ArticleDiscover oncology2023
The genes regulating sensitivity of tumor cells to T cell-mediated killing: could they be potential personalized immunotherapeutic targets in head and neck squamous cell carcinoma?
Article in Discover oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- T cell-mediated tumor killing sensitivity gene signature-based prognostic score for acute myeloid leukemia.Discover oncology · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo identify the pivotal genes, specifically the STTK genes, that govern the sensitivity of tumor cells to T cell-mediated killing in Head and Neck Squamous Cell Carcinoma (HNSC).
methodsThe differentially expressed genes (DEGs) in HNSC and STTK genes were overlapped to obtain the DE-STTK genes. Univariate and LASSO regression analyses were conducted to identify the pivotal DE-STTK genes that serve as hubs in HNSC (i.e., hub DE-STTK genes). The risk model was established to divide HNSC tumor samples into high- and low-risk groups based on the hub DE-STTK genes. Further investigations were carried out by examing the expression level, prognostic values, diagnostic values, enriched signaling pathways, correlation with tumor mutation burden (TMB), and association with tumor immune infiltration cells (TIICs).
resultsA total of 71 genes were found to be overlapped between DEGs in HNSC and STTK genes. Lasso regression analysis identified 9 hub genes which were MYF6, AATF, AURKA, CXCL9, DPM2, MYO1B, NCBP2, TNFRSF12A, and TRAF1. The network analysis of hub DE-STTK genes-pathway reveals that these 9 hub genes exhibit enrichment in multiple signaling pathways, including toll-like receptor signaling, TNF signaling, NF-kappa B signaling, cytokine-cytokine receptor interaction, spliceosome, mRNA surveillance pathway, nucleocytoplasmic transport, GPI-anchor biosynthesis, as well as N-Glycan biosynthesis. The Pearson correlation analysis showed that the majority of correlations between 9 hub DE-STTK genes and immune cells were positive.
conclusionThe 9 identified hub DE-STTK genes (MYF6, AATF, AURKA, CXCL9, DPM2, MYO1B, NCBP2, TNFRSF12A, and TRAF1) are presumptively implicated in the modulation of tumor immunity in HNSC. These genes, along with their enriched pathways, hold promise as potential personalized immunotherapeutic targets for the treatment of HNSC, thereby offering novel avenues for therapeutic intervention in this malignancy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.