The effect of chemotherapy on programmed cell death 1/programmed cell death 1 ligand axis: some chemotherapeutical drugs may finally work through immune response

Luo, Min; Fu, Liwu

doi:10.18632/oncotarget.7631

Cited by 51 publications

(51 citation statements)

References 64 publications

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“…Our results indicate that conventional front-line treatment is insufficient for these patients. 19,20 Comparison with previous studies regarding PD-1…”

Section: Pd-l1mentioning

confidence: 81%

High proportions of PD-1+ and PD-L1+ leukocytes in classical Hodgkin lymphoma microenvironment are associated with inferior outcome

et al. 2017

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Key Points• High proportions of PD-1 1 and PD-L1 1 leukocytes in the Hodgkin lymphoma microenvironment are associated with inferior outcome.• Expression of PD-L1 and PD-L2 on Hodgkin and Reed-Sternberg cells has no impact on outcome.Immune checkpoint inhibition targeting the programmed death receptor (PD)-1 pathway is a novel treatment approach in relapsed and refractory classical Hodgkin lymphoma (cHL). leukocytes was also associated with inferior OS in a multivariate analysis (HR, 3.46; 95% CI,. This is the first study to show a correlation after multivariate analysis between inferior outcome in cHL and a high proportion of both PD-1 1 and PD-L1 1 leukocytes in the tumor microenvironment.

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“…Our results indicate that conventional front-line treatment is insufficient for these patients. 19,20 Comparison with previous studies regarding PD-1…”

Section: Pd-l1mentioning

confidence: 81%

High proportions of PD-1+ and PD-L1+ leukocytes in classical Hodgkin lymphoma microenvironment are associated with inferior outcome

et al. 2017

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“…Chemotherapeutic agents could upregulate the PD‐L1 expression via IFN‐γ‐dependent and IFN‐γ‐independent modes. This upregulation could be exerted by activating different signals and releasing some immunosuppressive cytokines to reduce the antitumor immune response (Luo & Fu, 2016).…”

Section: Pd‐l1 and Colorectal Cancermentioning

confidence: 99%

“…To this end, combine the ICB with other therapies that stimulate T cell immunity (such as chemotherapy drugs) would be a more sufficient approach (Galluzzi et al, 2015). In this regard, the combination of immunotherapy and chemotherapy can maintain efficient and long‐lasting antitumor immune response via an effective alteration of the overall TME and immune tolerance (Luo & Fu, 2016). Some chemotherapies can enhance the efficacy of the anticancer effects of ICB according to the results of studies in preclinical models.…”

Section: Pd‐l1 and Colorectal Cancermentioning

confidence: 99%

PD‐1/PD‐L1‐dependent immune response in colorectal cancer

Payandeh

Khalili

Somi

et al. 2020

Journal Cellular Physiology

102

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Colorectal cancer (CRC) is still considered as the third most frequent cancer in the world. Microsatellite instability (MSI), inflammation, and microRNAs have been demonstrated as the main contributing factors in CRC. Subtype 1 CRC is defined by NK cells infiltration, induction of Th1 lymphocyte and cytotoxic T cell responses as well as upregulation of immune checkpoint proteins including programmed cell death‐1 (PD‐1). Based on the diverse features of CRC, such as the stage and localization of the tumor, several treatment approaches are available. However, the efficiency of these treatments may be decreased due to the development of diverse resistance mechanisms. It has been proven that monoclonal antibodies (mAbs) can increase the effectiveness of CRC treatments. Nowadays, several mAbs including nivolumab and pembrolizumab have been approved for the treatment of CRC. Immune checkpoint receptors including PD‐1 can be inhibited by these antibodies. Combination therapy gives an opportunity for advanced treatment for CRC patients. In this review, an update has been provided on the molecular mechanisms involved in MSI colorectal cancer immune microenvironment by focusing on PD‐ligand 1 (PD‐L1) and treatment of patients with advanced immunotherapy, which were examined in the different clinical trial phases. Considering induced expression of PD‐L1 by conventional chemotherapeutics, we have summarized the role of PD‐L1 in CRC, the chemotherapy effects on the PD‐1/PD‐L1 axis and novel combined approaches to enhance immunotherapy of CRC by focusing on PD‐L1.

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“…Anti-cancer agents, such as epothilone B, taxol and vinblastine, which are microtubule destabilizers, induced HLA class I surface protein expression and RNA transcription in a time- and concentration-dependent manner in ovarian cancer cells [49]. Microtubule destabilizers, such as these, potentially alter HLA expression by upregulating the production of cytokines (IFNα, IL-1β, IL-6, IL-12) involved in HLA expression or disrupt intracellular trafficking of HLA proteins, causing redistribution at the tumor surface [49,50]. In our laboratory, administration of type I IFNs (α, β) or type II IFN (γ) dose-dependently increased RNA transcription of HLA class I (A, B, C) and class II (DO, DM) molecules in the vast majority of epithelial cancers examined, while sensitizing HLA-A2 + malignancies to antigen-dependent, T cell attack, despite concurrent upregulation of PD-L1/2 [51].…”

Section: Impact Of Chemotherapy On Anti-tumor Immunity and Cancer mentioning

confidence: 99%

The Impact of Chemotherapy, Radiation and Epigenetic Modifiers in Cancer Cell Expression of Immune Inhibitory and Stimulatory Molecules and Anti-Tumor Efficacy

2016

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Genomic destabilizers, such as radiation and chemotherapy, and epigenetic modifiers are used for the treatment of cancer due to their apoptotic effects on the aberrant cells. However, these therapies may also induce widespread changes within the immune system and cancer cells, which may enable tumors to avoid immune surveillance and escape from host anti-tumor immunity. Genomic destabilizers can induce immunogenic death of tumor cells, but also induce upregulation of immune inhibitory ligands on drug-resistant cells, resulting in tumor progression. While administration of immunomodulatory antibodies that block the interactions between inhibitory receptors on immune cells and their ligands on tumor cells can mediate cancer regression in a subset of treated patients, it is crucial to understand how genomic destabilizers alter the immune system and malignant cells, including which inhibitory molecules, receptors and/or ligands are upregulated in response to genotoxic stress. Knowledge gained in this area will aid in the rational design of trials that combine genomic destabilizers, epigenetic modifiers and immunotherapeutic agents that may be synergized to improve clinical responses and prevent tumor escape from the immune system. Our review article describes the impact genomic destabilizers, such as radiation and chemotherapy, and epigenetic modifiers have on anti-tumor immunity and the tumor microenvironment. Although genomic destabilizers cause DNA damage on cancer cells, these therapies can also have diverse effects on the immune system, promote immunogenic cell death or survival and alter the cancer cell expression of immune inhibitor molecules.

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The effect of chemotherapy on programmed cell death 1/programmed cell death 1 ligand axis: some chemotherapeutical drugs may finally work through immune response

Cited by 51 publications

References 64 publications

High proportions of PD-1+ and PD-L1+ leukocytes in classical Hodgkin lymphoma microenvironment are associated with inferior outcome

High proportions of PD-1+ and PD-L1+ leukocytes in classical Hodgkin lymphoma microenvironment are associated with inferior outcome

PD‐1/PD‐L1‐dependent immune response in colorectal cancer

The Impact of Chemotherapy, Radiation and Epigenetic Modifiers in Cancer Cell Expression of Immune Inhibitory and Stimulatory Molecules and Anti-Tumor Efficacy

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