Invasive Lobular Cancer Arising in a Surgical Scar From Lumpectomy for a Previous Invasive Ductal Cancer of the Breast.

We describe a case of pathology-proven invasive lobular breast cancer (ILC) arising in a scar over 15 years after lumpectomy for previous invasive ductal carcinoma (IDC). The tumor was detected on screening mammography as a new focal asymmetry at the scar site and confirmed at diagnostic mammography. Ultrasound demonstrated an irregular, shadowing, hypoechoic mass at the scar site. Ultrasound-guided biopsy revealed poorly differentiated invasive lobular carcinoma. MRI and CT showed an irregular mass with pectoralis muscle invasion. Multimodality imaging findings are described. This is the first case to our knowledge reporting multimodality imaging findings of a breast cancer developing at the site of a surgical scar that is histologically different from the originally resected cancer.

JAM-A is both essential and inhibitory to development of hepatic polarity in WIF-B cells.

Junctional adhesion molecule (JAM) is involved in tight junction (TJ) formation in epithelial cells. Three JAMs (A, B, and C) are expressed in rat hepatocytes, but only rat JAM-A is present in polarized WIF-B cells, a rat-human hepatic line. We used knockdown (KD) and overexpression in WIF-B cells to determine the role of JAM-A in the development of hepatic polarity. Expression of rat JAM-A short hairpin RNA resulted in approximately 50% KD of JAM-A and substantial loss of hepatic polarity, as measured by the absence of apical cysts formed by adjacent cells and sealed by TJ belts. When inhibitory RNA-resistant human JAM-A (huWT) was expressed in KD cells, hepatic polarity was restored. In contrast, expression of JAM-A that either lacked its PDZ-binding motif (huDeltaC-term) or harbored a point mutation (T273A) did not complement, indicating that multiple sites within JAM-A's cytoplasmic tail are required for the development of hepatic polarity. Overexpression of huWT in normal WIF-B cells unexpectedly blocked WIF-B maturation to the hepatic phenotype, as did expression of three huJAM-A constructs with single point mutations in putative phosphorylation sites. In contrast, huDeltaC-term was without effect, and the T273A mutant only partially blocked maturation. Our results show that JAM-A is essential for the development of polarity in cultured hepatic cells via its possible phosphorylation and recruitment of relevant PDZ proteins and that hepatic polarity is achieved within a narrow range of JAM-A expression levels. Importantly, formation/maintenance of TJs and the apical domain in hepatic cells are linked, unlike simple epithelia.