ArticleThe Journal of pathology2012
Genomic and mutational profiling of ductal carcinomas in situ and matched adjacent invasive breast cancers reveals intra-tumour genetic heterogeneity and clonal selection.
Article in The Journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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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.
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Who cites it
87 citing papers in PubMed, 152 citations in OpenAlex.
- Quantitative assessment of HER2 expression in invasive ductal carcinoma and co-existing DCIS.Breast cancer research and treatment · 2025Article
- Identification of a Growth-Promoting Gene Cluster in the Region 2q24 as a Driver of Tumorigenesis in Childhood Hepatoblastoma.The American journal of pathology · 2025Article
- Mutational landscape of pure ductal carcinoma in situ and associations with disease prognosis and response to radiotherapy.Breast cancer research : BCR · 2025Article
- DCIS Progression and the Tumor Microenvironment: Molecular Insights and Prognostic Challenges.Cancers · 2025Review
- Article
- The Microenvironment in DCIS and Its Role in Disease Progression.Advances in experimental medicine and biology · 2025Review
- Article
- Impact of surgical types on overall survival in patients with ductal carcinomaGland surgery · 2024Article
- Multi-omic profiling of simultaneous ductal carcinoma in situ and invasive breast cancer.Breast cancer research and treatment · 2024Article
- Progression from ductal carcinoma in situ to invasive breast cancer: molecular features and clinical significance.Signal transduction and targeted therapy · 2024Review
- Article
- A living biobank of patient-derived ductal carcinoma in situ mouse-intraductal xenografts identifies risk factors for invasive progression.Cancer cell · 2023Article
- The most likely but largely ignored triggering factor for breast (or all) cancer invasion.Journal of Cancer · 2023Article
- Serial Tumor Molecular Profiling of Newly Diagnosed HER2-Negative Breast Cancers During Chemotherapy in Combination with Angiogenesis Inhibitors.Targeted oncology · 2022Article
- Heterogeneity of Circulating Tumor Cell-Associated Genomic Gains in Breast Cancer and Its Association with the Host Immune Response.Cancer research · 2021Article
- Breast Cancer Heterogeneity.Diagnostics (Basel, Switzerland) · 2021Review
- Transcriptome and genome evolution during HER2-amplified breast neoplasia.Breast cancer research : BCR · 2021Article
- Morphological intratumor heterogeneity in ductal carcinoma in situ of the breast.Virchows Archiv : an international journal of pathology · 2021Article
- Article
- Genomic Alterations during theMolecular cancer research : MCR · 2021Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 4 countries.
Funding
Abstract
The mechanisms underlying the progression from ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) of the breast are yet to be fully elucidated. Several hypotheses have been put forward to explain the progression from DCIS to IDC, including the selection of a subpopulation of cancer cells with specific genetic aberrations, and the acquisition of new genetic aberrations or non-genetic mechanisms mediated by the tumour microenvironment. To determine whether synchronously diagnosed ipsilateral DCI and IDCs have modal populations with distinct repertoires of gene copy number aberrations and mutations in common oncogenes, matched frozen samples of DCIS and IDC were retrieved from 13 patients and subjected to microarray-based comparative genomic hybridization (aCGH) and Sequenom MassARRAY (Oncocarta v 1.0 panel). Fluorescence in situ hybridization and Sanger sequencing were employed to validate the aCGH and Sequenom findings, respectively. Although the genomic profiles of matched DCI and IDCs were similar, in three of 13 matched pairs amplification of distinct loci (ie 1q41, 2q24.2, 6q22.31, 7q11.21, 8q21.2 and 9p13.3) was either restricted to, or more prevalent in, the modal population of cancer cells of one of the components. Sequenom MassARRAY identified PIK3CA mutations restricted to the DCIS component in two cases, and in a third case the frequency of the PIK3CA mutant allele reduced from 49% in the DCIS to 25% in the IDC component. Despite the genomic similarities between synchronous DCIS and IDC, our data provide strong circumstantial evidence to suggest that in some cases the progression from DCIS to IDC is driven by the selection of non-modal clones that harbour a specific repertoire of genetic aberrations.
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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.