Original ContributionsMolecular and genetic abnormalities in radial scar*,**
Section snippets
Histology and immunostaining
Blocks and slides of 17 patients with RS were retrieved from the files of the Pathology Department of the Royal Liverpool University Hospital, spanning an 11-year period. Slides stained with hematoxylin and eosin were reviewed to identify foci of different histologies within and outside RS. Cases that contained invasive or in situ carcinoma were excluded from the study. The cases of RS selected were from patients age 40 to 67 years.
For immunostaining, tissue samples were processed and stained
Distribution of ER+ cells in HUT
Seventy-one foci of HUT within RS (mean, 4.2 per patient; range, 1 to 11) were studied by a dual-labeled immunofluorescent technique, using ER and Ki67 antibodies. Like HUT foci outside RS, reported earlier,11 the staining pattern was heterogeneous (Table 1) and ER expression was positively correlated with age (Spearman's rho, r = 0.34, P = 0.001).HUT Subgroup N (%) % ER+: Mean (SD) % Dual+ Cells: Mean (SD) Dual+ ER+ HUT HUT in RS HUT HUT in RS HUT
Discussion
In the current study we looked at the same molecular markers in HUT foci within RS as we previously studied in HUT independent of RS11 and additional markers of AI at 2 loci implicated in breast tumorigenesis. The RS identified and selected for the study were of larger size to allow for both microdissection and for counting of sufficient numbers of epithelial cells, but did not show any concurrent malignant component. Such lesions are associated with a higher relative risk of malignancy.6, 7
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Cited by (23)
Diagnostic Pathology: Cytopathology
2018, Diagnostic Pathology: CytopathologyBenign sclerosing lesions of the breast – an update
2017, Diagnostic HistopathologyCitation Excerpt :As previously mentioned, Jacobs et al12 reported similarities in the expression of factors involved in vascular stroma formation between the two lesions, suggesting similarities in the stromal–epithelial balance between them. Iqbal et al21 reported molecular and genetic changes in a minority of radial scars similar to those seen in breast carcinomas. The finding in follow-up studies of radial scars that subsequent malignancy is just as likely to occur in the contralateral as in the ipsilateral breast, and the conclusion of Sanders et al17 in the largest study to date of its kind that there is little increased risk of subsequent carcinoma above that of the background proliferative disease (typical or atypical), argues against radial scars being precursors to carcinoma.
Diagnostic Pathology: Breast
2017, Diagnostic Pathology: BreastRadial scars diagnosed on breast core biopsy: Frequency of atypia and carcinoma on excision and implications for management
2016, BreastCitation Excerpt :The exact nature of the relationship between radial scar and neoplasia remains poorly understood. Molecular studies of radial scars have demonstrated some features that are similar to invasive carcinomas [34,35]. Data from the Nurses' Health Study suggested the carcinomas that develop in patients with radial scar may be more likely to be hormone receptor-negative [14].
Benign sclerosing lesions of the breast
2009, Diagnostic HistopathologyCitation Excerpt :As previously mentioned, Jacobs et al12 reported similarities in the expression of factors involved in vascular stroma formation between the two lesions, suggesting similarities in the stromal–epithelial balance between them. Iqbal et al21 reported molecular and genetic changes in a minority of radial scars similar to those seen in breast carcinomas. The finding in follow-up studies of radial scars that subsequent malignancy is just as likely to occur in the contralateral as in the ipsilateral breast, and the conclusion of Sanders et al17 in the largest study to date of its kind that there is little increased risk of subsequent carcinoma above that of the background proliferative disease (typical or atypical), argues against radial scars being precursors to carcinoma.
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Supported in part by a Clatterbridge Cancer Research Trust Mavis Horwich Fellowship.
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Address correspondence and reprint request to Michael P.A. Davies, MD, Clatterbridge Cancer Research Trust, J.K. Douglas Laboratories, Clatterbridge Hospital, Bebington, CH63 4JY, UK.