ArticleOncoimmunology2022
Intratumoral T-cell repertoires in DNA mismatch repair-proficient and -deficient colon tumors containing high or low numbers of tumor-infiltrating lymphocytes.
Article in Oncoimmunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Degrees of H2AX phosphorylation correlate with unique features of the intratumoral immune microenvironment in colorectal carcinomas.The oncologist · 2026Article
- A laminin α4-CD8Oncoimmunology · 2025Article
- Tumor aggression-defense index-a novel indicator to predicts recurrence and survival in stage II-III colorectal cancer.Journal of translational medicine · 2025Article
- Article
- Mismatch repair-proficient tumor footprints in the sands of immune desert: mechanistic constraints and precision platforms.Frontiers in immunology · 2024Review
- Developments in Checkpoint Inhibitor Therapy for the Management of Deficient Mismatch Repair (dMMR) Rectal Cancer.Current oncology (Toronto, Ont.) · 2023Review
- Neoantigens: promising targets for cancer therapy.Signal transduction and targeted therapy · 2023Review
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Authors and funding
11 authors.
Funding
Abstract
Colon tumors with deficient DNA mismatch repair (dMMR) are generally infiltrated by T cells more densely than tumors with proficient mismatch repair (pMMR). However, high numbers of tumor-infiltrating lymphocytes (TILs) are found in select pMMR tumors, and low numbers of TILs are seen in select dMMR tumors. In this study, we compared T-cell repertoires in 20 pMMR and 27 dMMR colon tumors with high and low TIL counts. We found that T cells in dMMR tumors are more clonal and their repertoire is less rich compared with T cells in pMMR tumors. In the dMMR group, T cells in TIL-high tumors were more clonal and their repertoire was less rich compared with T cells in TIL-low tumors, but in the pMMR group, T-cell diversity in TIL-high tumors was comparable to T-cell diversity in TIL-low tumors. These findings suggest that T cells clonally expand in dMMR tumors, possibly in response to MMR deficiency-induced tumor neoantigens.
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