ArticleNature communications2017
Combating subclonal evolution of resistant cancer phenotypes.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 101 papers.
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.
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.
Who cites it
101 citing papers in PubMed.
- Molecular Profiling-Based Assignment of Cancer Therapy (NCI-MPACT): A Randomized Multicenter Phase II Trial.JCO precision oncology · 2021Trial
- Article
- Atypical fusion among non-malignant cells: Unveiling the link between post-fusion-induced genome chaos and cancer initiation.Cancer cell international · 2026Article
- Integrative pipeline to profile and target endocrine therapy-insensitive cell populations in ER+ breast cancer.bioRxiv : the preprint server for biology · 2026Article
- Therapy-Related Mutational Signatures in Subsequent Neoplasms among Survivors of Childhood Cancer.Cancer discovery · 2026Article
- CNVeil resolves haplotype-specific copy number and uncovers subclonal architecture hidden from total copy number profiling in single-cell cancer genomes.bioRxiv : the preprint server for biology · 2026Article
- Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Metabolic Response to CDK4/6 Inhibition in ER+ Breast Cancer Creates a Therapeutic Vulnerability in Drug-Tolerant Persister Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- A Tumor-Agnostic, Topology-Informed Scoring Framework for Drug Repurposing: Application to CDK4/6 Inhibitor Resistance in HRBiomedicines · 2026Article
- Strength through diversity: how cancers thrive when clones cooperate.Molecular oncology · 2026Review
- Single Cell RNA Sequencing in Colorectal Cancer Immunology: Recent Updates, Application, and Emerging Challenges.Current molecular medicine · 2026Review
- Chemoresistome mapping in individual breast cancer patients unravels diversity in dynamic transcriptional adaptation.Molecular oncology · 2025Article
- Understanding Enzalutamide-Resistance Based on a Functional Single-Cell Approach.The Prostate · 2025Article
- DiffInvex identifies evolutionary shifts in driver gene repertoires during tumorigenesis and chemotherapy.Nature communications · 2025Article
- Long-read single-cell RNA sequencing enables the study of cancer subclone-specific genotypes and phenotypes in chronic lymphocytic leukemia.Genome research · 2025Article
- 15 Years Old ALK Gene from Birth to Adolescence; Where to in NBL.Current oncology reports · 2025Review
- Inferring active mutational processes in cancer using single cell sequencing and evolutionary constraints.bioRxiv : the preprint server for biology · 2025Article
- Machine learning-derived prognostic signature integrating programmed cell death and mitochondrial function in renal clear cell carcinoma: identification of PIF1 as a novel target.Cancer immunology, immunotherapy : CII · 2025Article
- Advanced single-cell and spatial analysis with high-multiplex characterization of circulating tumor cells and tumor tissue in prostate cancer: Unveiling resistance mechanisms with the CoDuCo in situ assay.Biomarker research · 2024Article
- Early evolutionary branching across spatial domains predisposes to clonal replacement under chemotherapy in neuroblastoma.Nature communications · 2024Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
28 authors.
Funding
Abstract
Metastatic breast cancer remains challenging to treat, and most patients ultimately progress on therapy. This acquired drug resistance is largely due to drug-refractory sub-populations (subclones) within heterogeneous tumors. Here, we track the genetic and phenotypic subclonal evolution of four breast cancers through years of treatment to better understand how breast cancers become drug-resistant. Recurrently appearing post-chemotherapy mutations are rare. However, bulk and single-cell RNA sequencing reveal acquisition of malignant phenotypes after treatment, including enhanced mesenchymal and growth factor signaling, which may promote drug resistance, and decreased antigen presentation and TNF-α signaling, which may enable immune system avoidance. Some of these phenotypes pre-exist in pre-treatment subclones that become dominant after chemotherapy, indicating selection for resistance phenotypes. Post-chemotherapy cancer cells are effectively treated with drugs targeting acquired phenotypes. These findings highlight cancer's ability to evolve phenotypically and suggest a phenotype-targeted treatment strategy that adapts to cancer as it evolves.
Indexed as
Identifiers
What OpenQuestion holds
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.