Presentation Abstract

Abstract Number: 2779
Presentation Title: Relationship of mammographic density with breast cancer subtypes
Presentation Time: Monday, Apr 19, 2010, 2:00 PM - 5:00 PM
Location: Exhibit Hall A-C, Poster Section 34
Poster Section: 34
Poster Board Number: 4
Author Block: Gretchen L. Gierach1, Jolanta Lissowska2, Montserrat Garcia-Closas1, Xiaohong R. Yang1, Jonine D. Figueroa1, Sarah Anzick1, Ewa Wesolowska2, Louise A. Brinton1, Paul S. Meltzer1, Norman F. Boyd3, Mark E. Sherman1. 1National Cancer Institute, Bethesda, MD; 2Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Warsaw, Poland; 3Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, Toronto, ON, Canada
Abstract Body: Background: Mammographic density (MD), a measure of the amount of radiologically dense breast tissue, is one of the strongest breast cancer risk factors. Studies have found that high MD increases risk for both estrogen receptor (ER)-negative and positive breast cancers, but data relating MD to breast cancer subtypes are limited.
Methods: We used data from the population-based Polish Breast Cancer Study to explore relationships between MD and breast cancer characteristics. This analysis includes 227 invasive breast cancers, which were available as frozen samples and used for mRNA and cytogenetic profiling, and fixed tissues, which were prepared as tissue microarrays for immunohistochemical analysis. Pre-treatment mammograms of the unaffected breast were retrieved for 184 (81%) cases ages 28-75 years. Craniocaudal views of digitized films were used to assess percent MD with Cumulus, a computer-assisted thresholding method. Analysis of variance (ANOVA) models were used to test the null hypothesis of no mean difference in MD between the breast cancer subtypes.
Results: Tumor subtypes were classified by key immunohistochemical markers as luminal A (ER+ and/or progesterone receptor (PR)+, human epidermal growth factor receptor-2 (HER2)-; n=129), luminal B (ER+ and/or PR+, HER2+; n=6), HER2-expressing (ER-, PR-, HER2+; n=13), basal-like (ER-, PR-, HER2-, cytokeratin 5+, and/or HER1+; n=23), and unclassified (negative for all five markers; n=8). Five cases did not have interpretable staining for all five markers and were excluded. MD values were approximately normally distributed. Preliminary ANOVA models revealed no differences in mean percent MD by tumor subtypes (p=0.29) as follows: luminal A, 27.5% (95% confidence interval (CI): 24.9-30.2); luminal B, 27.0% (95% CI: 14.8-39.2); HER2-expressing, 27.2% (95% CI: 18.9-35.5); basal-like, 24.6% (95% CI: 18.4-30.8); and unclassified, 15.7% (95% CI: 5.2-26.3). In analysis of covariance models adjusted for age there was marginal evidence of elevated MD with the HER2-expressing subtype (p=0.04), but we cannot exclude the possibility that this is a chance finding.
Conclusions: Our results do not provide strong support for an association between percent MD and breast cancer subtypes. To identify additional clues as to the biology underlying the MD-breast cancer relationship, ongoing analyses will relate MD to mRNA and cytogenetic profiles and data for protein expression via immunohistochemistry available for additional markers as previously reported.