Evidence map›Paper›PMID 41975515›Full record

ArticleGenome biology2026

Proteogenomic decoding of chemotherapy resistance in patients with triple-negative breast cancer.

Dong Ki Lee, Min Hwan Kim, Yumi Hwang, Seul-Gi Kim, Won-Ji Ryu, Geon-Uk Kim, Hyun Myoung Yun, Shinyoung Park, Jeong Dong Lee, Hyun Ju Han and 11 more

Abstract read
In one paragraph

Article in Genome biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors.

Dong Ki Lee *Department of Pharmacology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Min Hwan Kim *Division of Medical Oncology, Department of Internal Medicine, Yonsei Cancer Center, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Yumi HwangAvison Biomedical Research Center, Yonsei University College of Medicine, Seoul, Republic of Korea.
Seul-Gi KimDivision of Hematology and Oncology, Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, Republic of Korea.
Won-Ji RyuAvison Biomedical Research Center, Yonsei University College of Medicine, Seoul, Republic of Korea.
Geon-Uk KimAvison Biomedical Research Center, Yonsei University College of Medicine, Seoul, Republic of Korea.
Hyun Myoung YunAvison Biomedical Research Center, Yonsei University College of Medicine, Seoul, Republic of Korea.
Shinyoung ParkAvison Biomedical Research Center, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jeong Dong LeeAvison Biomedical Research Center, Yonsei University College of Medicine, Seoul, Republic of Korea.
Hyun Ju HanAvison Biomedical Research Center, Yonsei University College of Medicine, Seoul, Republic of Korea.
Gun Min KimDivision of Medical Oncology, Department of Internal Medicine, Yonsei Cancer Center, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Kyung-Hee KimBiopharmaceutical Chemistry Major, Department of Applied Chemistry, School of Science and Technology, Kookmin University, Seoul, Republic of Korea.
Jong Bae ParkDepartment of Medicine, Kyung Hee University School of Medicine, Seoul, Republic of Korea.
Min Jung KimDepartment of Radiology, Research Institute of Radiologic Science, Yonsei University College of Medicine, Seoul, Korea.
Ja Seung KooDepartment of Pathology, Yonsei University College of Medicine, Seoul, Korea.
Jee Ye KimDivision of Breast Surgery, Department of Surgery, Yonsei Cancer Center, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Hyung Seok ParkDivision of Breast Surgery, Department of Surgery, Yonsei Cancer Center, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Seung Il KimDivision of Breast Surgery, Department of Surgery, Yonsei Cancer Center, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Heon Yung GeeDepartment of Pharmacology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Seho Park *Division of Breast Surgery, Department of Surgery, Yonsei Cancer Center, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea. psh1025@yuhs.ac.
Joohyuk Sohn *Division of Medical Oncology, Department of Internal Medicine, Yonsei Cancer Center, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea. oncosohn@yuhs.ac.

Funding

Korea Health Industry Development Institute MD-PhD/Medical Scientist Training ProgramKorea Health Industry Development Institute RS-2024-00439841Korea Health Industry Development Institute (KHIDI) RS-2025-25459146Ministry of Health & Welfare, Republic of Korea HA22C0086National Cancer Center, Korea NCC-1810861National Research Foundation of Korea RS-2024-00452509
6 · The paper itself

Abstract

backgroundThe clinical utility of integrated proteogenomic biomarkers for predicting chemotherapy response in triple-negative breast cancer remains underexplored. We prospectively analyzed paired baseline and post-treatment tumor samples from 50 patients with stage II-III TNBC treated with anthracycline- and taxane-based neoadjuvant chemotherapy, integrating whole-exome sequencing, RNA sequencing, global proteomics, and phosphoproteomics.

resultsNon-negative matrix factorization clustering identifies five proteogenomic subtypes. The immune-enriched subtype demonstrates the highest pathologic complete response rate (55.6%), whereas no pathologic complete response was observed in the xenobiotic metabolism or epithelial-mesenchymal transition subtypes. Immune-related pathways are enriched in tumors with pathologic complete response, while epithelial-mesenchymal transition pathways are enriched in non-pathologic complete response tumors. The estrogen response pathway is selectively enriched in non-pathologic complete response tumors at the proteomic level and inversely correlated with immune activation. Post-translational modification and in vitro analyses suggest estrogen-linked GRK2 activation contributes to chemotherapy resistance. ITGB8 copy number loss is associated with higher pathologic complete response rates and immune activation, while non-pathologic complete response tumors of the immunomodulatory subtype show increased expression of AKR1C2 and ABCA13. Comparison of baseline and post-treatment tumors reveals AURKB pathway activation in residual disease, with Aurora B kinase inhibition synergizing with paclitaxel. A predictive model incorporating these biomarkers outperforms RNA-based models in predicting response.

conclusionIntegrative proteogenomic profiling enables robust prediction of chemotherapy resistance in triple-negative breast cancer and identifies actionable biomarkers providing a framework for advancing personalized therapeutic strategies.

Indexed as

Drug Resistance, NeoplasmProteogenomicsTriple Negative Breast NeoplasmsBiomarkers, TumorFemaleGene Expression Regulation, NeoplasticHumansNeoadjuvant TherapyBiomarkers, TumorBiomarkerChemotherapy responseNeoadjuvant chemotherapyProteogenomicsTriple-negative breast cancer

Identifiers

PMID41975515
PMCPMC13077823

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.