ArticleThe Journal of clinical investigation2017
Metabolic shifts in residual breast cancer drive tumor recurrence.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
What it found
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Who cites it
101 citing papers in PubMed, 172 citations in OpenAlex.
- Spatiotemporal organisation of residual disease in mouse and human BRCA1-deficient mammary tumours and breast cancer.Nature communications · 2026Article
- Biomaterial-based strategies for postoperative residual tumors: From margin clearance to immune control and tissue repair.Materials today. Bio · 2026Review
- Radiation-induced autophagy regulates fibroblast mitochondrial metabolism and crosstalk with triple-negative breast cancer cells.Cell reports · 2026Article
- Lipid Metabolism and Ferroptosis Resistance in Dormant Breast Cancer Cells: Emerging Therapeutic Vulnerabilities.Diagnostics (Basel, Switzerland) · 2026Review
- Picosecond infrared laser mass spectrometry for 10-second identification of lymphoproliferative imposter tumours in patient-derived xenografts.Scientific reports · 2026Article
- CPT1A as a metabolic gatekeeper linking fatty acid oxidation, ferroptosis resistance, and breast cancer stemness.Frontiers in oncology · 2026Review
- High CD36 Expression Predicts Aggressive Invasion and Recurrence in Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2025Article
- Metabolic Regulation of Ferroptosis in Breast Cancer.International journal of molecular sciences · 2025Review
- The pleiotropic roles of non-hormonal receptor basigin and regulatory microRNAs in breast cancer.NPJ breast cancer · 2025Review
- Understanding Tumor Dormancy: from Experimental Models to Mechanisms and Therapeutic Strategies.Biomolecules & therapeutics · 2025Review
- The Key Role of COA6 in Pancreatic Ductal Adenocarcinoma: Metabolic Reprogramming and Regulation of the Immune Microenvironment.Journal of cellular and molecular medicine · 2025Article
- CREB1-BCL2 drives mitochondrial resilience in RAS GAP-dependent breast cancer chemoresistance.Oncogene · 2025Article
- Peroxisomal membrane protein PMP70 confers drug resistance in colorectal cancer.Cell death & disease · 2025Article
- Structural variant and nucleosome occupancy dynamics postchemotherapy in a HER2+ breast cancer organoid model.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genetic advancements in breast cancer treatment: a review.Discover oncology · 2025Review
- Lung cancer and obesity: A contentious relationship (Review).Oncology reports · 2024Review
- Longitudinal multiomics analysis of aggressive pituitary neuroendocrine tumors: comparing primary and recurrent tumors from the same patient, reveals genomic stability and heterogeneous transcriptomic profiles with alterations in metabolic pathways.Acta neuropathologica communications · 2024Article
- FADS1/2 control lipid metabolism and ferroptosis susceptibility in triple-negative breast cancer.EMBO molecular medicine · 2024Article
- Article
- Cancer radioresistance is characterized by a differential lipid droplet content along the cell cycle.Cell division · 2024Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor recurrence is the leading cause of breast cancer-related death. Recurrences are largely driven by cancer cells that survive therapeutic intervention. This poorly understood population is referred to as minimal residual disease. Here, using mouse models that faithfully recapitulate human disease together with organoid cultures, we have demonstrated that residual cells acquire a transcriptionally distinct state from normal epithelium and primary tumors. Gene expression changes and functional characterization revealed altered lipid metabolism and elevated ROS as hallmarks of the cells that survive tumor regression. These residual cells exhibited increased oxidative DNA damage, potentiating the acquisition of somatic mutations during hormonal-induced expansion of the mammary cell population. Inhibition of either cellular fatty acid synthesis or fatty acid transport into mitochondria reduced cellular ROS levels and DNA damage, linking these features to lipid metabolism. Direct perturbation of these hallmarks in vivo, either by scavenging ROS or by halting the cyclic mammary cell population expansion, attenuated tumor recurrence. Finally, these observations were mirrored in transcriptomic and histological signatures of residual cancer cells from neoadjuvant-treated breast cancer patients. These results highlight the potential of lipid metabolism and ROS as therapeutic targets for reducing tumor recurrence in breast cancer patients.
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Registered trials
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 OpenQuestion graph.