ArticleNature medicine2015
Evolution of metastasis revealed by mutational landscapes of chemically induced skin cancers.
Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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
77 citing papers in PubMed, 113 citations in OpenAlex.
- Coexisting genomic aberrations associated with lymph node metastasis in breast cancer.The Journal of clinical investigation · 2018Trial
- Trial
- Chemically induced skin tumors arise from long-lived stem cells of the upper hair follicle.Science (New York, N.Y.) · 2026Article
- CIT tumor lines: A series of immunogenic murine cutaneous squamous cell carcinoma cell lines derived from chemical carcinogenesis.JID innovations : skin science from molecules to population health · 2026Article
- Epidermal PPARγ Signaling as a Suppressor of Toll-like Receptor-Mediated Inflammation and Fibrosis: Relevance to Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2026Article
- Tumour promotion through the lens of evolution.Nature · 2026Review
- Article
- Loss of the translational repressor 4E-BP1 promotes skin carcinogenesis.Frontiers in pharmacology · 2026Article
- Tumor cell heterogeneity drives spatial organization of the intratumoral immune response.The Journal of experimental medicine · 2025Article
- Exploring the Genetic Landscape of Vitiligo in the Pura Raza Español Horse: A Genomic Perspective.Animals : an open access journal from MDPI · 2024Article
- Article
- Patterns of Aneuploidy and Signaling Consequences in Cancer.Cancer research · 2024Review
- Stem-cell states converge in multistage cutaneous squamous cell carcinoma development.Science (New York, N.Y.) · 2024Article
- Mutations, Bottlenecks, and Clonal Sweeps: How Environmental Carcinogens and Genomic Changes Shape Clonal Evolution during Tumor Progression.Cold Spring Harbor perspectives in medicine · 2024Review
- Tracking tumor heterogeneity and progression with near-infrared II fluorophores.Exploration (Beijing, China) · 2023Review
- Aristolochic acid-associated cancers: a public health risk in need of global action.Nature reviews. Cancer · 2022Review
- Induction of potassium channel regulator KCNE4 in a submandibular lymph node metastasis model.Scientific reports · 2022Article
- Loss of Integrin α9β1 on Tumor Keratinocytes Enhances the Stromal Vasculature and Growth of Cutaneous Tumors.The Journal of investigative dermatology · 2022Article
- Article
- Integrated DNA and RNA sequencing reveals early drivers involved in metastasis of gastric cancer.Cell death & disease · 2022Article
17 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
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Human tumors show a high level of genetic heterogeneity, but the processes that influence the timing and route of metastatic dissemination of the subclones are unknown. Here we have used whole-exome sequencing of 103 matched benign, malignant and metastatic skin tumors from genetically heterogeneous mice to demonstrate that most metastases disseminate synchronously from the primary tumor, supporting parallel rather than linear evolution as the predominant model of metastasis. Shared mutations between primary carcinomas and their matched metastases have the distinct A-to-T signature of the initiating carcinogen dimethylbenzanthracene, but non-shared mutations are primarily G-to-T, a signature associated with oxidative stress. The existence of carcinomas that either did or did not metastasize in the same host animal suggests that there are tumor-intrinsic factors that influence metastatic seeding. We also demonstrate the importance of germline polymorphisms in determining allele-specific mutations, and we identify somatic genetic alterations that are specifically related to initiation of carcinogenesis by Hras or Kras mutations. Mouse tumors that mimic the genetic heterogeneity of human cancers can aid our understanding of the clonal evolution of metastasis and provide a realistic model for the testing of novel therapies.
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.