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Targeting the programmed death-1 pathway in lymphoid neoplasms
1The Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Abstract:
Programmed death-1 (PD-1) is a co-inhibitory molecule and is seen in CD4+ and CD8+ T cells. Upon binding to its ligands, programmed death ligand-1 (PD-L1) and -2 (PD-L2), PD-1 negatively regulates interleukin 2 (IL-2) production and T cell proliferation. Activated effector T-cells, which kill cancer cells, can be affected by PD-1 signaling in some lymphoid neoplasm that express PD-L1 or PD-L2. PD-L1 expression in tumor cells can be induced by extrinsic signal (i.e. interferon gamma) or intrinsic signals, such as genetic aberrations involving 9p24.1, latent Epstein-Barr virus infection, PD-L1 3'- untranslated region disruptions, and activated Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Anti-PD-1 therapy improves the overall response rate to treatment in patients with lymphoid neoplasms, particularly relapsed/refractory classical Hodgkin lymphoma. Inspired by their success in treating patients with classical Hodgkin lymphoma, medical practitioners have expanded PD-1 therapy, given as a single therapy or in combination with other drugs, to patients with other types of lymphoma. In this review, current clinical trials with anti-PD-1 or anti-PD-L1 drugs are summarized. The results of numerous clinical trials will broaden our understanding of PD-1 pathway and shall expand the list of patients who will get benefit from these agents including those who suffer from lymphoid neoplasms.
Insights
Programmed death-1 (PD-1) therapy shows promise for lymphoid neoplasms. Clinical trials are expanding the use of anti-PD-1 agents to improve treatment responses in patients with these cancers.
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- Programmed death-1 (PD-1) is a co-inhibitory molecule on T cells that regulates immune responses.
- PD-1 ligands, programmed death ligand-1 (PD-L1) and -2 (PD-L2), can suppress anti-tumor immunity in lymphoid neoplasms.
- Tumor PD-L1 expression is influenced by various intrinsic and extrinsic factors, including genetic aberrations and inflammatory signals.
Purpose of the Study:
- To review current clinical trials evaluating anti-PD-1 and anti-PD-L1 therapies in lymphoid neoplasms.
- To summarize the efficacy of PD-1 pathway inhibitors in treating these cancers.
- To explore the potential expansion of PD-1-targeted therapies for a broader patient population.
Main Methods:
- Review of current clinical trials involving anti-PD-1 or anti-PD-L1 drugs.
- Analysis of treatment response rates in patients with lymphoid neoplasms.
- Synthesis of data on PD-1 pathway modulation in cancer treatment.
Main Results:
- Anti-PD-1 therapy has demonstrated improved response rates in lymphoid neoplasms, notably in classical Hodgkin lymphoma.
- Therapeutic strategies involving PD-1 inhibitors are being extended to other lymphoma subtypes.
- Ongoing clinical trials aim to further elucidate the benefits of PD-1 pathway inhibition.
Conclusions:
- PD-1 pathway inhibitors represent a significant advancement in treating lymphoid neoplasms.
- Expanding PD-1-targeted therapies holds promise for improving outcomes in a wider range of patients.
- Further research will broaden the application of these immunotherapies in hematologic malignancies.
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