Cell Stress最新文献_第8页

Inflammation induced PD-L1-specific T cells 炎症诱导的PD-L1特异性T细胞

IF 6.4

Cell Stress Pub Date : 2019-09-13 DOI: 10.15698/cst2019.10.201

Shamaila Munir, M. Lundsager, M. Jørgensen, M. Hansen, Trine H Petersen, C. Bonefeld, C. Friese, Ö. Met, P. Straten, M. Andersen

引用次数: 13

Gold Nanoparticles sensitize pancreatic cancer cells to gemcitabine. 金纳米粒子使癌症胰腺细胞对吉西他滨敏感。

IF 6.4

Cell Stress Pub Date : 2019-07-31 DOI: 10.15698/cst2019.08.195

Yanyan Huai, Yushan Zhang, Xunhao Xiong, Shamik Das, Resham Bhattacharya, Priyabrata Mukherjee

{"title":"Gold Nanoparticles sensitize pancreatic cancer cells to gemcitabine.","authors":"Yanyan Huai, Yushan Zhang, Xunhao Xiong, Shamik Das, Resham Bhattacharya, Priyabrata Mukherjee","doi":"10.15698/cst2019.08.195","DOIUrl":"10.15698/cst2019.08.195","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest solid cancers with dismal prognosis. Several mechanisms that are mainly responsible for aggressiveness and therapy resistance of PDAC cells include epithelial to mesenchymal transition (EMT), stemness and Mitogen Activated Protein Kinase (MAPK) signaling. Strategies that inhibit these mechanisms are critically important to improve therapeutic outcome in PDAC. In the current study, we wanted to investigate whether gold nanoparticles (AuNPs) could sensitize pancreatic cancer cells to the chemotherapeutic agent gemcitabine. We demonstrated that treatment with AuNPs of 20 nm diameter inhibited migration and colony forming ability of pancreatic cancer cells. Pre-treatment with AuNPs sensitized pancreatic cancer cells to gemcitabine in both viability and colony forming assays. Mechanistically, pre-treatment of pancreatic cancer cells with AuNPs decreased gemcitabine induced EMT, stemness and MAPK activation. Taken together, these findings suggest that AuNPs could be considered as a potential agent to sensitize pancreatic cancer cells to gemcitabine.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"3 8","pages":"267-279"},"PeriodicalIF":6.4,"publicationDate":"2019-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6702449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41180164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immunosurveillance of cancer cell stress. 癌症细胞应激的免疫监测

IF 4.1

Cell Stress Pub Date : 2019-07-03 DOI: 10.15698/cst2019.09.198

Seila Lorenzo-Herrero, Christian Sordo-Bahamonde, Segundo González, Alejandro López-Soto

引用次数: 0

Impact of prophylactic TNF blockade in the dual PD-1 and CTLA-4 immunotherapy efficacy and toxicity 预防性TNF阻断对PD-1和CTLA-4双重免疫疗法疗效和毒性的影响

IF 6.4

Cell Stress Pub Date : 2019-06-26 DOI: 10.15698/cst2019.07.193

Maite Álvarez, I. Otano, Luna Minute, M. Ochoa, E. Pérez-Ruiz, I. Melero, P. Berraondo

{"title":"Impact of prophylactic TNF blockade in the dual PD-1 and CTLA-4 immunotherapy efficacy and toxicity","authors":"Maite Álvarez, I. Otano, Luna Minute, M. Ochoa, E. Pérez-Ruiz, I. Melero, P. Berraondo","doi":"10.15698/cst2019.07.193","DOIUrl":"https://doi.org/10.15698/cst2019.07.193","url":null,"abstract":"The TNF blockade therapy is currently a well-established treatment option for a variety of autoimmune diseases such as rheumatoid arthritis (RA), psoriasis or Crohn's disease, given the proinflammatory role of TNF in the course of these diseases. Importantly, TNF neutralization is also used for the treatment of corticosteroid-refractory immune-related adverse events (irAEs) induced by the combined anti-PD-1 and anti-CTLA-4 immunotherapy. The manifestation of these toxicities is an important limiting factor for the successful implementation of the inhibitory checkpoint blockade therapy (ICB), restraining its anti-tumor efficacy. In our recent study (Perez-Ruiz et al., Nature 569(7756): 428-432.), we analyzed the potential impact of prophylactic TNF neutralization therapy in the anti-PD1/CTLA-4 efficacy. Through several mouse models, we demonstrated that TNF neutralization ameliorated ICB-exacerbated colitis in addition to improving ICB-dependent anti-tumor efficacy. Similar results were obtained after prophylactic TNF blockade in graft vs host xenografted mouse models with human immune cells, which showed a reduction in colitis and hepatitis. Importantly, there was a preservation of the immunotherapeutic control of xenografted tumors after ICB treatment. Moreover, TNF and TNF-dependent gene expression is upregulated in the colon mucosa from patients affected by colitis as a side effect of ipilimumab and nivolumab. Our results, thus, provide evidence of the successful combination of prophylactic TNF neutralization with ICB therapy strategy to ameliorate toxicities, while keeping or even ameliorating anti-tumor efficacy. The prophylactic TNF blockade strategy is clinically feasible since excellent TNF inhibitors have been approved for the treatment of autoimmunity and are used for the immune-related serious adverse events in immunotherapy.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"3 1","pages":"236 - 239"},"PeriodicalIF":6.4,"publicationDate":"2019-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46976440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 16

Immunometabolic cross-talk in the inflamed heart. 炎症心脏的免疫代谢串扰

IF 4.1

Cell Stress Pub Date : 2019-06-07 DOI: 10.15698/cst2019.08.194

Federica M Marelli-Berg, Dunja Aksentijevic

{"title":"Immunometabolic cross-talk in the inflamed heart.","authors":"Federica M Marelli-Berg, Dunja Aksentijevic","doi":"10.15698/cst2019.08.194","DOIUrl":"10.15698/cst2019.08.194","url":null,"abstract":"Inflammatory processes underlie many diseases associated with injury of the heart muscle, including conditions without an obvious inflammatory pathogenic component such as hypertensive and diabetic cardiomyopathy. Persistence of cardiac inflammation can cause irreversible structural and functional deficits. Some are induced by direct damage of the heart muscle by cellular and soluble mediators but also by metabolic adaptations sustained by the inflammatory microenvironment. It is well established that both cardiomyocytes and immune cells undergo metabolic reprogramming in the site of inflammation, which allow them to deal with decreased availability of nutrients and oxygen. However, like in cancer, competition for nutrients and increased production of signalling metabolites such as lactate initiate a metabolic cross-talk between immune cells and cardiomyocytes which, we propose, might tip the balance between resolution of the inflammation versus adverse cardiac remodeling. Here we review our current understanding of the metabolic reprogramming of both heart tissue and immune cells during inflammation, and we discuss potential key mechanisms by which these metabolic responses intersect and influence each other and ultimately define the prognosis of the inflammatory process in the heart.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"3 1","pages":"240-266"},"PeriodicalIF":4.1,"publicationDate":"2019-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6702448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42407725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Stress and catecholamines modulate the bone marrow microenvironment to promote tumorigenesis 应激和儿茶酚胺调节骨髓微环境促进肿瘤发生

IF 6.4

Cell Stress Pub Date : 2019-06-04 DOI: 10.15698/cst2019.07.192

Pauline Hanns, Anna M. Paczulla, M. Medinger, M. Konantz, C. Lengerke

引用次数: 22

Remodeling of mitochondrial morphology and function: an emerging hallmark of cellular reprogramming. 线粒体形态和功能的重塑:细胞重编程的一个新兴标志。

IF 6.4

Cell Stress Pub Date : 2019-05-27 DOI: 10.15698/cst2019.06.189

Anuj Rastogi, Piyush Joshi, Ela Contreras, Vivian Gama

引用次数: 20

Biology and clinical relevance of EpCAM. EpCAM的生物学和临床意义。

IF 6.4

Cell Stress Pub Date : 2019-05-21 DOI: 10.15698/cst2019.06.188

Laura Keller, Stefan Werner, Klaus Pantel

引用次数: 115

Recent progress in the role of autophagy in neurological diseases. 神经系统疾病中自噬作用的最新进展。

IF 6.4

Cell Stress Pub Date : 2019-04-29 DOI: 10.15698/cst2019.05.186

Tian Meng, Shiyin Lin, Haixia Zhuang, Haofeng Huang, Zhengjie He, Yongquan Hu, Qing Gong, Du Feng

引用次数: 36

Tissue-resident memory T cells orchestrate tumour-immune equilibrium. 组织驻留记忆T细胞协调肿瘤免疫平衡。

IF 6.4

Cell Stress Pub Date : 2019-04-26 DOI: 10.15698/cst2019.05.187

Simone L Park, Laura K Mackay, Jason Waithman, Thomas Gebhardt

{"title":"Tissue-resident memory T cells orchestrate tumour-immune equilibrium.","authors":"Simone L Park, Laura K Mackay, Jason Waithman, Thomas Gebhardt","doi":"10.15698/cst2019.05.187","DOIUrl":"https://doi.org/10.15698/cst2019.05.187","url":null,"abstract":"The immune system can prevent tumour development by engaging in a process termed cancer immunosurveillance, during which immune cells such as T cells restrict tumour growth either by completely eradicating cancer cells in a process of 'elimination' or by suppressing cancer cell outgrowth by establishing a state of tumour-immune 'equilibrium'. Most cancers develop within epithelial layers of tissues but circulating T cells are largely excluded from these epithelial tissue compartments in the absence of infection or overt inflammation. In contrast, CD8+ tissue-resident memory T (TRM) cells reside permanently within epithelial layers of peripheral tissues without recirculating in blood. Accumulating evidence suggests that TRM cells are found in diverse human solid cancers where they correlate with improved prognosis and can protect against tumour challenge in mice. However, the mechanisms through which these cells mediate cancer protection are poorly understood. In our recent study (Park SL et al, Nature 565(7739), 2019) we developed a melanoma model that allowed us to identify a critical role for TRM cells in the establishment and maintenance of tumour-immune equilibrium in skin. Our findings provide insight into the immune cell populations important for maintaining long-term tumour dormancy in peripheral tissues and imply that targeting TRM cells may serve as a novel cancer treatment strategy.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"3 5","pages":"162-164"},"PeriodicalIF":6.4,"publicationDate":"2019-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6551858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37352652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6