Introduction to Pd L1 Blockade
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Pd L1 Blockade sentence examples within programmed death ligand
To overcome the limitation of antibody therapeutics, we have explored PD-1/PD-L1 (programmed death-ligand 1) blockades in traditional oriental medicine, which has a long history but has not yet studied PD-1/PD-L1 blockades.
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ERK pathway regulated the programmed death ligand-1 (PD-L1) expression which was linked to the response of programmed death-1 (PD-1)/PD-L1 blockade therapy.
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The further knock-out of PD-L1 in BMFs rescues the sensitivity of BMF-mixed tumor xenografts to PD-L1 blockade therapy.
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PD-1/PD-L1 blockade has become an important therapy in the anti-cancer armamentarium.
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Conclusions: CTX-8371 displays multiple mechanisms of action over monoclonal PD1/PD-L1 blockade.
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In this review, we have highlighted new viewpoints regarding improving the therapeutic effect of PD-1 and PD-L1 blockades in cancer therapy.
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Here, we tested whether the combination of a PD-L1 blockade and therapeutic vaccination with functionalized nanoparticles is a potent therapy during chronic Friend retrovirus infection.
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The PD-L1 blockade increased the production of interleukin-2 from swine PBMCs.
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We also show that a combination of SC-oHSV and PD-L1 blockade increases IFNγ-producing CD8+ tumor-infiltrating T lymphocytes and results in a profound extension of the median survival in syngeneic brain metastatic melanoma mouse models.
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The combination therapy was able to reduce M2 macrophage and increasing PD-L1 blockade sensitivity.
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Positive response to PD-1/PD-L1 blockades was observed in the treatment of solidtumors.
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PD-1/PD-L1 blockade could induce thyroiditis by diminishing regulatory T cells function.
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Moreover, the use of PD-1/PD-L1 blockade prior to or concurrent with osimertinib has been reported to increase the risk of pulmonary toxicity.
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Here, we show that MEK inhibition enhanced PD-L1 expression while PD-L1 blockade upregulated MAPK signaling in mutant KRAS lung tumors.
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BACKGROUND
PD-1/PD-L1 blockade immunotherapies have changed the landscape of cancer therapy.
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In addition, the serum thyroxine was mardedly decreased to 1/3 of that in the control group mice, and the blood pressure and body temperature were abnormally decreased in mice upon treatment with PD-L1 blockade.
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Further studies show that the pCCL2 trap could facilitate PD-L1 blockade immunotherapy, demonstrating its translation potential.
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Aim PD-1/PD-L1 blockade therapy is now widely used for the treatment of advanced malignancies.
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Tumor immunotherapy by PD-1/PD-L1 blockade (PPB) has emerged as a standard of care treatment and can bring long-lasting clinical benefits, yet less than one-third of patients respond to it.
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Fibrocytes express functional PD-L1; PD-L1 blockade further activates CD8+ T cells.
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This finding means that compensation for the potential sequestration of antibodies needs to be considered in the optimization of PD-L1 blockade therapies.
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Therapy with immune check-point inhibitors target PD-1/PD-L1 blockade inducing tumor regression.
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Of these three subtypes, two were associated with low response rates to PD-1/PD-L1 blockade, suggesting the existence of distinct avenues toward resistance.
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Importantly, the WM_Score was associated with the therapeutic efficacy of PD-L1 blockade, suggesting that the development of potential drugs targeting these “writers” to aid the clinical benefits of immunotherapy.
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These alterations were not observed in papillomas treated with PD-L1 blockade alone.
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We highlight the gaps in the field that need to be addressed to improve patient outcome including biomarkers for response stratification and potentially synergistic combination therapy regimens with PD-1/PD-L1 blockade.
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11551 Background: Based on the central role played by the vascular endothelial growth factor receptor (VEGFR) in immunosuppression, we assessed the activity and safety of VEGFR inhibitor pazopanib plus anti-PD-L1 blockade durvalumab in soft tissue sarcoma (STS).
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PD-1/PD-L1 blockade therapies provide notable clinical benefits for patients with advanced cancers, but the factors influencing the effectiveness of the treatment remain incompletely cataloged.
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The patients at high risk may get survival benefit from PD-1/PD-L1 blockade (stage I) or combined with chemotherapy (stage II).
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In this review, we discuss the main preclinical and clinical evidence on strategies that can lead to an enhanced response to PD-1/PD-L1 blockade in combination with radiation therapy.
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The nanoassembly has been reprogrammed with peptide-containing moieties for tumor-targeting and PD-1/PD-L1 blockade.
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Combined apatinib and PD-L1 blockade therapy synergistically delayed tumor growth and increased survival in MFC-bearing immunocompetent mice.
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Tfh TIL, regulated by functional Tfr TIL, are an expected key target of PD-1/PD-L1 blockade.
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The effect of Niraparib and PD-L1 blockade in ovarian cancer progression was investigated in vivo.
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Avelumab was tolerable and demonstrated antitumor activity in heavily pretreated patients with cHL, suggesting that PD-L1 blockade may be sufficient for therapeutic benefit in cHL.
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These patients at higher risk might be more suitable to benefit from PD-L1 blockade or other checkpoint blockade immunotherapies.
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Unfortunately, the main dilemma is that a large number of patients remain refractory to CTLA-4, PD-1, and PD-L1 blockade therapies.
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As a very promising immunotherapy, PD-1/PD-L1 blockade has revolutionized the treatment of a variety of tumor types, resulting in significant clinical efficacy and lasting responses.
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In MSI-H endometrial cancers specifically, response rates of over 50% to single agent PD-1/PD-L1 blockade have been reported across a number of studies.
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To identify strategies to overcome resistance to PD-L1 blockade, the transcriptional programs associated with PD-L1 and/or TGF-β blockade in the tumor microenvironment should be further elucidated.
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However, its anti-tumor response and mechanism combined with PD-L1 blockade in PC remain unclear.
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However, only a subset of cancers exhibits a durable response to PD-1/PD-L1 blockade.
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The mechanisms by which the same PD-1/PD-L1 blockades lead to two distinct therapeutic responses in CRC patients with different MSI statuses remain poorly understood and become a topic of great interest in both basic research and clinical practice.
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Moreover, (iv) the implication of PD-L1 in obese ASC-mediated T cell dysfunction was demonstrated through PD-L1 blockade.
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In vitro responsiveness to PD-L1 blockade varied with defined CD4+ T cell functions rather than IC expression levels: frequencies of cells with TH1- and TH17/TH22-, but not TFH-related functions, increased.
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Consistent with this, pharmacologic inhibition of PIM kinase by AZD1208 treatment significantly disrupted the myeloid cell–mediated immunosuppressive microenvironment and unleashed CD8+ T-cell–mediated antitumor immunity, which enhanced PD-L1 blockade in preclinical cancer models.
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Anti-PD-1/PD-L1 checkpoint inhibitors disrupt the engagement of PD-1 on T-cells and their ligands on tumor or other target cells and reactivate the tumor-specific T infiltrating lymphocytes (TILs), which are mostly in a state of anergy before the PD-1/PD-L1 blockade.
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Recent studies have shown that photodynamic therapy (PDT) which could effectively enhance PD-L1 blockade therapeutical effect, while its reason is still unclear.
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CONCLUSION
Our results suggest that the mIHC/IF platform is a clinically relevant method to assess CD39+CD8+ T cell proportion and this marker can serve as a potential biomarker that predicts response to PD-1/PD-L1 blockade in NSCLC patients.
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Most patients are resistant to PD-1/PD-L1 blockade therapy but mechanisms are not well defined.
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We observed a statistically significant association between PD1/PD-L1 blockade and pCR (SOR = 1.
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In contrast to other tumor indications, objective response rates to single-agent PD-1/PD-L1 blockade in ovarian cancer are limited, suggesting a need to identify combinatorial approaches that lead to tumor regression in a setting where checkpoint blockade alone is ineffective.
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An alarmin HMGN1 peptide combined with PD-L1 blockade improves antitumor responses in multiple murine tumor models.
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The emergence of immune checkpoint inhibitors (ICIs), mainly based on PD-1/PD-L1 blockade has revolutionized the therapeutic landscape of cancer.
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However, associated with T-cell regulation, the immunomodulatory effect of PD-L1 blockade and its biomarker in peripheral immunity remains elusive.
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Furthermore, we outlined the emerging biomarkers for the efficacy of PD-1/PD-L1 blockades and radiation therapy and discussed their predictive value in NSCLC.
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Mutations in the STK11 (LKB1) gene regulate resistance to PD-1/PD-L1 blockade.
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Additionally, compounds 24e, 24m, and 25a markedly improved the antitumor activity of PD-1/PD-L1 blockade.
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Importantly, the HOXscore was associated with the therapeutic efficacy of PD-L1 blockade, suggesting that the development of potential drugs targeting these HOX genes to aid the clinical benefits of immunotherapy.
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MATERIALS/METHODS
We looked at two groups of non-small cell lung cancer (NSCLC) patients drawn from two institutions: patients with metastatic disease treated with non-curative intent and normal lung in the radiation field, and patients receiving definitive chemo-radiation (CRT) followed by adjuvant PD-L1 blockade (durvalumab), some of which received durvalumab also concurrently.
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Therefore, the identification of new target molecules acting in distinct or complementary pathways in monotherapy or combination therapy with PD-1/PD-L1 blockade is gaining immense interest.
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Combination with PD-1/PD-L1 blockade aims at enhanced efficacy.
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Immune checkpoint inhibitor (ICI), PD-1/PD-L1 blockade has been approved for various cancers.
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In addition, the efficacy of PD-1/PD-L1 blockade as a therapeutic strategy to reverse myeloma immune suppression and inhibit myeloma cell survival still remains unknown.
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Immunotherapy approaches that improve the antitumor activity and proliferation of CD8+ T and NK cells include PD-1/PD-L1 blockade, CAR T cell therapy, or ex vivo-stimulated NK cells.
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However, whether regulating lipid accumulation in MDSCs by targeting FATP2 could block MDSCs reactive oxygen species (ROS) production and enhance PD-L1 blockade-mediated tumor immunotherapy remains unexplored.
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Similarly, we found that nobiletin assisted the induction of PD-1/PD-L1 blockade, which is a key factor for the immune escape mechanism.
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In the present work, we further tested the versatility of this approach in the case of an anti-PD-L1 blockade VHH (KN035).
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An intriguing prediction that emerges from the virtual patient simulations is that PD-1 blocking antibody results in higher response rate than PD-L1 blockade and that PD-L1 expression density on non-tumor immune cells rather than tumor cells is a predictor of response.
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In addition, SM also possesses natural TME-modulating ability; therefore, RBC-SLip can synergize with the PD1/PD-L1 blockade immunotherapy when encapsulated with PTX to achieve enhanced chemoimmunotherapy.
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Furthermore, PD-L1 blockade increased IFN-γ production in the presence of Rm-saliva, suggesting that Rm-saliva suppresses Th1 responses via the PD-1/PD-L1 pathway.
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Further cell-based PD-1/PD-L1 blockade bioassays indicated that these C2-symmetric molecules could significantly inhibit the PD-1/PD-L1 interaction at the cellular level and restore T cells' immune function at the safety concentrations.
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Purpose: To define dominant molecular and cellular features associated with PD-1/PD-L1 blockade resistance in metastatic urothelial cancer.
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And PD-L1 blockade therapy may be more effective in BC patients with the activation of some cancer-related pathways.
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To explore the possible synergistic effects of immunotherapy combined with chemotherapy, MC38 xenografts with different sensitivity to PD-L1 blockade were established.
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NEK2 inhibition thereby sensitizes PD-L1 blockade, synergically enhancing the anti-pancreatic cancer immune response.
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