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Non-Hodgkin Lymphoma
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Piers Blombery, David C. Linch
Classified as a separate disease entity in the current WHO classification, primary mediastinal (thymic) large B-cell lymphoma (PMBCL) usually presents in younger females with a large mediastinal mass.1 Pathologically, PMBCL is composed of large lymphocytes that express CD20, CD23 (a marker of thymic B-cells), and CD30 (weakly). The tumor often shows compartmentalizing sclerosis redolent of HL and indeed GEP data have shown PMBCL to be more similar to HL than to DLBCL.47 Other recurrent genetic abnormalities in this entity include amplifications of 9p (involving JAK2 as well as CD274 [PD-L1] and PDCD1LG2 [PD-L2]) and oncogenic mutations involving the JAK/STAT and NF-kB pathways. 48
Gastric Cancer
Published in Dongyou Liu, Tumors and Cancers, 2017
Occurring mainly in the gastric fundus or corpus and accounting for 10% of gastric cancer, EBV-associated tumors (or EBV-associated gastric cancer) demonstrate frequent DNA hypermethylation involving both promoter (e.g., cyclin-dependent kinase inhibitor 2A [CDKN2A] promoter) and nonpromoter CpG islands; somatic gene alterations in phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), AT-rich interactive domain 1A (ARID1A), and BCL6 corepressor (BCOR), TP53, janus kinase 2 (JAK2), CD274, and programmed cell death 1 ligand 2 (PDCD1LG2) [1,4,5].
Hodgkin Lymphoma
Published in Tariq I. Mughal, Precision Haematological Cancer Medicine, 2018
Studies have also defined the role of the programmed (cell) death protein 1 (PD-1) ligands, CD274(PD-L1) and PDCD1LG2(PD-L2), in the molecular pathogenesis of cHL and its impact on clinical outcome (Figure 10.6). Several alterations in the chromosome 9p24.1 amplicon, which not only contains the PD-L1 and PD-L2, but also the JAK2 gene, which affects the JAK-STAT pathway in a copy-number-dependent manner, have been observed. The amplification of 9p24.1 and the PD-1/PD-L2 alterations are now considered not only as a cardinal feature of cHL, but also predict for poor prognosis and shorter progression-free survival following conventional treatment. Furthermore, the almost uniform alterations of the PD-1 ligands are predictive for response to PD-1 blockade and outcome following treatment with immune checkpoint inhibitors. Interestingly, EBV infection can also result in an increased expression of PD-1 ligands in EBV-positive HL, but the impact of this requires additional study. A topical challenge is the methodology available for detection of the PD-1 ligands, PD-L1 and PD-L2. The very low purity of HRS cells and the unique composition of the surrounding inflammatory/immune infiltrate, tends to result in the most available molecular methodologies, including quantitative PCR and assay-based NGS platforms, to underestimate the frequency of the molecular aberrations and copy number alterations (CNA). Efforts are now assessing the clinical utility of both blood- and tissue-based NGS assays focused on tumour mutational burden (TMB) as a tool for predicting responses to immune-checkpoint therapy.
Integrated analyses of m1A regulator-mediated modification patterns in tumor microenvironment-infiltrating immune cells in colon cancer
Published in OncoImmunology, 2021
Yuzhen Gao, Hao Wang, Huiming Li, Xinxin Ye, Yan Xia, Shijin Yuan, Jie Lu, Xinyou Xie, Liangjing Wang, Jun Zhang
Similarly, in terms of immunotherapy, we found that the m1AScore could predict the OS for patients who had undergone anti-PD-L1 treatment (IMvigor210, Figure 7d, log-rank test, p = .041). Also, significant differences of m1AScore among patients with different main responses were observed and shown in Figure 7eand 7f (all p < .05). Patients with low m1AScore also had a higher neoantigen burden (Figure 7g, p< .001). Pan-cancer analysis showed that the m1AScore was negatively related to PD-L1 expression in most cancer patients, such as the TCGA-COAD and TCGA-READ cohorts (Figure 7h, all r > 0.3, P < .001), indicating that patients with low m1AScore may have had a potential response to anti-PD-L1 immunotherapy similar to that of the IMvigor210 cohort. However, we could not find any significant relationship between m1AScore and the responses of patients who had undergone anti-PD1 treatment (GSE78220, Figure 7iand 7j, P = .322). The correlations of m1AScore with CTLA4, PDCD1 (PD1), CD274 (PD-L1) and PDCD1LG2 (PD-L2) and their detail results in all pan-cancers were also listed in Supplemental Figure S9 and TableS12. In summary, our work indicated that the construction of m1A gene signatures could help in predicting the response to chemotherapy and anti-PDL1 immunotherapy.
Dissecting the heterogeneity of the microenvironment in primary and recurrent nasopharyngeal carcinomas using single-cell RNA sequencing
Published in OncoImmunology, 2022
Wen-Sa Peng, Xin Zhou, Wen-Bin Yan, Yu-Jiao Li, Cheng-Run Du, Xiao-Shen Wang, Chun-Ying Shen, Qi-Feng Wang, Hong-Mei Ying, Xue-Guan Lu, Ting-Ting Xu, Chao-Su Hu
As Tregs are chemoattracted by chemokine gradients, increased chemokine interactions could explain the enrichment of Tregs in the rNPC samples. In the recurrent group, CCL22/CCR4, expressed by cDC2 and mature DCs, and CCL17/CCR4, expressed by mature DCs, could recruit Tregs into tumor tissue, consistently with the increased chemotactic ability of rNPC-derived DCs. CD8+ T cells and NK cells in rNPC highly expressed CCL5 and CCL4, which showed ligand–receptor binding to CCR5 and CCR4 on Tregs, respectively, suggesting a potential interaction and chemotaxis between Tregs and CTLs/NK cells. For costimulatory modules, CD8+ T cells and mature DCs in rNPC were uniquely predicted to interact with Tregs via TNFSF4–TNFRSF4. A subset of TNFRSF4+ Tregs was reported based on NPC scRNA-seq data to have high activation and immunosuppressive potential, explaining Treg activation in rNPC.9 Inhibitory signals from Tregs to immune cells were commonly identified in both pNPC and rNPC, while suppressive signals from immune cells to Tregs were different. In pNPC, PDCD1LG2/FAM3C/CD274–PDCD1 interactions were commonly identified. In the absence of PDCD1 expression on Tregs, rNPC showed increased suppressive signals from DCs and macrophages to Tregs via LGALS9–HAVCR2. As TIM-3 (encoded by HAVCR2)-positive Tregs have been shown to express higher levels of IL-10 compared with those in TIM-3-negative Tregs and a higher capacity for inhibiting IFN-γ and TNF-α secretion by effector T cells, a recent study in HNSCC showed that treatment with anti-TIM-3 concurrently with anti-PD-L1 and radiotherapy led to a significant tumor growth delay, enhanced T cell cytotoxicity, decreased numbers of Tregs, and improved survival.45 Taken together, the different Treg communications identified in rNPC can be potential targets for immunotherapy.
Expression of genes and pathways associated with the B7-CD28 superfamily in response to irradiation of blood cells using 137Cs
Published in International Journal of Radiation Biology, 2021
Daner A. Silveira, Fernanda M. Ribeiro, Éder M. Simão, Viviane L. D. Mattos, Evamberto G. Góes
In summary, we detected activation of the immune system in the response of IR through the activation of the innate immune system, co-stimulation by the CD28 family, and CD28 co-stimulation pathways for the 300 cGy dose. Also, such a dose induces the overexpression of CD80, an important inducer of immune activation. This is corroborated by the downregulation of PDCD1LG2, which inhibits the induction of immune cells. Thus, the results obtained in this study indicate that 300 cGy is likely more efficient in activating the immune system.