Fig. 2: Bcl9 and Bcl9L are highly expressed in invasive breast cancers.

A Malignant tumor progression in MMTV-PyMT transgenic mice. Histological sections taken from tumors of MMTV-PyMT transgenic mice were stained with hematoxylin and eosin to visualize the different cancer progression stages (hyperplasia: increased amount of single cell layer epithelial tissue: adenoma: increased volumes of multi-layered epithelial structures; early invasive ductal carcinoma: invasion of tumor fronts, loss of epithelial differentiation; late invasive ductal carcinoma: single cell invasion, substantial loss of epithelial differentiation). The expression of estrogen receptor (ER), progesterone receptor (PR), and Her2 in the different progression stages is indicated below the panels. B Bcl9, Bcl9L, and β-catenin protein expression during MMTV-PyMT tumor progression. Histological sections taken from tumors of MMTV-PyMT transgenic mice were stained for Bcl9, Bcl9L, and β-catenin protein in different stages of MMTV-PyMT tumor progression. Rectangles indicate higher magnifications to visualize nuclear localization of Bcl9, Bcl9L, and β-catenin. Scale bar, 100 μm. C Analysis of BCL9 and BCL9L copy number alterations frequencies in different human breast cancer (BRCA) subtypes reveals a high enrichment of BCL9 amplifications in basal, Her2, luminal A and B breast cancer subtypes and, in comparison, a lower enrichment of BCL9L amplifications in the luminal B subtype. NA not annotated. D Disease/progression-free Kaplan–Meier (disease free status since initial treatment) estimate for patients with and without BCL9 gene alterations (cBioportal online tool). In contrast to BCL9, BCL9L gene alterations showed no significant impact on clinical outcome in this data set (not shown).