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• W4362546700 abstract "<div>Abstract<p>Impaired DNA repair drives mutagenicity, which increases neoantigen load and immunogenicity. We investigated the expression of proteins involved in the DNA damage response (ATM, Chk2), double-strand break repair (BRCA1, BLM, WRN, RECQL4, RECQL5, TOPO2A, DNA-PKcs, Ku70/Ku80), nucleotide excision repair (ERCC1), base excision repair (XRCC1, pol β, FEN1, PARP1), and immune responses (CD8, PD-1, PD-L1, FOXP3) in 1,269 breast cancers and validated our findings in an independent estrogen receptor–negative (ER⁻) cohort (<i>n</i> = 279). Patients with tumors that expressed low XRCC1, low ATM, and low BRCA1 were not only associated with high numbers of CD8⁺ tumor-infiltrating lymphocytes, but were also linked to higher grades, high proliferation indexes, presence of dedifferentiated cells, ER⁻ cells, and poor survival (all <i>P</i> ≤ 0.01). PD-1⁺ or PD-L1⁺ breast cancers with low XRCC1 were also linked to an aggressive phenotype that was high grade, had high proliferation indexes, contained dedifferentiated cells and ER⁻ (all with <i>P</i> values ≤ 0.01), and poor survival (<i>P</i> = 0.00021 and <i>P</i> = 0.00022, for PD-1⁺ and PD-L1⁺ cancers, respectively) including in an independent ER⁻ validation cohort (<i>P</i> = 0.007 and <i>P</i> = 0.047, respectively). We conclude that the interplay between DNA repair, CD8, PD-L1, and PD-1 can promote aggressive tumor phenotypes. XRCC1-directed personalization of immune checkpoint inhibitor therapy may be feasible and warrants further investigation in breast cancer. <i>Cancer Immunol Res; 5(4); 292–9. ©2017 AACR</i>.</p></div>" @default.
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• W4362546700 date "2023-04-03" @default.
• W4362546700 modified "2023-09-24" @default.
• W4362546700 title "Data from Clinical Impact of Tumor DNA Repair Expression and T-cell Infiltration in Breast Cancers" @default.
• W4362546700 doi "https://doi.org/10.1158/2326-6066.c.6548779.v1" @default.
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