ArticleThe American journal of pathology1998
Genetically abnormal clones in histologically normal breast tissue.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 119 citations in OpenAlex.
- Margin of Error: The Emerging Role of Field Cancerization in Predicting Recurrence Risk of Ductal Carcinoma In Situ.International journal of molecular sciences · 2026Review
- Mapping genomic and transcriptomic alterations spatially in epithelial cells adjacent to human breast carcinoma.Nature communications · 2017Article
- DFNA5 promoter methylation a marker for breast tumorigenesis.Oncotarget · 2017Article
- The role of molecular biomarkers for predicting adjacent breast cancer of Atypical Ductal Hyperplasia diagnosed on core biopsy.Cancer biomarkers : section A of Disease markers · 2016Article
- Molecular Portrait of the Normal Human Breast Tissue and Its Influence on Breast Carcinogenesis.Journal of breast cancer · 2016Review
- Computational Cancer Biology: An Evolutionary Perspective.PLoS computational biology · 2016Review
- 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
- Spontaneous slow replication fork progression elicits mitosis alterations in homologous recombination-deficient mammalian cells.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Nuclear nano-morphology markers of histologically normal cells detect the "field effect" of breast cancer.Breast cancer research and treatment · 2012Article
- Gene expression profiles of estrogen receptor-positive and estrogen receptor-negative breast cancers are detectable in histologically normal breast epithelium.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Novel molecular markers of malignancy in histologically normal and benign breast.Pathology research international · 2011Article
- AKT1/BRCA1 in the control of homologous recombination and genetic stability: the missing link between hereditary and sporadic breast cancers.Oncotarget · 2010Review
- Quantitative evaluation of DNA hypermethylation in malignant and benign breast tissue and fluids.International journal of cancer · 2010Article
- SNAI1 expression in colon cancer related with CDH1 and VDR downregulation in normal adjacent tissue.Oncogene · 2009Article
- Cell-cell contact interactions conditionally determine suppression and selection of the neoplastic phenotype.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- [The significance of "normal tissue" in the development of breast cancer: new concepts of early carcinogenesis].Der Pathologe · 2006Article
- p16(INK4a) prevents centrosome dysfunction and genomic instability in primary cells.PLoS biology · 2006Article
- 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
- Missense mutations but not allelic variants alter the function of ATM by dominant interference in patients with breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Breast cancer is believed to develop as multiple genetic abnormalities accumulate, each conferring some growth advantage, but the timing and nature of the earliest steps in this progression are not yet elucidated. Proliferative breast lesions, associated with an increased risk of breast cancer although considered benign, recently were shown to contain clonal genetic abnormalities. Therefore, we hypothesized that clonal genetic abnormalities might be detectable before any phenotypic abnormalities are evident, ie, in histologically normal breast tissue. We examined DNA extracted from 95 normal-appearing breast ducts or terminal ductal-lobular units from 20 individuals at varying degrees of risk (those undergoing reduction mammoplasties, those with atypical hyperplastic proliferative lesions, and those already diagnosed with breast cancer). Using nine microsatellite markers, we sought evidence of genetic instability or of allelic imbalance (most likely representing loss of heterozygosity). We found genetically abnormal clones in 21/95 (22%) seemingly normal samples from 10/20 (50%) women from all three risk groups. In women under age 50, trends toward increased rates of abnormalities were noted with increased cancer risk. The abnormalities identified were more likely to be at sites of known or postulated tumor suppressor genes rather than at random or neutral loci. Our data indicate that genetic abnormalities potentially critical to breast tumorigenesis accumulate before pathological detection even of high-risk lesions and are detectable in tissue that is not only histologically benign but also completely normal.
Indexed as
Identifiers
9626062PMC1858443W2415836231What OpenQuestion holds
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.