Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance
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Neoadjuvant chemotherapy (NAC) induces a pathological complete response (pCR) in ~30% of patients with breast cancer. However, many patients have residual cancer after chemotherapy, which correlates with a higher risk of metastatic recurrence and poorer outcome than those who achieve a pCR. We hypothesized that molecular profiling of tumors after NAC would identify genes associated with drug resistance. Digital transcript counting was used to profile surgically resected breast cancers after NAC. Low concentrations of dual specificity protein phosphatase 4 (DUSP4), an ERK phosphatase, correlated with high post-NAC tumor cell proliferation and with basal-like breast cancer (BLBC) status. BLBC had higher DUSP4 promoter methylation and gene expression patterns of Ras-ERK pathway activation relative to other breast cancer subtypes. DUSP4 overexpression increased chemotherapy-induced apoptosis, whereas DUSP4 depletion dampened the response to chemotherapy. Reduced DUSP4 expression in primary tumors after NAC was associated with treatment-refractory high Ki-67 scores and shorter recurrence-free survival. Finally, inhibition of mitogen-activated protein kinase kinase (MEK) synergized with docetaxel treatment in BLBC xenografts. Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response to anti-cancer chemotherapy.
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Drug-resistant residual cancers should harbor mechanisms and/or biomarkers of resistance to the primary therapy.
“These ‘drug resistant’ residual cancers should harbor mechanisms and/or biomarkers of resistance to the primary therapy”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Balko et al., 2012
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- Authors
- Balko, J. M., Cook, R. S., Vaught, D. B., Kuba, M. G., Miller, T. W., Bhola, N. E., Sanders, M. E., Granja-Ingram, N. M., Smith, J. J., Meszoely, I. M., Salter, J., Dowsett, M., Stemke-Hale, K., González-Angulo, A. M., Mills, G. B., Pinto, J. A., Gómez, H. L., & Arteaga, C. L.
- Affiliations
- Vanderbilt University (US)
- Institute of Cancer Research (GB)
- The University of Texas MD Anderson Cancer Center (US)
- Instituto Nacional de Enfermedades Neoplásicas (PE)
- Corresponding author
- Arteaga, Carlos L
- ORCID
- Venue
- Nature Medicine
- Published
- 2012-06-10
- Volume
- 18
- Issue
- 7
- Pages
- 1052-1059
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3693569
- OpenAlex
- W2063432148
- Cited by
- 262
- References
- 51
- Citations by year
- 2026: 5 · 2025: 13 · 2024: 13 · 2023: 15 · 2022: 23 · 2021: 26 · 2020: 15 · 2019: 26 · 2018: 16 · 2017: 13 · 2016: 26 · 2015: 16 · 2014: 25 · 2013: 26 · 2012: 4
- FWCI
- 7.54
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P50 CA98131, P30 CA 68485, R01CA143126, P50CA098258, K99CA142899, R00CA142899, P01CA099031, P50CA098131, P30CA016672, P30CA068485)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- residual breast cancer, neoadjuvant chemotherapy, drug resistance, DUSP4, Ras/ERK pathway, MEK inhibitors, basal-like breast cancer, chemotherapy-induced apoptosis, Ki-67, tumor recurrence, docetaxel, tumor cell proliferation
- MeSH terms
- Animals, Breast Neoplasms, Cell Survival, Enzyme Activation, Female, Humans, RNA, Messenger, Tissue Banks, Gene Expression Regulation, Neoplastic, Paraffin Embedding, Tissue Fixation, Treatment Outcome, Apoptosis, Neoplasm, Residual, ras Proteins, Drug Resistance, Neoplasm, Ki-67 Antigen, Neoadjuvant Therapy, Gene Expression Profiling, Mitogen-Activated Protein Kinase Kinases, MAP Kinase Signaling System, Extracellular Signal-Regulated MAP Kinases, Mice, Genes, Neoplasm, Dual-Specificity Phosphatases, Mitogen-Activated Protein Kinase Phosphatases, Gene Knockdown Techniques
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