Статті в журналах: "Programmed cell death ligand 1"

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Liu, Qiang, and Chun-Sheng Li. "Programmed Cell Death-1/Programmed Death-ligand 1 Pathway." Chinese Medical Journal 130, no. 8 (April 2017): 986–92. http://dx.doi.org/10.4103/0366-6999.204113.

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Jaafar, Jaafar, Eugenio Fernandez, Heba Alwan, and Jacques Philippe. "Programmed cell death-1 and programmed cell death ligand-1 antibodies-induced dysthyroidism." Endocrine Connections 7, no. 5 (May 2018): R196—R211. http://dx.doi.org/10.1530/ec-18-0079.

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Background Monoclonal antibodies blocking the programmed cell death-1 (PD-1) or its ligand (PD-L1) are a group of immune checkpoints inhibitors (ICIs) with proven antitumor efficacy. However, their use is complicated by immune-related adverse events (irAEs), including endocrine adverse events (eAEs). Purpose We review the incidence, time to onset and resolution rate of dysthyroidism induced by PD-1/PD-L1 Ab, and the clinical, biological and radiological findings. We aim to discuss the potential mechanisms of PD-1/PD-L1 Ab-induced dysthyroidism, and to propose a management algorithm. Methods We performed a literature search of available clinical trials regarding PD-1/PD-L1 Ab in the PubMed database. We selected all English language clinical trials that included at least 100 patients. We also present selected case series or reports, retrospective studies and reviews related to this issue. Findings In patients treated with PD-1 Ab, hypothyroidism occurred in 2–10.1% and hyperthyroidism occurred in 0.9–7.8%. When thyroiditis was reported separately, it occurred in 0.34–2.6%. Higher rates were reported when PD-1 Ab were associated with other ICI or chemotherapy. The median time to onset of hyperthyroidism and hypothyroidism after PD-1 Ab initiation was 23–45 days and 2–3.5 months, respectively. Regarding PD-L1 Ab, hypothyroidism occurred in 0–10% and hyperthyroidism in 0.5–2% of treated patients. The average time to onset of dysthyroidism after PD-L1 Ab was variable and ranged from 1 day after treatment initiation to 31 months. Conclusion Dysthyroidism occurs in up to 10% of patients treated with PD-1/PD-L1 Ab. Hypothyroidism and reversible destructive thyroiditis are the most frequent endocrine adverse events (eAE) in PD-1/PD-L1 treated patients. Immune and non-immune mechanisms are potentially involved, independently of the presence of thyroid antibodies.

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Verhoeff, Sarah R., Michel M. van den Heuvel, Carla M. L. van Herpen, Berber Piet, Erik H. J. G. Aarntzen, and Sandra Heskamp. "Programmed Cell Death-1/Ligand-1 PET Imaging." PET Clinics 15, no. 1 (January 2020): 35–43. http://dx.doi.org/10.1016/j.cpet.2019.08.008.

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Fang, Xiao-Na, and Li-Wu Fu. "Predictive Efficacy Biomarkers of Programmed Cell Death 1/Programmed Cell Death 1 Ligand Blockade Therapy." Recent Patents on Anti-Cancer Drug Discovery 11, no. 2 (April 15, 2016): 141–51. http://dx.doi.org/10.2174/1574892811666160226150506.

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Yu, Wesley Y., Timothy G. Berger, Jeffrey P. North, Zoltan Laszik, and Jarish N. Cohen. "Expression of programmed cell death ligand 1 and programmed cell death 1 in cutaneous warts." Journal of the American Academy of Dermatology 81, no. 5 (November 2019): 1127–33. http://dx.doi.org/10.1016/j.jaad.2019.02.063.

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Tamura, Akihiro, Makiko Yoshida, Nobuyuki Yamamoto, Nanako Nino, Naoko Nakatani, Takayuki Ichikawa, Sayaka Nakamura, et al. "Programmed Death-1 and Programmed Death-Ligand 1 Expression Patterns in Pediatric Lymphoma." Blood 132, Supplement 1 (November 29, 2018): 5316. http://dx.doi.org/10.1182/blood-2018-99-110732.

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Abstract Introduction The programmed death-1 (PD-1)-programmed death-ligand 1 (PD-L1) pathway is an inhibitory immune checkpoint that can suppress T-cell-mediated tumor cytotoxicity. Anti-PD-1 monoclonal antibodies have recently been recognized as promising therapy for adult patients with lymphoma, particularly in classical Hodgkin's lymphoma. However, little information is available regarding the expression patterns of PD-1 and PD-L1 in pediatric lymphoma. Therefore, this study aimed to investigate the expression patterns of PD-1 and PD-L1 in pediatric lymphoma. Methods Immunohistochemical analysis was performed on paraffin-embedded pretherapeutic tumor biopsies from 36 newly diagnosed pediatric patients (aged 0-15 years) with lymphoma or lymphoproliferative disorders treated at Kobe Children's Hospital (Kobe, Japan) from 2003 to 2018. Results Thirty-six samples comprising 11 of Burkitt lymphoma (BL), 7 of anaplastic large-cell lymphoma (ALCL), 6 of T-lymphoblastic lymphoma (T-LBL), 5 of diffuse large B-cell lymphoma (DLBCL), 3 of Hodgkin's lymphoma (HL), 2 of chronic active EBV-associated lymphoproliferative disorders (CAEBV-LPD), 1 of T cell/histiocyte rich B-cell lymphoma (T/HRBCL), and 1 of subcutaneous panniculitis-like T-cell lymphoma (SPTCL) were evaluated. PD-L1 and PD-1 staining results in each lymphoma type are explained below and in Table. Burkitt lymphoma None of the 11 samples stained for PD-L1 or PD-1 in BL cells. PD-1 was expressed in a small proportion of tumor-infiltrating lymphocytes (TIL) in 3 of the 11 samples. Anaplastic large-cell lymphoma PD-L1 was robustly expressed in ALCL cells in 5 of the 7 samples. However, PD-1 was not expressed in any ALCL cell samples but expressed in a small proportion of TIL in only 1 sample. T-lymphoblastic lymphoma None of the 6 samples stained for PD-L1 in T-LBL cells. PD-1 was stained in T-LBL cells in only 1 sample. Moreover, PD-1 was not stained in TIL in any samples. Diffuse large B-cell lymphoma None of the 3 samples with DLBCL-not otherwise specified (DLBCL-NOS) or 1 sample with DLBCL with IRF4 rearrangement expressed PD-L1 on tumor cells. Conversely, PD-L1 was overexpressed in tumor cells in 1 sample with DLBCL with an interfollicular pattern of proliferation (DLBCL-IF). However, PD-1 was not expressed in any DLBCL cell samples. PD-1 was expressed in a small proportion of TIL in 1 sample with DLBCL with IRF4 rearrangement. Hodgkin's lymphoma PD-L1 was overexpressed in HL cells in both nodular sclerosis classic HL (NScHL), whereas PD-L1 was not expressed in nodular lymphocyte predominant HL (NLPHL) cells. PD-1 was not expressed in HScHL or NLPHL cells but was expressed in a small proportion of TIL in 1 sample with NLPHL. Chronic active EBV-associated lymphoproliferative disorders PD-L1 was overexpressed in tumor cells in both samples with CAEBV-LPD. PD-1 was not expressed in tumor cells but was expressed in a small proportion of TIL in 1 sample. T cell/histiocyte-rich B-cell lymphoma PD-L1 was overexpressed on tumor cells in T/HRBCL. PD-1 was weakly expressed in a part of T/HRBCL cells but strongly expressed in TIL. Subcutaneous panniculitis-like T cell lymphoma PD-L1 was overexpressed in tumor cells in SPTCL. However, PD-1 was not expressed in SPTCL cells or TIL. Discussion In this pediatric cohort, PD-L1 was overexpressed in tumor cells in ALCL (5/7), DLBCL-IF (1/1), NScHL (2/2), CAEBV-LPD (2/2), T/HRBCL (1/1), and SPTCL (1/1), but not in BL, T-LBL, DLBCL-NOS, or NLPHL. While the PD-L1 expression in EBV-positive lymphoma cells has been reported before, this study demonstrated the PD-L1 overexpression in CAEBV-LPD. In addition, we demonstrated the PD-L1 overexpression on SPTCL and DLBCL-IF cells, whereas the PD-L1 overexpression in T/HRBCL cells was consistent with previous reports. This study demonstrated that the PD-1 expression in tumor cells was rare in pediatric lymphoma. In addition, PD-1 expressions in TIL tended to be low in pediatric lymphoma, except for NLPHL and T/HRBCL. Besides classic HL, PD-1 blockade might be a promising treatment strategy for ALCL, DLBCL-IF, CAEBV-LPD, T/HRBCL, and SPTCL in children. Indeed, anectodal reports showed promising efficacy in ALCL. Therefore, further investigations are required to assess the role of the PD-1-PD-L1 pathway in pediatric lymphoma. Disclosures No relevant conflicts of interest to declare.

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Zhang, Ni, Jingyao Tu, Xue Wang, and Qian Chu. "Programmed cell death-1/programmed cell death ligand-1 checkpoint inhibitors: differences in mechanism of action." Immunotherapy 11, no. 5 (April 2019): 429–41. http://dx.doi.org/10.2217/imt-2018-0110.

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Zhao, Wanying, Yuanzheng Liang, and Liang Wang. "Advances in targeting programmed cell death 1/programmed cell death-ligand 1 therapy for hematological malignancies." Aging Pathobiology and Therapeutics 3, no. 4 (December 31, 2021): 84–94. http://dx.doi.org/10.31491/apt.2021.12.071.

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Programmed cell death 1 (PD-1) and programmed cell death-ligand 1 (PD-L1) are important immune checkpoints, and their interactions can mediate immune suppression in the tumor microenvironment. Targeting PD-1 and PD-L1 are immune checkpoint inhibitors that bind to PD-1 and PD-L1, respectively, to block the signal pathway between the two and increase the immune response. They are widely used in tumor treatment and have good efficacies for malignant melanoma, renal cell carcinoma, and non-small cell lung cancer, among others. In addition, for hematological malignancies, studies targeting PD-1 and PD-L1 have achieved gratifying results. This article briefly reviews the mechanisms of action and clinical and hematological malignancy applications of targeting PD-1 and PD-L1. Keywords: PD-1, PD-L1, mechanism of action, hematological malignancy

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Wang, Tianyu, Xiaoxing Wu, Changying Guo, Kuojun Zhang, Jinyi Xu, Zheng Li, and Sheng Jiang. "Development of Inhibitors of the Programmed Cell Death-1/Programmed Cell Death-Ligand 1 Signaling Pathway." Journal of Medicinal Chemistry 62, no. 4 (September 24, 2018): 1715–30. http://dx.doi.org/10.1021/acs.jmedchem.8b00990.

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Shen, Jacson K., Gregory M. Cote, Edwin Choy, Pei Yang, David Harmon, Joseph Schwab, G. Petur Nielsen, et al. "Programmed Cell Death Ligand 1 Expression in Osteosarcoma." Cancer Immunology Research 2, no. 7 (April 21, 2014): 690–98. http://dx.doi.org/10.1158/2326-6066.cir-13-0224.

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Wolkow, Natalie, Frederick A. Jakobiec, Amir H. Afrogheh, Ralph C. Eagle, Sara I. Pai, and William C. Faquin. "Programmed Cell Death 1 Ligand 1 and Programmed Cell Death 1 Ligand 2 Are Expressed in Conjunctival Invasive Squamous Cell Carcinoma: Therapeutic Implications." American Journal of Ophthalmology 200 (April 2019): 226–41. http://dx.doi.org/10.1016/j.ajo.2018.12.020.

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Niedźwiedzka-Rystwej, Paulina, Adam Majchrzak, Bogusz Aksak-Wąs, Karol Serwin, Zenon Czajkowski, Ewelina Grywalska, Izabela Korona-Głowniak, Jacek Roliński, and Miłosz Parczewski. "Programmed Cell Death-1/Programmed Cell Death-1 Ligand as Prognostic Markers of Coronavirus Disease 2019 Severity." Cells 11, no. 12 (June 20, 2022): 1978. http://dx.doi.org/10.3390/cells11121978.

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Current research proves that immune dysregulation is a common feature of coronavirus disease 2019 (COVID-19), and immune exhaustion is associated with increased disease mortality. Immune checkpoint molecules, including the programmed cell death-1 (PD-1)/PD-1 ligand (PD-L1) axis, may serve as markers of disease severity. Accordingly, in this study, we evaluated the expression of PD-1/PD-L1 in patients with COVID-19. Blood immunophenotypes of hospitalized patients with moderate (n = 17, requiring oxygen support) and severe (n = 35, requiring mechanical ventilation in the intensive care setting) COVID-19 were compared and associated with clinical, laboratory, and survival data. The associations between severity and lymphocyte profiles were analysed at baseline and after 7 and 14 days of in-hospital treatment. Forty patients without COVID-19 infection were used as controls. For PD-1-positive T and B lymphocyte subsets, notable increases were observed between controls and patients with moderate or severe COVID-19 for CD4+PD-1+ T cells, CD8+PD-1+ T and CD19+PD-1+ B cells. Similar trends were observed for PD-L1-positive lymphocytes, namely, CD4+PD-L1+ T cells, CD8+PD-L1+ T cells and CD19+PD-L1+ B cells. Importantly, all markers associated with PD-1 and PD-L1 were stable over time for the analysed time points in the moderate and severe COVID-19 groups. Increased abundances of PD-1+ and PD-L1+ lymphocytes were associated with disease severity and mortality and were stable over time in patients with moderate to severe COVID-19. These immune exhaustion parameters may be attractive biomarkers of COVID-19 severity.

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Zhang, Jingyi, Kexin Tan, Xuejiao Jiang, Shuyue Zheng, Jia Li, Chongxiang Xue, Xu Zhang, and Huijuan Cui. "The incidence of pseudoprogressive disease associated with programmed cell death 1/programmed cell death ligand 1 inhibitors." Medicine 100, no. 28 (July 16, 2021): e26649. http://dx.doi.org/10.1097/md.0000000000026649.

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Deng, Tuo, and Guohua Zeng. "Immunotherapy With Programmed Cell Death 1 vs Programmed Cell Death Ligand 1 Inhibitors in Patients With Cancer." JAMA Oncology 6, no. 7 (July 1, 2020): 1113. http://dx.doi.org/10.1001/jamaoncol.2020.0625.

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Bomze, David, Daniel Azoulay, and Tomer Meirson. "Immunotherapy With Programmed Cell Death 1 vs Programmed Cell Death Ligand 1 Inhibitors in Patients With Cancer." JAMA Oncology 6, no. 7 (July 1, 2020): 1114. http://dx.doi.org/10.1001/jamaoncol.2020.0628.

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Wang, Tao, Shiowjen Lee, and Gerald M. Feldman. "Immunotherapy With Programmed Cell Death 1 vs Programmed Cell Death Ligand 1 Inhibitors in Patients With Cancer." JAMA Oncology 6, no. 7 (July 1, 2020): 1115. http://dx.doi.org/10.1001/jamaoncol.2020.0631.

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Ghiorghiu, Serban, Pralay Mukhopadhyay, and Cristian Massacesi. "Immunotherapy With Programmed Cell Death 1 vs Programmed Cell Death Ligand 1 Inhibitors in Patients With Cancer." JAMA Oncology 6, no. 7 (July 1, 2020): 1115. http://dx.doi.org/10.1001/jamaoncol.2020.0637.

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Sun, Lejia, Huayu Yang, and Yilei Mao. "Programmed cell death protein 1/programmed death ligand-1 checkpoint blockade meets patient-derived organoids." Annals of Translational Medicine 7, S8 (December 2019): S287. http://dx.doi.org/10.21037/atm.2019.11.76.

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Naidoo, Jarushka, Xuan Wang, Kaitlin M. Woo, Tunc Iyriboz, Darragh Halpenny, Jane Cunningham, Jamie E. Chaft, et al. "Pneumonitis in Patients Treated With Anti–Programmed Death-1/Programmed Death Ligand 1 Therapy." Journal of Clinical Oncology 35, no. 7 (March 1, 2017): 709–17. http://dx.doi.org/10.1200/jco.2016.68.2005.

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Purpose Pneumonitis is an uncommon but potentially fatal toxicity of anti–programmed death-1 (PD-1)/programmed death ligand 1 (PD-L1) monoclonal antibodies (mAbs). Clinical, radiologic, and pathologic features are poorly described. Methods Patients who received anti–PD-1/PD-L1 monotherapy or in combination with anti–cytotoxic T-cell lymphocyte associated antigen-4 mAb were identified at two institutions (Memorial Sloan Kettering Cancer Center: advanced solid cancers, 2009 to 2014, and Melanoma Institute of Australia: melanomas only, 2013 to 2015). Pneumonitis was diagnosed by the treating investigator; cases with confirmed malignant lung infiltration or infection were excluded. Clinical, radiologic, and pathologic features of pneumonitis were collected. Associations among pneumonitis incidence, therapy received, and underlying malignancy were examined with Fisher’s exact test as were associations between pneumonitis features and outcomes. Results Of 915 patients who received anti–PD-1/PD-L1 mAbs, pneumonitis developed in 43 (5%; 95% CI, 3% to 6%; Memorial Sloan Kettering Cancer Center, 27 of 578 [5%]; Melanoma Institute of Australia, 16 of 337 [5%]). Time to onset of pneumonitis ranged from 9 days to 19.2 months. The incidence of pneumonitis was higher with combination immunotherapy versus monotherapy (19 of 199 [10%] v 24 of 716 [3%]; P < .01). Incidence was similar in patients with melanoma and non–small-cell lung cancer (overall, 26 of 532 [5%] v nine of 209 [4%]; monotherapy, 15 of 417 v five of 152 [ P = 1.0]; combination, 11 of 115 v four of 57 [ P = .78]). Seventy-two percent (31 of 43) of cases were grade 1 to 2, and 86% (37 of 43) improved/resolved with drug holding/immunosuppression. Five patients worsened clinically and died during the course of pneumonitis treatment; proximal cause of death was pneumonitis (n = 1), infection related to immunosuppression (n = 3), or progressive cancer (n = 1). Radiologic and pathologic features of pneumonitis were diverse. Conclusion Pneumonitis associated with anti–PD-1/PD-L1 mAbs is a toxicity of variable onset and clinical, radiologic, and pathologic appearances. It is more common when anti–PD-1/PD-L1 mAbs are combined with anti–cytotoxic T-cell lymphocyte associated antigen-4 mAb. Most events are low grade and improve/resolve with drug holding/immunosuppression. Rarely, pneumonitis worsens despite immunosuppression, and may result in infection and/or death.

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Fakhri, Ghina, Reem Akel, Ibrahim Khalifeh, Hassan Chami, Adel Hajj Ali, Majd Al Assaad, Haneen Atwi, Humam Kadara, and Arafat Tfayli. "Prevalence of programmed death ligand-1 in patients diagnosed with non-small cell lung cancer in Lebanon." SAGE Open Medicine 9 (January 2021): 205031212110437. http://dx.doi.org/10.1177/20503121211043709.

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Introduction: Programmed death ligand-1 expression has been shown to be a good predictor of response to cancer therapy with checkpoint inhibitors. Its expression varies among different tumor types and among non-small cell lung cancer patients with different clinical and demographic characteristics. The prevalence and determinants of programmed death ligand-1 expression have been previously reported from various regions of the world, but data from Lebanon are lacking. This study examines the prevalence and the clinical, demographic and pathological predictors of programmed death ligand-1 expression in patients diagnosed with non-small cell lung cancer in Lebanon. Methods: Medical records of 180 patients diagnosed with primary non-small cell lung cancer at our institution and tested for programmed death ligand-1 expression were reviewed. Clinical, demographic and pathological information were collected and correlated with programmed death ligand-1 expression using the chi-square test and logistic regression. Results: One hundred eleven of the 180 non-small cell lung cancer tumor samples tested positive for programmed death ligand-1 expression (61.7%). 27.2% of those tumor samples expressed programmed death ligand-1 in 1%–49% of tumor cells, while 34.4% of tumor samples expressed programmed death ligand-1 in 50% or more of their cells. Squamous histology and advanced stage were significant predictors of programmed death ligand-1 expression (odds ratio = 2.79, 95% confidence interval [1.13–6.90], p = 0.012 and odds ratio = 2.48, 95% confidence interval [1.23–4.99], p = 0.044, respectively). Conclusion: Similar to reports from other populations, our results suggest that programmed death ligand-1 expression in non-small cell lung cancer is highly prevalent in the Lebanese population, especially in patients with advanced stage at diagnosis or squamous cell carcinoma histology. Because of the small sample size, while more that 60% of the patients are Lebanese, the results of this article cannot be extrapolated to the Middle Eastern and the Levantine population.

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Kim, J., J. H. Choi, J. Kong, W. Yang, H. Cho, D. B. Chay, and J. H. Kim. "Prognostic implication of programmed cell death 1 protein and programmed cell death 1 ligand 1 expression in endometrial cancer." Gynecologic Oncology 149 (June 2018): 47. http://dx.doi.org/10.1016/j.ygyno.2018.04.100.

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Xu, Dongmei, Hongmei Liu, Meiyi Xiang, Alei Feng, Mei Tian, Donghua Li, Yantao Mao, Li Zhang, Shuisheng Zhang, and Yuan Tian. "The relationship between pneumonitis and programmed cell death-1/programmed cell death ligand 1 inhibitors among cancer patients." Medicine 99, no. 41 (October 9, 2020): e22567. http://dx.doi.org/10.1097/md.0000000000022567.

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Hu-Lieskovan, Siwen, and Antoni Ribas. "New Combination Strategies Using Programmed Cell Death 1/Programmed Cell Death Ligand 1 Checkpoint Inhibitors as a Backbone." Cancer Journal 23, no. 1 (2017): 10–22. http://dx.doi.org/10.1097/ppo.0000000000000246.

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Qin, Mingze, Qi Cao, Xia Wu, Chunyang Liu, Shuaishuai Zheng, Hongbo Xie, Ye Tian, et al. "Discovery of the programmed cell death-1/programmed cell death-ligand 1 interaction inhibitors bearing an indoline scaffold." European Journal of Medicinal Chemistry 186 (January 2020): 111856. http://dx.doi.org/10.1016/j.ejmech.2019.111856.

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Wang, Zhijie, Zhengyi Zhao, and Jie Wang. "Immunotherapy With Programmed Cell Death 1 vs Programmed Cell Death Ligand 1 Inhibitors in Patients With Cancer—Reply." JAMA Oncology 6, no. 7 (July 1, 2020): 1116. http://dx.doi.org/10.1001/jamaoncol.2020.0646.

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London, Nyall, Justin Bishop, Lisa Rooper, Janis Taube, Masaru Ishii, and Gary Gallia. "Expression of Programmed Cell Death-Ligand 1 in Esthesioneuroblastoma." Journal of Neurological Surgery Part B: Skull Base 79, S 01 (February 2018): S1—S188. http://dx.doi.org/10.1055/s-0038-1633448.

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Zhang, Guo-Qiang, Wei-Jun Wei, Hong-Jun Song, Zhen-Kui Sun, Chen-Tian Shen, Xin-Yun Zhang, Xiao-Yue Chen, Zhong-Ling Qiu, and Quan-Yong Luo. "PROGRAMMED CELL DEATH–LIGAND 1 OVEREXPRESSION IN THYROID CANCER." Endocrine Practice 25, no. 3 (March 2019): 279–86. http://dx.doi.org/10.4158/ep-2018-0342.

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Wakeley, Michelle E., Monique E. De Paepe, Chun-Shiang Chung, and Alfred Ayala. "Programmed Cell Death Ligand 1 Protects Against Death in Neonatal Sepsis." Journal of the American College of Surgeons 229, no. 4 (October 2019): S214. http://dx.doi.org/10.1016/j.jamcollsurg.2019.08.467.

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Kawashita, Seiji, Koichi Aoyagi, Hiroshi Yamanaka, Rie Hantani, Shiori Naruoka, Atsuo Tanimoto, Yuji Hori, et al. "Symmetry-based ligand design and evaluation of small molecule inhibitors of programmed cell death-1/programmed death-ligand 1 interaction." Bioorganic & Medicinal Chemistry Letters 29, no. 17 (September 2019): 2464–67. http://dx.doi.org/10.1016/j.bmcl.2019.07.027.

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Chang, Katherine, Catherine Svabek, Cristina Vazquez-Guillamet, Bryan Sato, David Rasche, Strother Wilson, Paul Robbins, et al. "Targeting the programmed cell death 1: programmed cell death ligand 1 pathway reverses T cell exhaustion in patients with sepsis." Critical Care 18, no. 1 (2014): R3. http://dx.doi.org/10.1186/cc13176.

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Jo, Jae-Cheol, Misung Kim, Yunsuk Choi, Hyun-Jung Kim, Ji Eun Kim, Seoung Wan Chae, Hawk Kim, and Hee Jeong Cha. "Expression of programmed cell death 1 and programmed cell death ligand 1 in extranodal NK/T-cell lymphoma, nasal type." Annals of Hematology 96, no. 1 (October 3, 2016): 25–31. http://dx.doi.org/10.1007/s00277-016-2818-4.

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Jo, Jae-Cheol, Yunsuk Choi, Hee Jeong Cha, Eun Hee Lee, Eun Kyoung Kang, and Hawk Kim. "Expression of Programmed Cell Death 1 and Programmed Cell Death Ligand 1 in Extranodal NK/T-Cell Lymphoma, Nasal Type." Blood 126, no. 23 (December 3, 2015): 1461. http://dx.doi.org/10.1182/blood.v126.23.1461.1461.

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Abstract Background Programmed cell death ligand 1 (PD-L1) is expressed on extranodal NK/T-cell lymphoma, nasal type (ENKL) tumor cells. The programmed cell death 1 (PD-1) and PD-L1 pathway inhibits host antitumor responses; however, little is known about how this pathway functions in ENKL. The aim of this study was to investigate the expression of PD-1 and PD-L1 and to determine the clinicopathological impact of PD-1 and PD-L1 positivity in ENKL. Methods We performed PD-1 and PD-L1 immunostaining in 79 ENKL biopsy samples and retrospectively analyzed medical records of all 79 patients from 4 tertiary referral hospitals. The demographic features, performance status, stage, LDH, primary sites, nodal sites, hemoglobin, white blood cell, platelet, creatinine, international prognostic index (IPI), and prognostic index for T-cell lymphoma (PIT) were recorded. Results The expression rates of PD-1-positive and PD-L1-positive ENKL were 7.6% and 88.6%, respectively (Figure 1A & 1B). PD-L1-negative ENKL (n=9) was significantly associated with high intermediate or high risk IPI (n=7, P=0.002) and group 3 or 4 PIT (n=6, P=0.043). Patients with PD-1-positive ENKL (n=6) had a trend toward better overall survival (OS) compared with that in patients with PD-1-negative ENKL (P = 0.090, Figure 2A). In contrast, there was no significant difference in OS between PD-L1-positive and -negative ENLK (P = 0.428, Figure 2B). Conclusions This is the first report describing the clinicopathological features and survival outcome according to expression of PD-1 and PD-L1 in ENKL. PD-1 expression rate is very low, and PD-L1 negativity is associated with poor risk groups of IPI and PIT in ENKL Disclosures Kim: Alexion Pharmaceuticals: Research Funding; Il-Yang: Research Funding; Celgene: Research Funding; Novartis: Research Funding.

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Lee, Joo Sang, and Eytan Ruppin. "Multiomics Prediction of Response Rates to Therapies to Inhibit Programmed Cell Death 1 and Programmed Cell Death 1 Ligand 1." JAMA Oncology 5, no. 11 (November 1, 2019): 1614. http://dx.doi.org/10.1001/jamaoncol.2019.2311.

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Guan, Xiuwen, Haijuan Wang, Fei Ma, Haili Qian, Zongbi Yi, and Binghe Xu. "The Efficacy and Safety of Programmed Cell Death 1 and Programmed Cell Death 1 Ligand Inhibitors for Advanced Melanoma." Medicine 95, no. 11 (March 2016): e3134. http://dx.doi.org/10.1097/md.0000000000003134.

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35

Zhao, Bin, Hong Zhao, and Jiaxin Zhao. "Fatal adverse events associated with programmed cell death protein 1 or programmed cell death-ligand 1 monotherapy in cancer." Therapeutic Advances in Medical Oncology 12 (January 2020): 175883591989575. http://dx.doi.org/10.1177/1758835919895753.

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Background: The introduction of antibodies targeting programmed cell death protein 1 (PD-1) and programmed cell death-ligand 1 (PD-L1) into clinical practice has had a revolutionary effect on cancer treatment. However, the incidence and risk of fatal adverse events (FAEs) following PD-1/PD-L1 inhibitor administration are controversial. Methods: We performed a systematic search for randomized controlled trials (RCTs) of PD-1/PD-L1 inhibitors (atezolizumab, avelumab, durvalumab, nivolumab, and pembrolizumab) in Embase, PubMed, the Cochrane database, and abstracts presented at American Society of Clinical Oncology and European Society of Medical Oncology from inception to July 2018. FAEs were extracted from each study and pooled to calculate overall incidence and odds ratios (ORs). Results: In total, 20 RCTs involving 12,398 patients with solid tumors were included in this study. The overall incidence of FAEs with PD-1/PD-L1 inhibitors was 0.43% [95% confidence interval (CI), 0.25–0.66%]. However, the incidences of FAEs varied significantly by tumor type and median follow-up time. Compared with conventional agents, the application of PD-1/PD-L1 inhibitors significantly reduced the risk of FAEs (OR, 0.56; 95% CI, 0.35–0.89; p = 0.015). Moreover, trial sequential analysis confirmed that our results were solid and reliable; further studies were unlikely to alter this conclusion. FAEs occurred dispersed in major organ systems, with the most common mortalities appearing in the respiratory system (46.2%). Conclusions: Compared with conventional treatment, PD-1/PD-L1 blockade monotherapy is associated with a significantly reduced risk of mortality in patients with solid tumors.

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Li, Mingkai, Linlin Huang, Xiuhong Ren, Lixia Liu, Qinghong Shi, Ling Liu, Xiao Wang, Yuan Tian, Lili Yu, and Fuli Mi. "The incidence risk of programmed cell death-1/programmed cell death ligand 1 inhibitor-related alopecia for cancer patients." Medicine 99, no. 42 (October 16, 2020): e22555. http://dx.doi.org/10.1097/md.0000000000022555.

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Duan, Jianchun, Longgang Cui, Xiaochen Zhao, Hua Bai, Shangli Cai, Guoqiang Wang, Zhengyi Zhao, et al. "Use of Immunotherapy With Programmed Cell Death 1 vs Programmed Cell Death Ligand 1 Inhibitors in Patients With Cancer." JAMA Oncology 6, no. 3 (March 1, 2020): 375. http://dx.doi.org/10.1001/jamaoncol.2019.5367.

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Greaves, Paul, and John G. Gribben. "The role of B7 family molecules in hematologic malignancy." Blood 121, no. 5 (January 31, 2013): 734–44. http://dx.doi.org/10.1182/blood-2012-10-385591.

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AbstractThe B7 family consists of structurally related, cell-surface proteins that regulate immune responses by delivering costimulatory or coinhibitory signals through their ligands. Eight family members have been identified to date including CD80 (B7-1), CD86 (B7-2), CD274 (programmed cell death-1 ligand [PD-L1]), CD273 (programmed cell death-2 ligand [PD-L2]), CD275 (inducible costimulator ligand [ICOS-L]), CD276 (B7-H3), B7-H4, and B7-H6. B7 ligands are expressed on both lymphoid and nonlymphoid tissues. The importance of the B7 family in regulating immune responses is clear from their demonstrated role in the development of immunodeficiency and autoimmune diseases. Manipulation of the signals delivered by B7 ligands shows great potential in the treatment of cancers including leukemias and lymphomas and in regulating allogeneic T-cell responses after stem cell transplantation.

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Kim, Jong Hoon, Young Joon Choi, Byung Ha Lee, Mi-Young Song, Chae Yeon Ban, Jihye Kim, Junsik Park, et al. "Programmed cell death ligand 1 alleviates psoriatic inflammation by suppressing IL-17A production from programmed cell death 1–high T cells." Journal of Allergy and Clinical Immunology 137, no. 5 (May 2016): 1466–76. http://dx.doi.org/10.1016/j.jaci.2015.11.021.

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Tay, Woan Ting, Yi-Hsien Fang, Suet Theng Beh, Yen-Wen Liu, Ling-Wei Hsu, Chia-Jui Yen, and Ping-Yen Liu. "Programmed Cell Death-1: Programmed Cell Death-Ligand 1 Interaction Protects Human Cardiomyocytes Against T-Cell Mediated Inflammation and Apoptosis Response In Vitro." International Journal of Molecular Sciences 21, no. 7 (March 31, 2020): 2399. http://dx.doi.org/10.3390/ijms21072399.

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Aim: Immunological checkpoint therapy is considered a powerful method for cancer therapy and acts by re-activating autologous T cells to kill the cancer cell. Myocarditis cases have been reported in cancer patients after immunological therapy; for example, nivolumab treatment is a monoclonal antibody that blocks programmed cell death-1/programmed cell death ligand-1 ligand interaction. This project provided insight into the inflammatory response as a benchmark to investigate the potential cardiotoxic effect of T cell response to the programmed cell death-1 (PD-1)/programmed cell death ligand-1 (PD-L1) axis in regulating cardiomyocyte injury in vitro. Methods and Results: We investigated cardiomyopathy resulted from the PD-1/PD-L1 axis blockade using the anti-PD-1 antibody in Rockefeller University embryonic stem cells-derived cardiomyocytes (RUES2-CMs) and a melanoma tumor-bearing murine model. We found that nivolumab alone did not induce inflammatory-related proteins, including PD-L1 expression, and did not induce apoptosis, which was contrary to doxorubicin, a cardiotoxic chemotherapy drug. However, nivolumab was able to exacerbate the immune response by increasing cytokine and inflammatory gene expression in RUES2-CMs when co-cultured with CD4+ T lymphocytes and induced apoptosis. This effect was not observed when RUES2-CMs were co-cultured with CD8+ T lymphocytes. The in vivo model showed that the heart function of tumor-bearing mice was decreased after treatment with anti-PD-1 antibody and demonstrated a dilated left ventricle histological examination. The dilated left ventricle was associated with an infiltration of CD4+ and CD8+ T lymphocytes into the myocardium. PD-L1 and inflammatory-associated gene expression were significantly increased in anti-PD-1-treated tumor-bearing mice. Cleaved caspase-3 and mouse plasma cardiac troponin I expressions were increased significantly. Conclusion: PD-L1 expression on cardiomyocytes suppressed T-cell function. Blockade of PD-1 by nivolumab enhanced cardiomyocyte inflammation and apoptosis through the enhancement of T-cell response towards cardiomyocytes.

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Yang, Lu-Lu, and Yi-Long Wu. "Recent advances of immunotherapy in lung cancer: anti-programmed cell death-1/programmed death ligand-1 antibodies." Lung Cancer Management 3, no. 2 (April 2014): 175–90. http://dx.doi.org/10.2217/lmt.13.80.

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Muszak, Damian, Ewa Surmiak, Jacek Plewka, Katarzyna Magiera-Mularz, Justyna Kocik-Krol, Bogdan Musielak, Dominik Sala, et al. "Terphenyl-Based Small-Molecule Inhibitors of Programmed Cell Death-1/Programmed Death-Ligand 1 Protein–Protein Interaction." Journal of Medicinal Chemistry 64, no. 15 (July 27, 2021): 11614–36. http://dx.doi.org/10.1021/acs.jmedchem.1c00957.

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Feng, Jamie, and Natasha B. Leighl. "There Is an Unmet Need for Another Programmed Cell Death Protein 1/Programmed Death-Ligand 1 Inhibitor." Journal of Thoracic Oncology 17, no. 10 (October 2022): 1175–77. http://dx.doi.org/10.1016/j.jtho.2022.07.1150.

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Geisler, Benjamin P., Leesa L. Pridham, M. Cecilia Monge B., Tali M. Johnson, Jonathan Karnon, and Elad Sharon. "Cost-effectiveness of programmed cell death protein 1/programmed death-ligand 1 inhibitors (aPD1/aPDL1) varies widely." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e18351-e18351. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e18351.

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e18351 Background: Immunotherapy with aPD1/aPDL1 has been shown to be efficacious for a range of indications. However, cost-effectiveness has only been demonstrated for some. Our goal was to compare incremental costs and effects across Food and Drug Administration (FDA) approved aPD1/aPDL1 using a standardized value framework. Methods: aPD1/aPDL1 randomized controlled trials (RCTs) were obtained from the FDA's 2014-18 approval lists. Restricted mean Overall (OS) and Progression-Free Survival (PFS) were extrapolated to 10 years via best-fitting (Akaike/Bayesian information criterion) parametric function (Kaplan-Meier survival curves digitized via Henley&Hoyle approach). Average wholesale price for experimental and comparator regimens from approval year’s Micromedex Red Book (IBM Watson Health, Cambridge, MA) were applied to either median treatment duration or mean extrapolated PFS, assuming the entire cohort was treated with no dose reductions. For multicenter RCTs with physician’s choice of the comparator, we assumed the regimen most likely used in the U.S. Incremental cost-effectiveness ratios (ICER) were discounted at 3% per annum. Results: Undiscounted OS gains with aPD1/aPDL1 after extrapolation to 10 years ranged from 0.72 to 1.89 LYs as compared to between 0.13 and 0.27 LYs at the end of the RCT. Discounted additional costs for aPD1/aPDL1 ranged from about -$1,700 to $348,312. Crude estimates of the incremental cost per LY gained vary widely, with ICERs for PACIFIC and Impower150 beyond $150,000/LY in both analyses, and additionally Keynote 024 and Checkmate 214 in the analysis that assumed treatment to the end of PFS. Conclusions: Value for money appears to vary widely across indications and comparators, from cost-saving to low-value. Common extrapolation-based analyses of aPD1/aPDL1-based regimens can help elucidate differences in value. The presented analyses are preliminary. Further assessment of extrapolation methods, downstream costs and quality of life effects are required. [Table: see text]

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Almahmoud, Suliman, and Haizhen A. Zhong. "Molecular Modeling Studies on the Binding Mode of the PD-1/PD-L1 Complex Inhibitors." International Journal of Molecular Sciences 20, no. 18 (September 19, 2019): 4654. http://dx.doi.org/10.3390/ijms20184654.

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The programmed cell death protein 1 (PD-1)/programmed cell death ligand 1 (PD-L1) is an immune checkpoint (ICP) overexpressed in various types of tumors; thus, it has been considered as an important target for cancer therapy. To determine important residues for ligand binding, we applied molecular docking studies to PD-1/PD-L1 complex inhibitors against the PD-L1 protein. Our data revealed that the residues Tyr56, Asp122, and Lys124 play critical roles in ligand binding to the PD-L1 protein and they could be used to design ligands that are active against the PD-1/PD-L1 complex. The formation of H-bonds with Arg125 of the PD-L1 protein may enhance the potency of the PD-1/PD-L1 binding.

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Kojima, Kensuke, Tetsuki Sakamoto, Takahiko Kasai, Shinji Atagi, and Hyungeun Yoon. "A quantitative evaluation of the histological type dependence of the programmed death-ligand 1 expression in non-small cell lung cancer including various adenocarcinoma subtypes: a cross-sectional study." Japanese Journal of Clinical Oncology 52, no. 3 (December 29, 2021): 281–85. http://dx.doi.org/10.1093/jjco/hyab202.

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Abstract The association between non-small cell lung cancer histology and programmed death-ligand 1 expression remains controversial. We retrospectively analyzed histological dependence of the programmed death-ligand 1 expression by a multiple regression analysis of 356 non-small cell lung cancer patients. The programmed death-ligand 1 expression patterns of adenocarcinoma were consistent with a pathological predominant growth pattern as a reference to papillary adenocarcinoma: minimally invasive adenocarcinoma[partial regression coefficient (B), 0.17; 95% confidence interval, 0.05–0.59], lepidic adenocarcinoma (B, 0.46; 95% confidence interval, 0.23–0.90), acinar adenocarcinoma (B, 1.98; 95% confidence interval, 1.05–3.76) and solid adenocarcinoma (B, 5.11; 95% confidence interval, 2.20–11.9). In histology other than adenocarcinoma, the programmed death-ligand 1 expression tended to be high with poor differentiation: adenosquamous carcinoma (B, 4.17; 95% confidence interval, 1.05–16.6), squamous cell carcinoma (B, 4.32; 95% confidence interval, 2.45–7.62) and pleomorphic carcinoma (B, 13.0; 95% confidence interval, 4.43–38.2). We showed quantitatively that the programmed death-ligand 1 expression in non-small cell lung cancer tended to be clearly histology-dependent, with more poorly differentiated histology showing a higher expression.

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Xia, Yunfei, Zilu Huang, Shuohan Zheng, Shirong Ding, Yinghong Wei, Chen Chen, Xing Liu, and He Li. "Prognostic role of programmed cell death ligand-1 expression in head and neck cancer treated with programmed cell death protein-1/programmed cell death ligand-1 inhibitors: A meta-analysis based on clinical trials." Journal of Cancer Research and Therapeutics 17, no. 3 (2021): 676. http://dx.doi.org/10.4103/jcrt.jcrt_1606_20.

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Desforges, Ploa, Khashayar Esfahani, and Nathaniel Bouganim. "Programmed Cell Death Ligand 1–Induced Coma From Diffuse Cerebritis." Journal of Oncology Practice 14, no. 2 (February 2018): 134–35. http://dx.doi.org/10.1200/jop.2017.024992.

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Chandrasekaran, Deepika, Sandhya Sundaram, Kadhiresan N, and Padmavathi R. "Programmed Death Ligand 1; An Immunotarget for Renal Cell Carcinoma." Asian Pacific Journal of Cancer Prevention 20, no. 10 (October 1, 2019): 2951–57. http://dx.doi.org/10.31557/apjcp.2019.20.10.2951.

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Kerr, Keith M., and Fred R. Hirsch. "Programmed Death Ligand-1 Immunohistochemistry: Friend or Foe?" Archives of Pathology & Laboratory Medicine 140, no. 4 (January 12, 2016): 326–31. http://dx.doi.org/10.5858/arpa.2015-0522-sa.

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The approval of anti-programmed death receptor (PD)-1 therapies for non–small cell lung cancer has directed the spotlight on programmed death ligand-1 (PD-L1) immunohistochemistry as the latest predictive biomarker potentially required in this disease. Several other drugs in this class will likely be approved in the future and each has been developed with a unique anti–PD-L1 immunohistochemistry test. The prospect of 5 drugs competing in the same treatment area, each possibly requiring PD-L1 immunohistochemistry testing, presents a challenge for pathologists unlike any previously faced. The key issue is whether laboratories will attempt to deliver the trial-validated assays for one or more of these treatments, or introduce instead one or more laboratory developed tests, or attempt to provide a single PD-L1 immunohistochemistry assay for all possible anti–PD-1 and anti–PD-L1 treatments that may be used. This paper discusses some of the issues, challenges, hazards, and possible solutions that have recently emerged in this most complex interface between cancer therapeutics and laboratory biomarker testing.

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