ArticleGenes, chromosomes & cancer2012
Differential copy number aberrations in novel candidate genes associated with progression from in situ to invasive ductal carcinoma of the breast.
Article in Genes, chromosomes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- High-throughput proteomics of breast cancer interstitial fluid: identification of tumor subtype-specific serologically relevant biomarkers.Molecular oncology · 2021Trial
- Clinicopathological predictive factors for ipsilateral and contralateral events following initial surgery to treat ductal carcinoma in situ.Breast cancer (Tokyo, Japan) · 2016Trial
- Identification and bioinformatics analysis of cilia-associated gene families inFrontiers in microbiology · 2025Article
- Progression from ductal carcinoma in situ to invasive breast cancer: molecular features and clinical significance.Signal transduction and targeted therapy · 2024Review
- Upregulation of CELSR1 expression promotes ovarian cancer cell proliferation, migration, and invasion.Medical oncology (Northwood, London, England) · 2023Article
- Article
- Bioinformatics and integrated analyses of prognosis-associated key genes in lung adenocarcinoma.Journal of thoracic disease · 2021Article
- Article
- A retrospective alternative for active surveillance trials for ductal carcinoma in situ of the breast.International journal of cancer · 2020Review
- CELSR1 Acts as an Oncogene Regulated by miR-199a-5p in Glioma.Cancer management and research · 2020Article
- Genomic landscape of ductal carcinoma in situ and association with progression.Breast cancer research and treatment · 2019Article
- Intratumoral Heterogeneity in Ductal Carcinoma In Situ: Chaos and Consequence.Journal of mammary gland biology and neoplasia · 2018Review
- Genome evolution in ductal carcinoma in situ: invasion of the clones.The Journal of pathology · 2017Review
- Adhesion GPCRs in Tumorigenesis.Handbook of experimental pharmacology · 2016Review
- Expression profiling of in vivo ductal carcinoma in situ progression models identified B cell lymphoma-9 as a molecular driver of breast cancer invasion.Breast cancer research : BCR · 2015Article
- Copy number analysis of ductal carcinoma in situ with and without recurrence.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2015Article
- Appraisal of the technologies and review of the genomic landscape of ductal carcinoma in situ of the breast.Breast cancer research : BCR · 2015Review
- Impact of the presence and quantity of ductal carcinoma in situ component on the outcome of invasive breast cancer.International journal of clinical and experimental pathology · 2015Article
- Expression QTL-based analyses reveal candidate causal genes and loci across five tumor types.Human molecular genetics · 2014Article
- The SMRT coregulator enhances growth of estrogen receptor-α-positive breast cancer cells by promotion of cell cycle progression and inhibition of apoptosis.Endocrinology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Only a minority of intraductal carcinomas of the breast give rise to stromally invasive disease. We microdissected 206 paraffin blocks representing 116 different cases of low-grade ductal carcinoma in situ (DCIS). Fifty-five were pure DCIS (PD) cases without progression to invasive carcinoma. Sixty-one cases had a small invasive component. DNA was extracted from microdissected sections and hybridized to high-density bacterial artificial chromosome arrays. Array comparative genomic hybridization analysis of 118 hybridized DNA samples yielded data on 69 samples that were suitable for further statistical analysis. This cohort included 20 pure DCIS cases, 25 mixed DCIS (MD), and 24 mixed invasive carcinoma samples. PD cases had a higher frequency of DNA copy number changes than MD cases, and the latter had similar DNA profiles compared to paired invasive carcinomas. Copy number changes on 13 chromosomal arms occurred at different rates in PD versus MD lesions. Eight of 19 candidate genes residing at those loci were confirmed to have differential copy number changes by quantitative PCR. NCOR2/SMRT and NR4A1 (both on 12q), DYNLRB2 (16q), CELSR1, UPK3A, and ST13 (all on 22q) were more frequently amplified in PD. Moreover, NCOR2, NR4A1, and DYNLRB2 showed more frequent copy number losses in MD. GRAP2 (22q) was more often amplified in MD, whereas TAF1C (16q) was more commonly deleted in PD. A multigene model comprising these candidate genes discriminated between PD and MD lesions with high accuracy. These findings suggest that the propensity to invade the stroma may be encoded in the genome of intraductal carcinomas.
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Registered trials
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