ArticleNature communications2016
The landscape of chromosomal aberrations in breast cancer mouse models reveals driver-specific routes to tumorigenesis.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 54 citations in OpenAlex.
- Development and Application of MiMouse, a Comprehensive Genomic Profiling Panel for Credentialing Mouse Tumor Models.Cancer research communications · 2025Article
- Molecular Markers for Thyroid Cancer Diagnosis: Insights from MAPK Pathway Gene Expression Analysis.Biomedicines · 2025Article
- Aneuploidy as a driver of human cancer.Nature genetics · 2024Review
- Exploring the prognostic significance of arm-level copy number alterations in triple-negative breast cancer.Oncogene · 2024Article
- Machine-learning analysis reveals an important role for negative selection in shaping cancer aneuploidy landscapes.Genome biology · 2024Article
- Dissecting metastasis using preclinical models and methods.Nature reviews. Cancer · 2023Review
- Characterization of Mammary Tumors Arising from MMTV-PyVT Transgenic Mice.Current issues in molecular biology · 2023Article
- Mesenchymal tumor cells drive adaptive resistance of Trp53Molecular oncology · 2022Article
- Whole-Genome Duplication Shapes the Aneuploidy Landscape of Human Cancers.Cancer research · 2022Article
- Article
- Article
- Aneuploidy as a promoter and suppressor of malignant growth.Nature reviews. Cancer · 2021Review
- Insights from transgenic mouse models of PyMT-induced breast cancer: recapitulating human breast cancer progression in vivo.Oncogene · 2021Review
- Conservation of copy number profiles during engraftment and passaging of patient-derived cancer xenografts.Nature genetics · 2021Article
- Cathepsin D deficiency in mammary epithelium transiently stalls breast cancer by interference with mTORC1 signaling.Nature communications · 2020Article
- mRNAs, proteins and the emerging principles of gene expression control.Nature reviews. Genetics · 2020Review
- Cross-species oncogenic signatures of breast cancer in canine mammary tumors.Nature communications · 2020Article
- Alzheimer's Disease, and Breast and Prostate Cancer Research: Translational Failures and the Importance to Monitor Outputs and Impact of Funded Research.Animals : an open access journal from MDPI · 2020Review
- Chemogenomic profiling of breast cancer patient-derived xenografts reveals targetable vulnerabilities for difficult-to-treat tumors.Communications biology · 2020Article
- Breast Cancer: A Molecularly Heterogenous Disease Needing Subtype-Specific Treatments.Medical sciences (Basel, Switzerland) · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aneuploidy and copy-number alterations (CNAs) are a hallmark of human cancer. Although genetically engineered mouse models (GEMMs) are commonly used to model human cancer, their chromosomal landscapes remain underexplored. Here we use gene expression profiles to infer CNAs in 3,108 samples from 45 mouse models, providing the first comprehensive catalogue of chromosomal aberrations in cancer GEMMs. Mining this resource, we find that most chromosomal aberrations accumulate late during breast tumorigenesis, and observe marked differences in CNA prevalence between mouse mammary tumours initiated with distinct drivers. Some aberrations are recurrent and unique to specific GEMMs, suggesting distinct driver-dependent routes to tumorigenesis. Synteny-based comparison of mouse and human tumours narrows critical regions in CNAs, thereby identifying candidate driver genes. We experimentally validate that loss of Stratifin (SFN) promotes HER2-induced tumorigenesis in human cells. These results demonstrate the power of GEMM CNA analysis to inform the pathogenesis of human cancer.
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.