An immunoinformatics assessment of the cancer testis antigen, DDX53, as a potential early esophageal cancer antigen
Abstract | PDF | Full Text | Supplementary Materials | Supplementary Table 1 | Supplementary Table 2 | Supplementary Table 3 | Supplementary Table 4 | Supplementary Table 5 | Supplementary Table 6 | Supplementary Table 7 | Supplementary Table 8 | How to Cite | Press Release
https://doi.org/10.18632/oncoscience.590
Peter Cheng1, Konrad J. Cios1, Mallika Varkhedi1, Vayda R. Barker1, Michelle Yeagley1, Andrea Chobrutskiy2, Boris I. Chobrutskiy3 and George Blanck1,4
1 Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, Florida (FL) 33612, USA
2 Department of Pediatrics, Oregon Health and Science University Hospital, Portland, Oregon (OR) 97239, USA
3 Department of Internal Medicine, Oregon Health and Science University Hospital, Portland, Oregon (OR) 97239, USA
4 Department of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida (FL) 33612, USA
Correspondence to:
George Blanck, email: [email protected]
Keywords: adaptive immune receptor recombinations; complementarity determining region-3; esophageal cancer survival rates; cancer testis antigens
Received: May 20, 2023 Accepted: October 16, 2023 Published: November 10, 2023
ABSTRACT
T-lymphocytes have been implicated in facilitating a pro-inflammatory, pro‑tumorigenic microenvironment that worsens prognosis for esophageal carcinoma (ESCA). In this study, we identified tumor resident, T-cell receptor (TCR) complementarity determining region-3 (CDR3) amino acid sequences and employed an algorithm particularly suited to the big data setting to evaluate TCR CDR3-cancer testis antigen (CTA) chemical complementarities. Chemical complementarity of the ESCA TCR CDR3s and the cancer testis antigen DDX53 represented a disease-free survival (DFS) distinction, whereby the upper fiftieth percentile complementarity group correlated with worse DFS. The high TCR CDR3-DDX53 complementarity group also represented a greater proportion of tumor samples lacking DDX53 expression. These data and analyses raise the question of whether the TCR CDR3-DDX53 chemical complementarity assessment detected an ESCA immune response that selected for DDX53-negative cells?
PII: 590