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Immunophenotypic Markers
Published in Wojciech Gorczyca, Atlas of Differential Diagnosis in Neoplastic Hematopathology, 2014
CD30 (Figure 5.15) is a transmembrane glycoprotein and a member of the tumor necrosis factor superfamily. CD30 is a promising target for antibody-based therapy in HL and ALCL, as well as in CD30+ DLBCL. CD30 cluster of antibodies (e.g., Ki-1, BerH2) recognizes an activation-associated protein that is expressed in activated B and T lymphocytes (with immunoblastic cytomorphology), classical HL, ALCL (systemic and primary cutaneous), subset of DLBCLs, neoplastic cells in LYG, PEL (most cases), PMBL, large cells in EATL, LYP, pagetoid reticulosis (a variant of MF), MF with large cell transformation, and occasional cases of FL and PCM. Benign mast cells are CD30−, but CD30 expression has been reported in aggressive systemic mastocytosis and occasional mast cell leukemias.
Thorax
Published in Tiziana Rancati, Claudio Fiorino, Modelling Radiotherapy Side Effects, 2019
Daniel Schanne, Jan Unkelbach, Matthias Guckenberger
Some studies have suggested the involvement of genetic differences in the individual susceptibility to pulmonary toxicity. Pang et al. focused on single-nucleotide polymorphisms (SNP) in heatshock proteins (HSP) which are expressed by cells after the influence of various stressors and confer improved cellular survival via multiple mechanisms. After genotyping 271 NSCLC patients, they selected 2 SNPs in the heat shock protein beta-1 (HSPB1) gene for further analysis and discovered a statistically significant difference in the occurrence of grade ≥ 3 radiation pneumonitis depending on the mean lung dose applied (Pang et al. 2013). Pu et al. chose a wider approach by identifying 11930 SNPs in 201 NSCLC patients. After mathematical modeling, they selected 19 SNPs and further validated them in lymphoblastoid cell lines. Finally, three genes Protein Kinase C Epsilon (PRKCE), DExD/H-Box Helicase 58 (DDX58), and Tumor Necrosis Factor SuperFamily 7 (TNFSF7), involved in cell signaling and immune response, were identified as predictors of pneumonitis and esophagitis with an area under the receiver-operator-characteristics (ROC) curve (AUC) of 0.79 and 0.94, respectively (in combination with clinical data) (Pu et al. 2014). Xiong et al. reported on 362 patients with NSCLC and found an increased risk of radiation pneumonitis for those with a SNP in the Ataxia Teleangiectatica Mutated gene (ATM) 46(Xiong et al. 2013). In another study of 165 patients with NSCLC, SNPs in the DNA-repair genes X-Ray Repair Cross Complementing 1 (XRCC1) and Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) correlated with grade ≥2 radiation pneumonitis (Yin et al. 2011). Further genes and genetic variants that have been implicated in increased risk for radiation pneumonitis are cytokines like Tumor Necrosis Factor alpha (TNFα), (Tucker et al. 2013b) the DNA-repair gene Ligase IV (LIG4) (Yin et al. 2012) and vascular endothelial growth factor (VEGF) (Guan et al. 2010). Of note, genomic studies associating SNPs with clinical phenotypes should be interpreted with care as the functional consequences of these genetic alterations are often under-explored and a clear cause-effect model is therefore lacking (Emahazion et al. 2001). Extensive preclinical and clinical validation is therefore needed to incorporate these parameters into clinical practice (Beaudet 2010).
Blood soluble Fas concentrations and ischemic stroke patient mortality
Published in Expert Review of Molecular Diagnostics, 2022
Leonardo Lorente, María M. Martín, Antonia Pérez-Cejas, Carmen Ferrer-Moure, Luis Ramos-Gómez, Jordi Solé-Violán, Juan J. Cáceres, Alejandro Jiménez, Agustín F. González-Rivero
Apoptosis is initiated by the release of cytochrome c from mitochondria into the cytosol (intrinsic or mitochondrial pathway) or by the activation of the cell death receptor on the cell surface (extrinsic pathway) [2–4]. The activation of the extrinsic apoptosis pathway is produced when a ligand from the tumor necrosis factor superfamily of ligands (TNFSF) binds with its receptor of tumor necrosis factor membrane receptor superfamily (TNFRSF). Fas receptor is one of the major TNFRSF receptors, and the Fas ligand is its ligand. When Fas and FasL join, activation of extrinsic pathway occurs with the appearance of a death signal that will activate caspase 8. Subsequently, activated caspase-8 is responsible for activating caspase-3, which is responsible for apoptotic cellular damage [2–4].
Targeting of keloid with TRAIL and TRAIL-R2/DR5
Published in Journal of Dermatological Treatment, 2021
Pengfei Sun, Zhensheng Hu, Bo Pan, Xiaosheng Lu
Tumor Necrosis Factor Related Apoptosis Inducing Ligand (TRAIL), is a member of Tumor Necrosis Factor Superfamily (TNF-SF). The TRAIL is a type II transmembrane protein, which can be expressed in soluble form from the cell surface by protein hydrolysis. It has strong antitumor activity and has no killing effect on normal cells (37,38). AND it is expressed in many tissues, mainly in digestive tract, spleen, lung, prostate, T cell and NK cell surface. Through the analysis of gene differential expression in Oncomine database, we can know that TRAIL is highly expressed in many kinds of malignant tumors, such as Bladder Cancer, Breast Cancer, Cervical Cancer, Esophageal Cancer, Head and Neck Cancer, Kidney Cancer, Liver Cancer, Lung Cancer, Lymphoma, Melanoma, Myeloma, Pancreatic Cancer, Prostate Cancer. And it also shows that TRAIL has great value in tumor detection and targeted treatment of tumors (39) (Figure 1).
Associations between TNFSF4 gene polymorphisms (rs2205960 G > A, rs704840 T > G and rs844648 G > A) and susceptibility to autoimmune diseases in Asians: a meta-analysis
Published in Immunological Investigations, 2021
Yangyang Yang, Xiahui Li, Bowen Li, Liying Mu, Jin Wang, Yunmeng Cheng, Yao Gu, Huijian Wu
TNFSF4 locates in human 1q25 and encodes a membrane-bound protein expressed on the surface of antigen-presenting cells including dendritic cells (Ohshima et al. 1997), B cells (Lee et al. 2010) and macrophages (Murata et al. 2000), and it also expresses on CD4 + T cells, CD8 + T cells and vascular endothelial cells (Imura et al. 1996) and is firstly identified on the surface of human T-cell leukemia virus type I-infected leukemic T cells (Baum et al. 1994). TNFSF4 belongs to tumor necrosis factor superfamily and serves as a ligand of a T cell co-stimulator, TNFRSF4, to regulate T cell-mediated immunity. The TNFSF4-TNFRSF4 pair plays a role in promoting the survival of effector T cells and generation of memory CD4 + T cells. Increasing number of studies consolidate the vital role of this pair of ligand-receptor in pathogenesis of multiple autoimmune and inflammatory diseases. This highlights the significant function of TNFSF4 in inflammation and immune response.