High‐dose cyclophosphamide for hard‐to‐treat patients with relapsed or refractory B‐cell non‐Hodgkin's lymphoma, a phase II result

Michot, Jean‐Marie; Annereau, Maxime; Danu, Alina; Legoupil, Colette; Chahine, Claude; Achab, Nadia; Antosikova, Anna; Cerutti, Ariane; Rossignol, Julien; Gourichon, David; Willekens, Christophe; Dartigues, Peggy; Lazarovici, Julien; Lemare, François; Ribrag, Vincent

doi:10.1111/ejh.13369

Cited by 4 publications

(2 citation statements)

References 39 publications

(75 reference statements)

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“…Cyclophosphamide (CP) is an alkylating chemotherapeutic agent broadly employed in the therapy of numerous human malignancies [ 1 , 2 , 3 ]. CP has been approved by the FDA for use in the treatment of stage III and IV lymphomas, including lymphocytic Hodgkin and non-Hodgkin lymphomas [ 4 , 5 ]. CP is used as an immunosuppressant to prevent post-transplant rejection and graft-vs.-host complications; however, its therapeutic application is associated with serious adverse effects, such as hemorrhagic cystitis, myelosuppression, kidney injury, amenorrhea, lung injury, cardiotoxicity, and hepatotoxicity [ 1 , 3 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of Nrf2/HO-1 Signaling and Attenuation of Oxidative Stress, Inflammation, and Cell Death Mediate the Protective Effect of Apigenin against Cyclophosphamide Hepatotoxicity

et al. 2022

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Liver injury is among the adverse effects of the chemotherapeutic agent cyclophosphamide (CP). This study investigated the protective role of the flavone apigenin (API) against CP-induced liver damage, pointing to the involvement of Nrf2/HO-1 signaling. Rats were treated with API (20 and 40 mg/kg) for 15 days and received CP (150 mg/kg) on day 16. CP caused liver damage manifested by an elevation of transaminases, alkaline phosphatase (ALP), and lactate dehydrogenase (LDH), and histological alterations, including granular vacuolation, mononuclear cell infiltration, and hydropic changes. Hepatic reactive oxygen species (ROS), malondialdehyde (MDA), and nitric oxide (NO) were increased and glutathione (GSH) and antioxidant enzymes were decreased in CP-administered rats. CP upregulated the inflammatory markers NF-κB p65, TNF-α, IL-6, and iNOS, along with the pro-apoptotic Bax and caspase-3. Pre-treatment with API ameliorated circulating transaminases, ALP, and LDH, and prevented histopathological changes in CP-intoxicated rats. API suppressed ROS, MDA, NO, NF-κB p65, iNOS, inflammatory cytokines, oxidative DNA damage, Bax, and caspase-3 in CP-intoxicated rats. In addition, API enhanced hepatic antioxidants and Bcl-2 and boosted the Nrf2 and HO-1 mRNA abundance and protein. In conclusion, API is effective in preventing CP hepatotoxicity by attenuating oxidative stress, the inflammatory response, and apoptosis. The hepatoprotective efficacy of API was associated with the upregulation of Nrf2/HO-1 signaling.

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Section: Introductionmentioning

confidence: 99%

Upregulation of Nrf2/HO-1 Signaling and Attenuation of Oxidative Stress, Inflammation, and Cell Death Mediate the Protective Effect of Apigenin against Cyclophosphamide Hepatotoxicity

et al. 2022

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“…In addition to the cited trails, a myriad of trials based on the targeting BCMA in MM ( [60][61][62][63][64][65], CD19 in ALL [32,[66][67][68][69][70][71][72][73][74] and non-Hodgkin's lymphoma (NHL) [69,[75][76][77][78][79], CD20 in BCL [70,[80][81][82], and CD22 in ALL [83][84][85][86] have shown the significant efficacy in the clinic.…”

Section: Hematological Malignanciesmentioning

confidence: 99%

A deep insight into CRISPR/Cas9 application in CAR-T cell-based tumor immunotherapies

et al. 2021

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To date, two chimeric antigen receptors (CAR)-T cell products from autologous T cells have been approved by The United States Food and Drug Administration (FDA). The case-by-case autologous T cell generation setting is largely considered as a pivotal restraining cause for its large-scale clinical use because of the costly and prolonged manufacturing procedure. Further, activated CAR-T cells mainly express immune checkpoint molecules, including CTLA4, PD1, LAG3, abrogating CAR-T anti-tumor activity. In addition, CAR-T cell therapy potently results in some toxicity, such as cytokine releases syndrome (CRS). Therefore, the development of the universal allogeneic T cells with higher anti-tumor effects is of paramount importance. Thus, genome-editing technologies, in particular, clustered regularly interspaced short palindromic repeat (CRISPR)-Cas9 are currently being used to establish “off-the-shelf” CAR-T cells with robust resistance to immune cell-suppressive molecules. In fact, that simultaneous ablation of PD-1, T cell receptor alpha constant (TRAC or TCR), and also β-2 microglobulin (B2M) by CRISPR-Cas9 technique can support the manufacture of universal CAR-T cells with robust resistance to PD-L1. . Indeed, the ablation of β2M or TARC can severely hinder swift elimination of allogeneic T cells those express foreign HLA-I molecules, and thereby enables the generation of CAR-T cells from allogeneic healthy donors T cells with higher persistence in vivo. Herein, we will deliver a brief overview of the CAR-T cell application in the context of tumor immunotherapy. More importantly, we will discuss recent finding concerning the application of genome editing technologies for preparing universal CAR-T cells or cells that can effectively counter tumor escape, with a special focus on CRISPR-Cas9 technology.

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Car T Cells in Solid Tumors: Overcoming Obstacles

Rojas-Quintero,

Díaz,

Palmar

et al. 2024

IJMS

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Chimeric antigen receptor T cell (CAR T cell) therapy has emerged as a prominent adoptive cell therapy and a therapeutic approach of great interest in the fight against cancer. This approach has shown notorious efficacy in refractory hematological neoplasm, which has bolstered its exploration in the field of solid cancers. However, successfully managing solid tumors presents considerable intrinsic challenges, which include the necessity of guiding the modified cells toward the tumoral region, assuring their penetration and survival in adverse microenvironments, and addressing the complexity of identifying the specific antigens for each type of cancer. This review focuses on outlining the challenges faced by CAR T cell therapy when used in the treatment of solid tumors, as well as presenting optimizations and emergent approaches directed at improving its efficacy in this particular context. From precise localization to the modulation of the tumoral microenvironment and the adaptation of antigen recognition strategies, diverse pathways will be examined to overcome the current limitations and buttress the therapeutic potential of CAR T cells in the fight against solid tumors.

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High‐dose cyclophosphamide for hard‐to‐treat patients with relapsed or refractory B‐cell non‐Hodgkin's lymphoma, a phase II result

Cited by 4 publications

References 39 publications

Upregulation of Nrf2/HO-1 Signaling and Attenuation of Oxidative Stress, Inflammation, and Cell Death Mediate the Protective Effect of Apigenin against Cyclophosphamide Hepatotoxicity

Upregulation of Nrf2/HO-1 Signaling and Attenuation of Oxidative Stress, Inflammation, and Cell Death Mediate the Protective Effect of Apigenin against Cyclophosphamide Hepatotoxicity

A deep insight into CRISPR/Cas9 application in CAR-T cell-based tumor immunotherapies

Car T Cells in Solid Tumors: Overcoming Obstacles

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