ArticleNature communications2020
Adaptation and selection shape clonal evolution of tumors during residual disease and recurrence.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy-Tolerant Persister Cells in ER+ Breast Cancer.Cancer research · 2025Trial
- Biomaterial-based strategies for postoperative residual tumors: From margin clearance to immune control and tissue repair.Materials today. Bio · 2026Review
- Recurrence in the chemotherapy regimen of bladder carcinoma originates from quiescent epidermoid-like cells.Nature communications · 2026Article
- Article
- Targeting tumor transition windows.Exploration of targeted anti-tumor therapy · 2026Review
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- Modeling tumor relapse using proliferation tracing and ablation transgenic mouse.NPJ breast cancer · 2025Article
- Establishment and characterization of 24 breast cancer cell lines and 3 breast cancer organoids reveals molecular heterogeneity and drug response variability in malignant pleural effusion-derived models.Breast cancer research : BCR · 2025Article
- LINC01235 Promotes Clonal Evolution through DNA Replication Licensing-Induced Chromosomal Instability in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Clonal expansion dictates the efficacy of mitochondrial lineage tracing in single cells.Genome biology · 2025Article
- Subclonal TP53 and KRAS variants combined with poor treatment response identify ultrahigh-risk pediatric patients with T-ALL.Blood advances · 2025Article
- Recording Lineage History with Cellular Barcodes in the Mammary Epithelium and in Breast Cancer.Advances in experimental medicine and biology · 2025Review
- Splicing inhibition mediated by reduced splicing factors and helicases is associated with the cellular response of lung cancer cells to cisplatin.Computational and structural biotechnology journal · 2024Article
- Exploring the clinical utility of liquid biopsy with cfDNA in cancer: A systematic review.The journal of liquid biopsy · 2024Review
- The Expression Profiles of lncRNAs Are Associated with Neoadjuvant Chemotherapy Resistance in Locally Advanced, Luminal B-Type Breast Cancer.International journal of molecular sciences · 2024Article
- Pharmacological targeting of the cancer epigenome.Nature cancer · 2024Review
- Cetuximab chemotherapy resistance: Insight into the homeostatic evolution of head and neck cancer (Review).Oncology reports · 2024Review
- Dormancy in Breast Cancer.Cold Spring Harbor perspectives in medicine · 2023Review
- Beyond Neoantigens: Antigens Derived from Tumor Drivers as Cancer Vaccine Targets.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Experimental and spontaneous metastasis assays can result in divergence in clonal architecture.Communications biology · 2023Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
The survival and recurrence of residual tumor cells following therapy constitutes one of the biggest obstacles to obtaining cures in breast cancer, but it remains unclear how the clonal composition of tumors changes during relapse. We use cellular barcoding to monitor clonal dynamics during tumor recurrence in vivo. We find that clonal diversity decreases during tumor regression, residual disease, and recurrence. The recurrence of dormant residual cells follows several distinct routes. Approximately half of the recurrent tumors exhibit clonal dominance with a small number of subclones comprising the vast majority of the tumor; these clonal recurrences are frequently dependent upon Met gene amplification. A second group of recurrent tumors comprises thousands of subclones, has a clonal architecture similar to primary tumors, and is dependent upon the Jak/Stat pathway. Thus the regrowth of dormant tumors proceeds via multiple routes, producing recurrent tumors with distinct clonal composition, genetic alterations, and drug sensitivities.
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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.