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随着程序性死亡受体1(PD-1)、程序性死亡配体1(PD-L1)以及细胞毒性T淋巴细胞抗原4(CTLA-4)等免疫检查点的发现,免疫检查点抑制剂(ICI)逐渐成为肿瘤治疗领域中最有前景的方法之一,已被证实可以提高晚期非小细胞肺癌(NSCLC)患者的生存率。与化疗相比,对于肿瘤细胞表面PD-L1高表达的晚期NSCLC患者,抗PD-1/PD-L1治疗后生存期显著延长且不良反应较少。抗CTLA-4药物单药治疗效果有限,通常与PD-1/PD-L1药物联合可进一步提高抗肿瘤效果。另外一些新型免疫检查点抑制剂,如依吉利单抗、替拉戈鲁单抗等在临床试验中也表现出一定的抗肿瘤作用,未来在晚期NSCLC患者的治疗中或许能提供帮助。对ICI在NSCLC治疗中的临床应用进行总结,同时对未来免疫治疗的发展和预测性生物标志物进行展望,可以为晚期NSCLC患者的治疗提供新的靶点和思路。 相似文献
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免疫检查点抑制剂(immune checkpointinhibitors, ICIs)是针对程序性死亡受体1(programmed cell death protein 1,PD-1)/程序性死亡受体配体1(programmed cell death protein ligand1,PD-L1)和细胞毒性T淋巴细胞相关抗原4(cytotoxic T lymphocyte associated antigen-4,CTLA-4)的单克隆抗体,主要通过阻断上述免疫检查点通路的抑制性免疫调节作用从而增强人体的抗肿瘤免疫反应。 相似文献
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肺癌已成为我国死亡率最高的恶性肿瘤,其中非小细胞肺癌占肺癌的85%~90%,且发病率呈逐年增高趋势[1]。大多数非小细胞肺癌诊断时已出现远处转移,无法手术治疗。放疗、化疗、靶向治疗和抗血管生成治疗是晚期非小细胞肺癌患者的主要治疗方法。而肿瘤免疫治疗在肺癌中的应用既往一直未有突破性的进展,其治疗策略主要集中于直接提高抗肿瘤主动免疫(如过继性细胞免疫治疗)[2]。随着对肿瘤免疫微环境研究的深入,免疫检查点(immune checkpoint)在肿瘤免疫逃逸中的作用逐渐被重视,而针对免疫检查点的抑制剂(immune checkpoint inhibitors,ICIs)开始进入临床应用,并显示出一定的治疗效果。其中,程序性死亡受体-1/配体-L1(programmed cell death 1,PD-1/Programmed cell death 1 ligand 1,PD-L1)抑制剂已经获批应用于晚期非小细胞肺癌的治疗。 相似文献
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肺癌仍然是世界范围内癌症死亡的主要原因,预后不良。非小细胞肺癌(non-small cell lung cancer,NSCLC)占肺癌总数的85%~90%,NSCLC一般分为鳞癌、腺癌、大细胞癌3种类型,其治疗方法和预后往往相似,晚期NSCLC的5年总生存率(overall survival,OS)约为13%[1]。随着免疫时代的到来,为NSCLC的治疗带来了重大突破,多项研究显示免疫联合治疗为各种类型的晚期NSCLC患者可带来显著的临床疗效[2],为晚期NSCLC患者生存率提高带来新的转机。近年来,以程序性死亡受体1(programmed death 1,PD-1)、程序性死亡配体-L1(programmed death ligand-1,PD-L1)和细胞毒性T淋巴细胞相关抗原4(cytotoxic T lymphocyte-associated antigen-4,CTLA-4)抑制剂为主的检查点抑制剂是晚期NSCLC治疗的研究热点。 相似文献
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肺癌仍然是世界范围内癌症死亡的主要原因,预后不良。非小细胞肺癌(non-small cell lung cancer,NSCLC)占肺癌总数的85%~90%,NSCLC一般分为鳞癌、腺癌、大细胞癌3种类型,其治疗方法和预后往往相似,晚期NSCLC的5年总生存率(overall survival,OS)约为13%[1]。随着免疫时代的到来,为NSCLC的治疗带来了重大突破,多项研究显示免疫联合治疗为各种类型的晚期NSCLC患者可带来显著的临床疗效[2],为晚期NSCLC患者生存率提高带来新的转机。近年来,以程序性死亡受体1(programmed death 1,PD-1)、程序性死亡配体-L1(programmed death ligand-1,PD-L1)和细胞毒性T淋巴细胞相关抗原4(cytotoxic T lymphocyte-associated antigen-4,CTLA-4)抑制剂为主的检查点抑制剂是晚期NSCLC治疗的研究热点。 相似文献
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<正>随着肿瘤免疫治疗进展,目前免疫检查点抑制剂(immune checkpoint inhibitor,ICI)的临床应用主要集中在细胞毒性T淋巴细胞相关抗原4(cytotoxic T lymphocyte associated antigen-4,CTLA-4)抑制剂、程序性死亡受体1(programmed death-1,PD-1)抑制剂及程序性死亡配体-1(programmed death ligand-1,PD-L1)抑制剂。免疫治疗有可能在多种恶性实体肿瘤中诱导持久反应,但因其作用机制,可导致不同于其他癌症疗法的免疫相关不良反应(immune-related adverse events,irAEs)。常见的irAEs包括皮肤毒性、结肠炎、肝炎、内分泌不良反应、肺炎、风湿病样免疫相关不良反应, 相似文献
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A. Rubbert-Roth T. Zander C. Kneitz C. Baerwald H. Wirtz C. Witt 《Zeitschrift für Rheumatologie》2016,75(1):47-53
Lung cancer is a frequently occurring disease, particularly in the elderly; however, within the last 10 years the pharmaceutical treatment of lung cancer has been significantly improved. Due to a better understanding of the pathophysiological events and the identification of molecular subgroups of lung tumors, new therapeutic drugs have been developed that significantly prolong survival of patients with the respective molecular pattern. In particular immunotherapeutic agents, such as programmed death-ligand 1 (PD-L1) and programmed death 1 (PD1) antibodies have shown promising clinical results in a subgroup of lung cancer patients. Due to the high incidence of both lung cancer and rheumatic diseases they often occur together, which necessitates an interdisciplinary management. The success of improved therapy of lung cancer has led to a greater focus on the treatment of comorbidities; however, interventions into the immune system by immune checkpoint inhibitors can lead to new challenges when an autoimmune disease is simultaneously present. The possibility of an effective screening for lung cancer in the future also presents the prospect of an improvement in mortality, which raises the question of the optimal monitoring of patients with rheumatoid arthritis (RA) under immunosuppressive therapy. The aim of this review is to discuss the interaction between lung cancer and RA with respect to the currently available data. 相似文献
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Rationale:The emergence of immune checkpoint inhibitors has brought new breakthroughs in the treatment of small cell lung cancer (SCLC). Programmed cell death-ligand 1 inhibitors combined with chemotherapy have been approved for the first-line treatment of extensive-stage small cell lung cancer (ES-SCLC). However, programmed death 1 inhibitors have limited efficacy in the treatment of SCLC. The reason may be related to the abnormal vascular state in the tumor microenvironment.Patient concerns:A 55-year-old male patient, presenting cough and sputum for 1 month.Diagnoses:The patient was clinically diagnosed with SCLC and staged as ES-SCLC.Interventions:Etoposide combined with lobaplatin treatment every 3 weeks for 4 cycles, evaluate as progressive disease. On the basis of the original plan, combined with camrelizumab for 2 cycles, evaluation as progressive disease. Then, the patient was treated with intravenous infusion of camrelizumab plus oral anlotinib. After 4 cycles, evaluation as partial response. Then we continued to use camrelizumab combined with anlotinib treatment for the patient. At the end of 26 cycles, the chest computed tomography examination revealed that the patient had achieved complete remission.Outcomes:After treated with carrelizumab combined with anlotinib for 26 cycles, the curative effect was evaluated as complete remission, progression-free survival was 24 months and there was no immune-related adverse reaction during treatment period. Besides, the patient developed complicated hand–foot syndrome, but this symptom was significantly relieved after reducing the dosage of anlotinib.Lessons:In this case, antiangiogenesis combined with programmed death 1 inhibitors significantly inhibited tumor progression. It also indicated that anlotinib concurrent carrelizumab may be a superior choice for ES-SCLC. Further clinical trials required to confifirm its effificacy and safety. 相似文献
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Background:Programmed cell death-1/programmed cell death 1 ligand 1 (PD-1/PD-L1) inhibitors are a group of immune checkpoint inhibitors immunotherapy for cancer treatment. These immune checkpoint inhibitors are becoming first-line treatments for several types of cancer. Radiotherapy for cancer is a traditional treatment and the therapeutic effect is not satisfactory due to the side effect of chemotherapeutic drugs. This study aims to evaluate the efficacy and safety of PD1/PD-L1 inhibitor immunotherapy combined chemotherapy for inoperable advanced lung cancer.Methods:We will utilize PubMed, PubMed Central, EMbase, Medline, CNKI, WAN FANG Database, and Web of Science to screen eligible studies published from January 1, 2015 to December 30, 2020. Two reviewers will extract data and evaluate the risk of bias independently. The quality of the included studies will be evaluated using the RevMan 5.3 software for data analysis.Results:This review will summarize high-quality evidence of trials to evaluate the precise medicine efficacy and safety of PD1/PD-L1 inhibitor combined radiotherapy for inoperable advanced lung cancer.Conclusions:The findings of the systematic review will provide scientific evidence of the efficacy and safety of PD1/PD-L1 inhibitor combined radiotherapy for inoperable advanced lung cancer to guide the clinician''s drug use.Ethics and dissemination:Not applicable.INPLASY registration number:INPLASY202140123. 相似文献
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Immunotherapy by means of checkpoint inhibition has been proven to be effective in non-small cell lung cancer (NSCLC). Inhibitors of the programmed cell death 1 (PD-1) receptor or its ligand PD-L1 in particular are more effective than conventional chemotherapy in many therapeutic settings. The role of cytotoxic T?lymphocyte-associated antigen 4 (CTLA-4) inhibitors as well as combination therapies are currently the subject of clinical investigations. Improved survival, better tolerability and long-lasting remission are the advantages but the excess costs and the lack of a valid biomarker are the drawbacks of this new therapeutic option. 相似文献
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In contrast to other tumor types, immunotherapy has not yet become a relevant part of the treatment landscape of unselected colorectal cancer. Beside the small subgroup of deficient mismatch repair or microsatellite instable tumors (about 5%) as a surrogate for high mutational burden and subsequently high neoantigen load and immunogenicity, inhibitors of programmed death 1 (PD-1), programmed death ligand 1 (PD-L1) and/or cytotoxic T lymphocyte-associated antigen-4 were not or only modestly effective in metastatic colorectal cancer. Thus, a variety of combination approaches with chemotherapy, targeted therapy, toll-like receptor agonists, local ablation or oncolytic viruses is currently being evaluated in different disease settings. Despite several encouraging single arm data already presented or published, available randomized data are unimpressive. Adding PD-1/PD-L1 inhibitors to fluoropyrimidines and bevacizumab maintenance showed no beneficial impact on delaying progression. In refractory disease, the combination of PD-1/PD-L1 and MEK inhibitor was not different from regorafenib, whereas a PD-1/PD-L1 and cytotoxic T lymphocyteassociated antigen-4 inhibitor combination demonstrated better overall survival compared to supportive care alone. Clinical trials in all disease settings applying different combination approaches are ongoing and may define the role of immunotherapy in colorectal cancer. 相似文献
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Motono Nozomu Mizoguchi Takaki Ishikawa Masahito Iwai Shun Iijima Yoshihito Uramoto Hidetaka 《Lung》2023,201(1):95-101
Lung - Although targeting programmed death-1 (PD-1) and its ligand, programmed death-ligand 1 (PD-L1), is an established treatment modality for non-small cell lung cancer (NSCLC), the prognostic... 相似文献
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近年来程序性死亡受体1/程序性死亡配体1(PD-1/PD-L1)免疫检测点阻滞剂在实体瘤治疗上取得振奋人心的效果。PD-1主要表达于活化的T、B细胞,在限制自身免疫及过度炎症反应方面起重要作用;肿瘤微环境中PD-1/PD-L1的高表达使T细胞活性受到过度抑制,从而发生肿瘤免疫逃逸;PD-L1表达水平可能是预测检测点阻滞剂疗效的标志物。免疫治疗因其持久的反应性及较小毒副作用使部分肿瘤患者获益明显。本文旨在阐述主要的PD-1/PD-L1检测点阻滞剂(单抗)近年来在恶性黑色素瘤、肺癌、尿路上皮癌、肾细胞癌等治疗上研究的现状并在获益人群中筛选出可能具有价值的生物学标志物。 相似文献
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Emily M Lin Jun Gong Samuel J Klempner Joseph Chao 《World journal of gastroenterology : WJG》2018,24(25):2686-2697
Blockade of the programmed death ligand 1(PD-L1) and programmed cell death 1(PD-1) receptor axis represents an effective form of cancer immunotherapy. Preclinical evidence initially suggested that gastric and gastroesophageal junction(GEJ) cancers are potentially immunotherapy-sensitive tumors. Early phase clinical trials have demonstrated promising antitumor activity with PD-1/PD-L1 blockade in advanced or metastatic gastric/GEJ cancer. Microsatellite instability(MSI) and PD-L1 expression have been shown to predict higher response to PD-1 inhibitors as highlighted by the recent approvals of pembrolizumab in treatmentrefractory solid tumors with MSI status and the thirdline or greater treatment of PD-L1 positive advanced gastric/GEJ cancers. However, predictive and prognostic biomarkers remain an ongoing need. In this review, we detail the preclinical evidence and early tissue biomarker analyses illustrating potential predictive biomarkers to PD-1/PD-L1 blockade in gastric/GEJ cancer. We also review the clinical development of PD-1/PD-L1 inhibitors in gastric/GEJ cancer and highlight several areas in need of future investigation in order to optimize the efficacy of PD-1/PD-L1 blockade in gastric/GEJ cancer. 相似文献
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《Seminars in arthritis and rheumatism》2019,48(6):907-910
ObjectiveImmune checkpoint inhibitors are effective cancer therapies that have been associated with immune-related adverse events (irAEs). Recent reports of irAEs describe symptoms resembling classic rheumatologic syndromes, most notably associated with cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) inhibitor blockade. Though cases have been described, there are fewer reports of rheumatologic disease associated with programmed cell death protein-1 (PD-1) inhibitors. Here, we describe a series of four patients presenting to the Brigham and Women’s Hospital (BWH) Arthritis Center with de novo polymyalgia rheumatica (PMR)-type conditions and/or peripheral synovitis after treatment with PD-1/PD-Ligand 1 (PD-L1) pathway inhibitors.MethodsPatients with metastatic renal cell carcinoma (RCC) who were treated with PD-1/PD-L1 pathway inhibitors and subsequently developed complaints of new joint pain were referred to the BWH Arthritis Center as part of routine care and identified retrospectively. The electronic medical record was reviewed for cancer history and treatment, rheumatologic symptoms, physical exam, laboratory testing, and clinical course.ResultsAll four patients developed irAEs consistent with a PMR-type syndrome and/or peripheral synovitis. Symptoms persisted despite discontinuation of the PD-1/PD-L1 pathway inhibitors; however, three of the patients responded well to oral glucocorticoids alone while one patient required the addition of oral methotrexate. All patients had an eventual decline in inflammatory markers.ConclusionThese cases highlight the need for both oncologists and rheumatologists to recognize the development of rheumatologic disease during treatment with immune checkpoint blockade. Further investigation is needed to optimize the management of irAEs, particularly considering the increasing use of checkpoint inhibitors to treat malignancies. 相似文献
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BACKGROUND & AIMS: Many reports indicate that nonsteroidal anti-inflammatory drugs (NSAIDs) have antineoplastic effects, but the precise molecular mechanism(s) responsible are unclear. We evaluated the effect of cyclooxygenase (COX) inhibitors (NSAIDs) on human colon carcinoma cells (HCA-7) and identified several genes that are regulated after treatment with NS-398, a selective COX-2 inhibitor. METHODS: Differential display polymerase chain reaction cloning techniques were used to identify genes regulated by treatment with NSAIDs and selective COX-2 inhibitors. RESULTS: A prostate apoptosis response 4 (Par-4) gene was up-regulated after NSAID treatment. Par-4 was first isolated from prostate carcinoma cells undergoing apoptosis, and expression of Par-4 sensitized cancer cells to apoptotic stimuli. Par-4 levels were increased in cells treated with COX inhibitors such as NS-398, nimesulide, SC-58125, and sulindac sulfide. Treatment of HCA-7 cells with these agents also induced apoptotic cell death. CONCLUSIONS: The results suggest that regulation of Par-4 contributes to the proapoptotic effects of high-dose COX inhibitors (NSAIDs) by serving as a downstream mediator leading to initiation of programmed cell death. 相似文献