ArticleOncogene2006
A comprehensive study of chromosome 16q in invasive ductal and lobular breast carcinoma using array CGH.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 69 citations in OpenAlex.
- Subtype-specific enhancer RNAs define transcriptional regulators and prognosis in breast cancers.Molecular oncology · 2026Article
- ATBF1 is a potential diagnostic marker of histological grade and functions via WNT5A in breast cancer.BMC cancer · 2022Article
- Aberrations of Chromosomes 1 and 16 in Breast Cancer: A Framework for Cooperation of Transcriptionally Dysregulated Genes.Cancers · 2021Article
- Lobular Breast Cancer: A Review.Frontiers in oncology · 2020Review
- Significant random signatures reveals new biomarker for breast cancer.BMC medical genomics · 2019Article
- LobSig is a multigene predictor of outcome in invasive lobular carcinoma.NPJ breast cancer · 2019Article
- Role of columnar cell lesions in breast carcinogenesis: analysis of chromosome 16 copy number changes by multiplex ligation-dependent probe amplification.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018Article
- Survival differences of CIMP subtypes integrated with CNA information in human breast cancer.Oncotarget · 2017Article
- Zinc Finger Homeodomain Factor Zfhx3 Is Essential for Mammary Lactogenic Differentiation by Maintaining Prolactin Signaling Activity.The Journal of biological chemistry · 2016Article
- Quantitative multigene FISH on breast carcinomas identifies der(1;16)(q10;p10) as an early event in luminal A tumors.Genes, chromosomes & cancer · 2015Article
- Invasive lobular carcinoma of the breast: morphology, biomarkers and 'omics.Breast cancer research : BCR · 2015Review
- Microsatellite stable colorectal cancers stratified by the BRAF V600E mutation show distinct patterns of chromosomal instability.PloS one · 2014Article
- Article
- An array CGH based genomic instability index (G2I) is predictive of clinical outcome in breast cancer and reveals a subset of tumors without lymph node involvement but with poor prognosis.BMC medical genomics · 2012Article
- Article
- Immunophenotypic and genomic characterization of papillary carcinomas of the breast.The Journal of pathology · 2012Article
- Atbf1 regulates pubertal mammary gland development likely by inhibiting the pro-proliferative function of estrogen-ER signaling.PloS one · 2012Article
- Identification of metastasis-associated breast cancer genes using a high-resolution whole genome profiling approach.Journal of cancer research and clinical oncology · 2011Article
- Merotelic attachments and non-homologous end joining are the basis of chromosomal instability.Cell division · 2010Article
- Genomic subtypes of breast cancer identified by array-comparative genomic hybridization display distinct molecular and clinical characteristics.Breast cancer research : BCR · 2010Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 1 country.
Funding
Abstract
We analysed chromosome 16q in 106 breast cancers using tiling-path array-comparative genomic hybridization (aCGH). About 80% of ductal cancers (IDCs) and all lobular cancers (ILCs) lost at least part of 16q. Grade I (GI) IDCs and ILCs often lost the whole chromosome arm. Grade II (GII) and grade III (GIII) IDCs showed less frequent whole-arm loss, but often had complex changes, typically small regions of gain together with larger regions of loss. The boundaries of gains/losses tended to cluster, common sites being 54.5-55.5 Mb and 57.4-58.8 Mb. Overall, the peak frequency of loss (83% cancers) occurred at 61.9-62.9 Mb. We also found several 'minimal' regions of loss/gain. However, no mutations in candidate genes (TRADD, CDH5, CDH8 and CDH11) were detected. Cluster analysis based on copy number changes identified a large group of cancers that had lost most of 16q, and two smaller groups (one with few changes, one with a tendency to show copy number gain). Although all morphological types occurred in each cluster group, IDCs (especially GII/GIII) were relatively overrepresented in the smaller groups. Cluster groups were not independently associated with survival. Use of tiling-path aCGH prompted re-evaluation of the hypothetical pathways of breast carcinogenesis. ILCs have the simplest changes on 16q and probably diverge from the IDC lineage close to the stage of 16q loss. Higher-grade IDCs probably develop from low-grade lesions in most cases, but there remains evidence that some GII/GIII IDCs arise without a GI precursor.
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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.