ArticleOncotarget2015
Genomic differences between pure ductal carcinoma in situ and synchronous ductal carcinoma in situ with invasive breast cancer.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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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.
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.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Prognostic significance of microinvasion with ductal carcinoma in situ of the breast: a meta-analysis.Breast cancer research and treatment · 2023Pooled it
- Comprehensive Genomic Analysis of Normal and Cancer Cells Elucidates the Elevated Mutational Burden in Cancer.Cancer research · 2026Article
- Racial Disparity in Ductal Carcinoma in Situ: Risk-Predictive and Actionable Biomarkers for Early Intervention.Cancers · 2026Review
- 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
- Exploring the Latent Information in Spatial Transcriptomics Data via Multi-View Graph Convolutional Network Based on Implicit Contrastive Learning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The end of the genetic paradigm of cancer.PLoS biology · 2025Review
- The Microenvironment in DCIS and Its Role in Disease Progression.Advances in experimental medicine and biology · 2025Review
- Radiology for Ductal Carcinoma In Situ of the Breast: Updates on Invasive Cancer Progression and Active Monitoring.Korean journal of radiology · 2024Review
- Unsupervised representation learning of chromatin images identifies changes in cell state and tissue organization in DCIS.Nature communications · 2024Article
- Multi-omic profiling of simultaneous ductal carcinoma in situ and invasive breast cancer.Breast cancer research and treatment · 2024Article
- Tumor microenvironmental determinants of high-risk DCIS progression.Research square · 2024Article
- Spatial Biology of Breast Cancer.Cold Spring Harbor perspectives in medicine · 2024Review
- 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
- Review
- Regulation of growth, invasion and metabolism of breast ductal carcinoma through CCL2/CCR2 signaling interactions with MET receptor tyrosine kinases.Neoplasia (New York, N.Y.) · 2022Article
- Ductal Carcinoma In Situ of Breast: From Molecular Etiology to Therapeutic Management.Endocrinology · 2022Review
- Ductal Carcinoma in Situ: Molecular Changes Accompanying Disease Progression.Journal of mammary gland biology and neoplasia · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although ductal carcinoma in situ (DCIS) precedes invasive ductal carcinoma (IDC), the related genomic alterations remain unknown. To identify the genomic landscape of DCIS and better understand the mechanisms behind progression to IDC, we performed whole-exome sequencing and copy number profiling for six cases of pure DCIS and five pairs of synchronous DCIS and IDC. Pure DCIS harbored well-known mutations (e.g., TP53, PIK3CA and AKT1), copy number alterations (CNAs) and chromothripses, but had significantly fewer driver genes and co-occurrence of mutation/CNAs than synchronous DCIS-IDC. We found neither recurrent nor significantly mutated genes with synchronous DCIS-IDC compared to pure DCIS, indicating that there may not be a single determinant for pure DCIS progression to IDC. Of note, synchronous DCIS genomes were closer to IDC than pure DCIS. Among the clinicopathologic parameters, progesterone receptor (PR)-negative status was associated with increased mutations, CNAs, co-occurrence of mutations/CNAs and driver mutations. Our results indicate that although pure DCIS has already acquired some drivers, more changes are needed to progress to IDC. In addition, IDC-associated DCIS is more aggressive than pure DCIS at genomic level and should really be considered IDC. Finally, the data suggest that PR-negativity could be used to predict aggressive breast cancer genotypes.
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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.