ArticleThe American journal of pathology2000
Loss of heterozygosity in fibrocystic change of the breast: genetic relationship between benign proliferative lesions and associated carcinomas.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- Is Cancer Reversible? Rethinking Carcinogenesis Models-A New Epistemological Tool.Biomolecules · 2023Review
- The matricellular protein CCN6 differentially regulates mitochondrial metabolism in normal epithelium and in metaplastic breast carcinomas.Journal of cell communication and signaling · 2022Article
- Paradoxical Behavior of Oncogenes Undermines the Somatic Mutation Theory.Biomolecules · 2022Article
- Genomic Changes in Normal Breast Tissue in Women at Normal Risk or at High Risk for Breast Cancer.Breast cancer : basic and clinical research · 2016Review
- Preinvasive breast cancer.Annual review of pathology · 2010Review
- Characterization of breast precancerous lesions and myoepithelial hyperplasia in sclerosing adenosis with apocrine metaplasia.Molecular oncology · 2007Article
- The enigmatic nature of apocrine breast lesions.Virchows Archiv : an international journal of pathology · 2006Review
- Of extracellular matrix, scaffolds, and signaling: tissue architecture regulates development, homeostasis, and cancer.Annual review of cell and developmental biology · 2006Review
- Function and regulation of melanoma-stromal fibroblast interactions: when seeds meet soil.Oncogene · 2003Review
- The diagnosis and management of pre-invasive breast disease: genetic alterations in pre-invasive lesions.Breast cancer research : BCR · 2003Review
- Loss of heterozygosity or allele imbalance in histologically normal breast epithelium is distinct from loss of heterozygosity or allele imbalance in co-existing carcinomas.The American journal of pathology · 2002Article
- Putting tumours in context.Nature reviews. Cancer · 2001Review
- High-resolution chromosome 3p allelotyping of breast carcinomas and precursor lesions demonstrates frequent loss of heterozygosity and a discontinuous pattern of allele loss.The American journal of pathology · 2001Article
- The tumor microenvironment is a dominant force in multidrug resistance.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapyReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of heterozygosity (LOH), a genetic change frequently detected in cancer, can also occur in benign epithelial foci in the breast. To characterize LOH in benign breast tissue, 32 cases containing the various components of fibrocystic change in the absence of malignancy were studied. Microdissected foci of ductal hyperplasia, apocrine metaplasia, sclerosing adenosis, and morphologically normal terminal duct lobular units (TDLUs) were analyzed for LOH at 14 polymorphic loci representing seven chromosomal arms. LOH was detected in 22% of normal TDLUs (6/27), 17% of adenosis (4/23), 19% of hyperplasia (4/21), and 53% of apocrine metaplasia (10/19) specimens. Because of the high percentage of LOH in apocrine metaplasia in nonneoplastic specimens, the genetic relationship between apocrine metaplasia and cancer was studied in a panel of breast cancer cases. Of 14 examples of apocrine metaplasia adjacent to a carcinoma, seven were found to have LOH with at least one marker. In all seven cases, the tumor and apocrine metaplasia shared LOH at one or more markers. The results demonstrate that LOH occurs frequently in the components of fibrocystic change as well as in normal TDLUs and suggest that foci of apocrine metaplasia can share a genetically altered precursor cell with an associated carcinoma.
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