risk-organ involvement exhibit poorer survival compared with those without. (Right) M... More about this image found in Evolution of prognostic systems in LCH. (Left) Traditional risk-organ–based...
Images
Enhancing PD-1 blockade efficacy through CD38 inhibition. The figure illustrates potential mechanisms through which combining the PD-1 inhibitor cemiplimab (orange) with the CD38 monoclonal antibody isatuximab (black) may amplify immune checkpoint blockade in ENKTL. (I) Direct CD38-mediated cell killing: isatuximab induces direct cytotoxicity against ENKTL cells (violet), which have CD38 expression that is further upregulated in response to PD-1 blockade.4 (II) Reducing Treg-mediated immunosuppression: isatuximab eliminates immunosuppressive CD38-positive Tregs (red), promoting a more immune-permissive tumor microenvironment and boosting antitumor immunity.4 (III) Restoring cytotoxic CD8+ T-cell function: PD-1 inhibition with cemiplimab activates cytotoxic T cells (green). However, compensatory upregulation of CD38 in malignant cells, driven by factors like ATRA and IFNβ (black arrows), suppresses cytotoxic T-cell function.8 CD38 plays an important role as an ectoenzyme in metabolizing NAD and generating adenosine, which activates ADORs on cytotoxic T cells, dampening their function (black dotted arrow).4 By blocking CD38, isatuximab disrupts this resistance mechanism (black inhibitor), potentially enhancing and prolonging the efficacy of PD-1 blockade. ADOR, adenosine receptor; ATRA, all-trans retinoic acid; IFNβ, interferon-β; NAD, nicotinamide adenine dinucleotide. Figure created in BioRender (https://BioRender.com/y93h678).
Published: 2025
Enhancing PD-1 blockade efficacy through CD38 inhibition. The figure illustrates potential mechanisms through which combining the PD-1 inhibitor cemiplimab (orange) with the CD38 monoclonal antibody isatuximab (black) may amplify immune checkpoint blockade in ENKTL. (I) Direct CD38-mediated cell kil... More about this image found in Enhancing PD-1 blockade efficacy through CD38 inhibition. The figure illust...
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