Abstract
Abstract The two main histological types of infiltrating breast cancer, lobular (ILC) and the more common ductal (IDC) carcinoma are morphologically and clinically distinct revealing different patterns of chromosomal aberrations and gene expression. Loss of heterozygosity (LOH) at chromosome 3p is frequently observed in breast tumors and a whole genome study utilizing a SNP array assay found a significantly higher frequency of LOH on 3p in ductal than lobular tumors. In order to investigate the molecular alterations at 3p associated with these breast cancer subtypes we analyzed LOH in 118 IDC and 18 ILC samples using seven microsatellite markers. Genomic DNA was obtained from frozen tumor tissue and peripheral blood was used as a normal reference. All samples were genotyped on a MegaBace® system and analyzed using Fragment Profiler® Version 2.1 software. Significance was determined using Chi-square test (X2). A significant higher frequency of LOH was observed in IDC (62.7%) when compared with ILC (38.9%) (X2=4.60 P<0.05). When the markers were analyzed separately, LOH at three of them, D3S1307 in 3p26.3, D3S1286 in 3p24.3 and D3S1300 (intragenic FHIT) in 3p14.2, were significantly more frequent in ductal than lobular tumors (X2= 4.66 P<0.05; X2= 3.99 P<0.05 and X2= 5.43 P<0.025, respectively). D3S1307 marker showed the highest frequency of LOH in IDC (47.8%) and associations between loss of this marker and loss of estrogen and progesterone receptors were found in these samples (X2= 4.61 P<0.05 and X2= 4.49 P<0.05, respectively) suggesting that there are genes on this region involved in the control of differentiation of ductal tumors. For lobular tumors, the highest loss (53.3%) was seen for D3S1274 on 3p12.3 (intragenic DUTT1). In addition to confirm previous studies these findings suggest that specific losses on 3p (3p26.3, 3p24.3 and 3p14.2) are more common in IDC when compared with ILC breast tumors. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2158.
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