Chimeric antigen receptor (CAR)-T therapy has demonstrated remarkable outcomes for B cell malignancies, however, its application for T cell lymphoma, particularly cutaneous T cell lymphoma (CTCL), has been limited. Barriers to effective CAR-T cell therapy in treating CTCL include T cell aplasia in autologous transplants, CAR-T product contamination with leukemic T cells, CAR-T fratricide (when the target antigen is present on normal T cells), and tumor heterogeneity. To address these critical challenges, innovative CAR engineering by targeting multiple antigens to strike a balance between efficacy and safety of the therapy is necessary. In this review, we discuss the current obstacles to CAR-T cell therapy and highlight potential targets in treating CTCL. Looking forward, we propose strategies to develop more powerful dual CARs that are advancing towards the clinic in CTCL therapy.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9433932PMC
http://dx.doi.org/10.3389/fimmu.2022.968395DOI Listing

Publication Analysis

Top Keywords

car-t cell
12
cell lymphoma
12
cutaneous cell
8
cell therapy
8
treating ctcl
8
cell
7
car-t
6
therapy
5
cell development
4
development cutaneous
4

Similar Publications

Purpose Of Review: Cutaneous T cell lymphomas (CTCLs) are comprised of a heterogenous group of non-Hodgkin lymphomas that can be difficult to treat and are often refractory to standard therapies. Mycosis fungoides (MF) and Sezary syndrome (SS) are the most common subtypes, accounting for the majority of CTCLs. There is no standard of care, and no treatments are curative.

View Article and Find Full Text PDF
Article Synopsis
  • FT596 is a novel cancer therapy using iPSC-derived CAR NK cells targeting CD19, designed to assess its safe dosage and effectiveness alone and with rituximab in patients with B-cell lymphoma.
  • This phase 1 trial involved patients with relapsed or refractory B-cell lymphoma, administering FT596 after chemotherapy, with separate regimens for those receiving rituximab and those who did not.
  • The study measured potential side effects while determining the optimal dose of FT596 and allowed modifications to the treatment based on patient tolerance and response.
View Article and Find Full Text PDF

Optimizing CAR-T cell function in solid tumor microenvironment: insights from culture media additives.

Curr Res Transl Med

December 2024

Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Sciences, Nanjing Normal University, Nanjing, 210023, China. Electronic address:

Cancer remains one of the most pressing health challenges worldwide. Recently, chimeric antigen receptor (CAR)-T cell therapy has emerged as a promising approach for treating hematological cancers. However, the translation of CAR-T cell therapy to solid tumors faces formidable obstacles, notably the immunosuppressive tumor microenvironment.

View Article and Find Full Text PDF

CAR-T cell therapy for breast cancer: Current status and future perspective.

Cancer Treat Rev

December 2024

Istituto Nazionale Tumori, IRCCS, Fondazione G. Pascale, Napoli, Italy. Electronic address:

Within the expanding therapeutic landscape for breast cancer (BC), metastatic breast cancer (MBC) remains virtually incurable and tend to develop resistance to conventional treatments ultimately leading to metastatic progression and death. Cellular immunotherapy (CI), particularly chimeric antigen receptor-engineered T (CAR-T) cells, has emerged as a promising approach for addressing this challenge. In the wake of their striking efficacy against hematological cancers, CAR-T cells have also been used where the clinical need is greatest - in patients with aggressive BCs.

View Article and Find Full Text PDF

Tumor-induced metabolic immunosuppression: Mechanisms and therapeutic targets.

Cell Rep

January 2025

Université Côte d'Azur, INSERM, C3M, Nice, France; Équipe labellisée LIGUE Contre le Cancer, Nice, France. Electronic address:

Metabolic reprogramming in both immune and cancer cells plays a crucial role in the antitumor immune response. Recent studies indicate that cancer metabolism not only sustains carcinogenesis and survival via altered signaling but also modulates immune cell function. Metabolic crosstalk within the tumor microenvironment results in nutrient competition and acidosis, thereby hindering immune cell functionality.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!