ArticleCellular oncology (Dordrecht, Netherlands)2011
Molecular differences between ductal carcinoma in situ and adjacent invasive breast carcinoma: a multiplex ligation-dependent probe amplification study.
Article in Cellular oncology (Dordrecht, Netherlands), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 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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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
21 citing papers in PubMed, 62 citations in OpenAlex.
- Matrix stiffness-induced IKBKE and MAPK8 signaling drives a phenotypic switch from DCIS to invasive breast cancer.Cell communication and signaling : CCS · 2025Article
- Progression from ductal carcinoma in situ to invasive breast cancer: molecular features and clinical significance.Signal transduction and targeted therapy · 2024Review
- Review
- The Research Progress in Physiological and Pathological Functions of TRAF4.Frontiers in oncology · 2022Review
- Multifaceted Role of PRDM Proteins in Human Cancer.International journal of molecular sciences · 2020Review
- Copy number changes at 8p11-12 predict adverse clinical outcome and chemo- and radiotherapy response in breast cancer.Oncotarget · 2018Article
- Article
- Modulation of Molecular Biomarker Expression in Response to Chemotherapy in Invasive Ductal Carcinoma.BioMed research international · 2018Article
- Glucose insult elicits hyperactivation of cancer stem cells through miR-424-cdc42-prdm14 signalling axis.British journal of cancer · 2017Article
- BIRC5 Genomic Copy Number Variation in Early-Onset Breast Cancer.Iranian biomedical journal · 2016Article
- Article
- Appraisal of the technologies and review of the genomic landscape of ductal carcinoma in situ of the breast.Breast cancer research : BCR · 2015Review
- Epigenetic Regulation of miRNAs and Breast Cancer Stem Cells.Current pharmacology reports · 2015Article
- Gene status in HER2 equivocal breast carcinomas: impact of distinct recommendations and contribution of a polymerase chain reaction-based method.The oncologist · 2014Article
- A comparison of the risks of in-breast recurrence after a diagnosis of dcis or early invasive breast cancer.Current oncology (Toronto, Ont.) · 2014Article
- PI3K pathway activation in high-grade ductal carcinoma in situ--implications for progression to invasive breast carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Progression from ductal carcinoma in situ to invasive breast cancer: revisited.Molecular oncology · 2013Review
- Chromosome 1q25.3 copy number alterations in primary breast cancers detected by multiplex ligation-dependent probe amplification and allelic imbalance assays and its comparison with fluorescent in situ hybridization assays.Cellular oncology (Dordrecht, Netherlands) · 2013Article
- FGFR-1 amplification in metastatic lymph-nodal and haematogenous lobular breast carcinoma.Journal of experimental & clinical cancer research : CR · 2012Article
- Genomic and mutational profiling of ductal carcinomas in situ and matched adjacent invasive breast cancers reveals intra-tumour genetic heterogeneity and clonal selection.The Journal of pathology · 2012Article
Corrections and comments
- Erratum issued
- Reprint of
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDuctal carcinoma in situ (DCIS) accounts for approximately 20% of mammographically detected breast cancers. Although DCIS is generally highly curable, some women with DCIS will develop life-threatening invasive breast cancer, but the determinants of progression to infiltrating ductal cancer (IDC) are largely unknown.
methodsIn the current study, we used multiplex ligation-dependent probe amplification (MLPA), a multiplex PCR-based test, to compare copy numbers of 21 breast cancer related genes between laser-microdissected DCIS and adjacent IDC lesions in 39 patients. Genes included in this study were ESR1, EGFR, FGFR1, ADAM9, IKBKB, PRDM14, MTDH, MYC, CCND1, EMSY, CDH1, TRAF4, CPD, MED1, HER2, CDC6, TOP2A, MAPT, BIRC5, CCNE1 and AURKA.
resultsThere were no significant differences in copy number for the 21 genes between DCIS and adjacent IDC. Low/intermediate-grade DCIS showed on average 6 gains/amplifications versus 8 in high-grade DCIS (p = 0.158). Furthermore, alterations of AURKA and CCNE1 were exclusively found in high-grade DCIS, and HER2, PRDM14 and EMSY amplification was more frequent in high-grade DCIS than in low/intermediate-grade DCIS. In contrast, the average number of alterations in low/intermediate and high grade IDC was similar, and although EGFR alterations were exclusively found in high grade IDC compared to low/intermediate-grade IDC, there were generally fewer differences between low/intermediate-grade and high-grade IDC than between low/intermediate-grade and high-grade DCIS.
conclusionIn conclusion, there were no significant differences in copy number for 21 breast cancer related genes between DCIS and adjacent IDC, indicating that DCIS is genetically as advanced as its invasive counterpart. However, high grade DCIS showed more copy number changes than low/intermediate grade DCIS with specifically involved genes, supporting a model in which different histological grades of DCIS are associated with distinct genomic changes that progress to IDC in different routes. These high grade DCIS specific genes may be potential targets for treatment and/or predict progression.
Identifiers
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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.