De novo programmed cell death in oral cancer

1999 ◽  
Vol 34 (3) ◽  
pp. 241 ◽  
Author(s):  
D Ravi
Keyword(s):  
Cell Death ◽  
Oral Cancer ◽  
Programmed Cell Death ◽  
De Novo

scholarly journals The mechanism of de novo expression of programmed cell death-ligand 1 in squamous cell carcinoma of the lung

2017 ◽  
Vol 38 (4) ◽  
pp. 2189-2196 ◽  
Author(s):  
Tomoyuki Igarashi ◽  
Koji Teramoto ◽  
Mitsuaki Ishida ◽  
Jun Hanaoka ◽  
Yataro Daigo
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
De Novo

scholarly journals Novel immune checkpoint targets: moving beyond PD-1 and CTLA-4

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Shuang Qin ◽  
Linping Xu ◽  
Ming Yi ◽  
Shengnan Yu ◽  
Kongming Wu ◽  
...  
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Programmed Cell Death ◽  
T Cell Activation ◽  
Immune Checkpoint ◽  
Cell Activation ◽  
De Novo ◽  
Checkpoint Inhibitors ◽  
Immune Checkpoints ◽  
Immune Checkpoint Molecules

Abstract The emergence of immune checkpoint inhibitors (ICIs), mainly including anti-programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) and anti-cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) monoclonal antibodies (mAbs), has shaped therapeutic landscape of some type of cancers. Despite some ICIs have manifested compelling clinical effectiveness in certain tumor types, the majority of patients still showed de novo or adaptive resistance. At present, the overall efficiency of immune checkpoint therapy remains unsatisfactory. Exploring additional immune checkpoint molecules is a hot research topic. Recent studies have identified several new immune checkpoint targets, like lymphocyte activation gene-3 (LAG-3), T cell immunoglobulin and mucin-domain containing-3 (TIM-3), T cell immunoglobulin and ITIM domain (TIGIT), V-domain Ig suppressor of T cell activation (VISTA), and so on. The investigations about these molecules have generated promising results in preclinical studies and/or clinical trials. In this review, we discussed the structure and expression of these newly-characterized immune checkpoints molecules, presented the current progress and understanding of them. Moreover, we summarized the clinical data pertinent to these recent immune checkpoint molecules as well as their application prospects.

scholarly journals Fibrinogen-like protein 1 (FGL1): the next immune checkpoint target

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Wenjing Qian ◽  
Mingfang Zhao ◽  
Ruoyu Wang ◽  
Heming Li
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Checkpoint ◽  
Epithelial To Mesenchymal Transition ◽  
Immune Escape ◽  
De Novo ◽  
Lymphocyte Activation ◽  
Response Prediction ◽  
Immune Checkpoint Blockade ◽  
Mesenchymal Transition

AbstractImmune checkpoint therapy has achieved significant efficacy by blocking inhibitory pathways to release the function of T lymphocytes. In the clinic, anti-programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) monoclonal antibodies (mAbs) have progressed to first-line monotherapies in certain tumor types. However, the efficacy of anti-PD-1/PD-L1 mAbs is still limited due to toxic side effects and de novo or adaptive resistance. Moreover, other immune checkpoint target and biomarkers for therapeutic response prediction are still lacking; as a biomarker, the PD-L1 (CD274, B7-H1) expression level is not as accurate as required. Hence, it is necessary to seek more representative predictive molecules and potential target molecules for immune checkpoint therapy. Fibrinogen-like protein 1 (FGL1) is a proliferation- and metabolism-related protein secreted by the liver. Multiple studies have confirmed that FGL1 is a newly emerging checkpoint ligand of lymphocyte activation gene 3 (LAG3), emphasizing the potential of targeting FGL1/LAG3 as the next generation of immune checkpoint therapy. In this review, we summarize the substantial regulation mechanisms of FGL1 in physiological and pathological conditions, especially tumor epithelial to mesenchymal transition, immune escape and immune checkpoint blockade resistance, to provide insights for targeting FGL1 in cancer treatment.

scholarly journals New-onset insulin-dependent diabetes due to nivolumab

2018 ◽  
Vol 2018 ◽  
Author(s):  
Ali A Zaied ◽  
Halis K Akturk ◽  
Richard W Joseph ◽  
Augustine S Lee
Keyword(s):  
Diabetes Mellitus ◽  
Cell Death ◽  
Metabolic Acidosis ◽  
Programmed Cell Death ◽  
Diabetic Ketoacidosis ◽  
De Novo ◽  
Autoimmune Diabetes ◽  
List Type ◽  
Programmed Cell Death 1 ◽  
Insulin Dependent

Summary Nivolumab, a monoclonal antibody against programmed cell death-1 receptor, is increasingly used in advanced cancers. While nivolumab use enhances cancer therapy, it is associated with increased immune-related adverse events. We describe an elderly man who presented in ketoacidosis after receiving nivolumab for metastatic renal cell carcinoma. On presentation, he was hyperpneic and laboratory analyses showed hyperglycemia and anion-gapped metabolic acidosis consistent with diabetic ketoacidosis. No other precipitating factors, besides nivolumab, were identified. Pre-nivolumab blood glucose levels were normal. The patient responded to treatment with intravenous fluids, insulin and electrolyte replacement. He was diagnosed with insulin-dependent autoimmune diabetes mellitus secondary to nivolumab. Although nivolumab was stopped, he continued to require multiple insulin injection therapy till his last follow-up 7 months after presentation. Clinicians need to be alerted to the development of diabetes mellitus and diabetic ketoacidosis in patients receiving nivolumab. Learning points: Diabetic ketoacidosis should be considered in the differential of patients presenting with metabolic acidosis following treatment with antibodies to programmed cell death-1 receptor (anti-PD-1). Autoimmune islet cell damage is the presumed mechanism for how insulin requiring diabetes mellitus can develop de novo following administration of anti-PD-1. Because anti-PD-1 works by the activation of T-cells and reduction of ‘self-tolerance’, other autoimmune disorders are likely to be increasingly recognized with increased use of these agents.

scholarly journals Ceramide Synthase-dependent Ceramide Generation and Programmed Cell Death

2011 ◽  
Vol 286 (18) ◽  
pp. 15929-15942 ◽  
Author(s):  
Thomas D. Mullen ◽  
Russell W. Jenkins ◽  
Christopher J. Clarke ◽  
Jacek Bielawski ◽  
Yusuf A. Hannun ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Programmed Cell Death ◽  
De Novo ◽  
Fumonisin B1 ◽  
Membrane Permeabilization ◽  
Ceramide Synthase ◽  
Plasma Membrane Permeabilization ◽  
Ceramide Generation ◽  
Uv C

The sphingolipid ceramide has been widely implicated in the regulation of programmed cell death or apoptosis. The accumulation of ceramide has been demonstrated in a wide variety of experimental models of apoptosis and in response to a myriad of stimuli and cellular stresses. However, the detailed mechanisms of its generation and regulatory role during apoptosis are poorly understood. We sought to determine the regulation and roles of ceramide production in a model of ultraviolet light-C (UV-C)-induced programmed cell death. We found that UV-C irradiation induces the accumulation of multiple sphingolipid species including ceramide, dihydroceramide, sphingomyelin, and hexosylceramide. Late ceramide generation was also found to be regulated by Bcl-xL, Bak, and caspases. Surprisingly, inhibition of de novo synthesis using myriocin or fumonisin B1 resulted in decreased overall cellular ceramide levels basally and in response to UV-C, but only fumonisin B1 inhibited cell death, suggesting the presence of a ceramide synthase (CerS)-dependent, sphingosine-derived pool of ceramide in regulating programmed cell death. We found that this pool did not regulate the mitochondrial pathway, but it did partially regulate activation of caspase-7 and, more importantly, was necessary for late plasma membrane permeabilization. Attempting to identify the CerS responsible for this effect, we found that combined knockdown of CerS5 and CerS6 was able to decrease long-chain ceramide accumulation and plasma membrane permeabilization. These data identify a novel role for CerS and the sphingosine salvage pathway in regulating membrane permeability in the execution phase of programmed cell death.

scholarly journals Transcriptome profiling of kenaf (Hibiscus cannabinus L.) under plumbic stress conditions implies the involvement of NAC transcription factors regulating reactive oxygen species-dependent programmed cell death

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e8733
Author(s):  
Xia An ◽  
Jie Chen ◽  
Guanrong Jin
Keyword(s):  
Reactive Oxygen Species ◽  
Heavy Metal ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Reactive Oxygen ◽  
Hibiscus Cannabinus ◽  
Differentially Expressed ◽  
Oxygen Species

Heavy metal contamination of soils has become a serious global issue, and bioremediation has been proposed as a potential solution. Kenaf (Hibiscus cannabinus L.) is a fast growing, non-woody multipurpose annual plant that is suitable for removing excess heavy metals from soils. However, there has been relatively little research on the kenaf molecular mechanisms induced in response to an exposure to heavy metal stress. Thus, whole kenaf seedlings grown under control (normal) and stress (plumbic treatment) conditions were sampled for transcriptome sequencing. Unigenes generated through the de novo assembly of clean reads were functionally annotated based on seven databases. Transcription factor (TF)-coding genes were predicted and the physiological traits of the seedlings were analyzed. A total of 44.57 Gb high-quality sequencing data were obtained, which were assembled into 136,854 unigenes. These unigenes included 1,697 that were regarded as differentially expressed genes (DEGs). A GO enrichment analysis of the DEGs indicated that many of them are related to catalytic activities. Moreover, the DEGs appeared to suggest that numerous KEGG pathways are suppressed (e.g., the photosynthesis-involving pathways) or enhanced (like the flavonoid metabolism pathways) in response to Pb stress. Of the 2,066 predicted TF-coding genes, only 55 were differentially expressed between the control and stressed samples. Further analyses suggested that the plumbic stress treatment induced reactive oxygen species-dependent programmed cell death in the kenaf plants via a process that may be regulated by the differentially expressed NAC TF genes.

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