Triple negative breast cancer phenotypes: a comparison between symptomatic and screening patients.

Abstract #2085 Body: Background: Triple-negative breast cancers are defined by a lack of expression of oestrogen, progesterone, and HER-2 receptors. Prognostically, they are associated with a poor clinical outcome. It is uncertain whether during growth and maturation of a breast cancer its phenotype may drift from one which over-expresses ER, PR and HER-2 towards a tumor type that loses this expression. In the UK women are screened for breast cancer between the ages of 50 and 70 years, which provides us with a cohort of patients whose breast cancers are at a much earlier stage than those presenting symptomatically. Thus if phenotypic drift occurred the screening population might have a lower incidence of triple negative tumors compared to those presenting symptomatically.
 Aim: To compare the incidence of triple negative tumors in a screening and symptomatic population. Materials and Methods: Pathology reports for 2002 to 2004 inclusive were scrutinized for ER PR and HER-2 expression. A list of screening patients was retrieved from our screening database and cross-referenced with pathology reports. Immunohistochemistry (IHC) was used to quantify ER and PR expression, a quick score of 4 or less was negative for over-expression. Similarly IHC was used to quantify HER-2 expression, and a score of 0 or 1+ was negative for over-expression. clinical data, such as patient age, lymphovascular invasion, lymph node status, tumor size, and grade were available for statistical analysis. Results: There were 213 screening patients of which, 31 (14.5%) had triple negative phenotypes and 443 symptomatic patients of which, 73 (16.4%) were triple negative. This difference was not statistically different. Discussion: The incidence of Basal-like breast tumors is similar in the screening group compared to the symptomatic population suggesting that this aspect of tumor biology is determined at a very early stage in the development of tumors and is not subject to phenotypic drift. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 2085.