Trial reportMolecular oncology2014
Breast tumor PDXs are genetically plastic and correspond to a subset of aggressive cancers prone to relapse.
Trial report in Molecular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled 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.
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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Pooled it
- Breast tumor PDXs are genetically plastic and correspond to a subset of aggressive cancers prone to relapse.Molecular oncology · 2014Trial
- Insights from Genomic Sequencing of Preclinical Breast Cancer Models Establish Human Parallels to Increase Therapeutic Applicability.Journal of mammary gland biology and neoplasia · 2026Review
- A clinically concordant vulvar cancer patient-derived xenograft model retaining primary molecular signature for preclinical drug sensitivity assessment.Open medicine (Warsaw, Poland) · 2026Article
- Zebrafish Avatar testing preclinical study predicts chemotherapy response in breast cancer.NPJ precision oncology · 2025Article
- Prognostic Value of Trop-2 Expression in Nonmetastatic Triple-Negative Breast Cancer and Correlation With Emerging Biomarkers.Cancer medicine · 2025Article
- Patient-Derived Xenografts of Breast Cancer.Advances in experimental medicine and biology · 2025Review
- A novel Fc-engineered cathepsin D-targeting antibody enhances ADCC, triggers tumor-infiltrating NK cell recruitment, and improves treatment with paclitaxel and enzalutamide in triple-negative breast cancer.Journal for immunotherapy of cancer · 2024Article
- SPARC in cancer-associated fibroblasts is an independent poor prognostic factor in non-metastatic triple-negative breast cancer and exhibits pro-tumor activity.International journal of cancer · 2023Article
- Biomimetic Gland Models with Engineered Stratagems.Research (Washington, D.C.) · 2023Review
- Article
- Article
- Multi-Level Control of the ATM/ATR-CHK1 Axis by the Transcription Factor E4F1 in Triple-Negative Breast Cancer.International journal of molecular sciences · 2022Article
- Patient-derived xenograft (PDX) models, applications and challenges in cancer research.Journal of translational medicine · 2022Review
- A human breast cancer-derived xenograft and organoid platform for drug discovery and precision oncology.Nature cancer · 2022Article
- Functional precision oncology: Testing tumors with drugs to identify vulnerabilities and novel combinations.Cancer cell · 2022Review
- Review: Sustainable Clinical Development of CAR-T Cells - Switching From Viral Transduction Towards CRISPR-Cas Gene Editing.Frontiers in immunology · 2022Review
- Toward improved models of human cancer.APL bioengineering · 2021Article
- Early stability and late random tumor progression of a HER2-positive primary breast cancer patient-derived xenograft.Scientific reports · 2021Article
- Experimental models of endocrine responsive breast cancer: strengths, limitations, and use.Cancer drug resistance (Alhambra, Calif.) · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patient derived xenografts (PDXs) are increasingly appreciated models in cancer research, particularly for preclinical testing, as they reflect the patient's tumor biology more accurately than cancer cell lines. We have established a collection of 20 breast PDXs and characterized their biological and clinical features, as well as their genetic stability. While most PDXs originated from triple negative breast cancers (70%), our collection comprised five ER + cases (25%). Remarkably, the tumors that produced PDXs derived from a subset of aggressive breast cancers with a high proportion of grade 3 tumors and reduced recurrence-free survival. Consistent with this, we found significant differences between the transcriptomic signatures of tumors that produced a PDX (Take) and those that did not (No Take). The PDXs faithfully recapitulate the histological features of their primary tumors, and retain an excellent conservation of molecular classification assignment and Copy Number Change (CNC). Furthermore, the CNC profiles of different PDXs established from the same tumor overlap significantly. However, a small fraction of CNCs in the primary tumor that correspond to oligoclonal events were gradually lost during sequential passaging, suggesting that the PDXs' genetic structure eventually stabilizes around a dominant clone present in the tumor of origin. Finally, de novo occurring genetic events covering up to 9% of the genome were found in only a minority of the PDXs, showing that PDXs have limited genetic instability. These data show that breast cancer PDXs represent a subset of aggressive tumors prone to relapse, and that despite of an excellent conservation of original features, they remain genetically dynamic elements.
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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.