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. 2021 Oct 5;9(10):e003371. doi: 10.1136/jitc-2021-003371

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© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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High homologous recombination deficiency in non-immune-inflamed TNBCs with HLA-I LOH. (A) Enrichment map shows pathways enriched in non-immune-inflamed TNBCs with HLA-I LOH when compared with non-immune-inflamed TNBCs with HLA-I non-LOH. Nodes in the network represent pathways, and similar pathways with many common genes are connected. Groups of similar pathways are indicated. The size and color of each node represent the p-value and NES value of each pathway, respectively. All pathways included were statistically significant (p-value <0.05 and q-value <0.25). (B) Cleveland plot shows the top 15 statistically significant pathways (p-value <0.05 and q-value <0.25) with the highest NES value. All pathways included are statistically significant. (C) Comparison of homologous recombination deficiency scores between the HLA-I LOH and non-LOH groups in non-immune-inflamed tumors. (D) Potential clinical translations of HLA-I LOH status. ***, p<0.001. HLA, human leukocyte antigen; LOH, loss of heterozygosity; NES, normalized enrichment score; TNBCs, triple-negative breast cancers.