Expression of E-cadherin, α-catenin, and β-catenin in tubulolobular carcinoma of the breast

Abstract

Tubulolobular carcinoma (TLC) of the breast is a rare subtype of breast carcinoma categorized by Fisher et al. (Hum Pathol 8:679-683, 1977) as a tubular variant of lobular carcinoma. E-cadherin is a transmembrane glycoprotein, and complete loss of E-cadherin expression has been observed in invasive lobular carcinoma. Ductal carcinoma retains at least some expression of E-cadherin. Moreover, the adhesive function of E-cadherin is dependent on the integrity of the catenin components, which link E-cadherin to the actin filaments. In order to achieve improved categorization of TLC, we decided to investigate both E-cadherin and the catenins in TLCs and invasive lobular carcinomas. We reviewed all 1,430 cases of primary breast carcinoma that were surgically resected at Saitama Medical Center, Saitama Medical School, and at Saitama Red Cross Hospital between 1990 and 2005. Among these, 16 cases of TLC were reported retrospectively. The results were compared with those of 20 cases of invasive lobular carcinomas that were included as controls. Tumor tissue was immunostained for E-cadherin, alpha-catenin, and beta-catenin. The presence of immunoreactivity in the TLC was seen in 12 (75%) cases for E-cadherin, in 8 (50%) cases for alpha-catenin, and in 10 (62.5%) cases for beta-catenin. However, plasma-membrane-associated staining for E-cadherin, alpha-catenin, and beta-catenin was completely absent in invasive lobular carcinomas. These results suggest the possibility that TLCs are not a variant of lobular carcinoma, but rather ductal carcinomas with a lobular growth pattern.

Bench to bedside and back again: Molecular mechanisms of α-catenin function and roles in tumorigenesis

“…These resulting juxta-membrane α-catenin dimers bundle actin filaments and suppress actin assembly by inhibiting the Arp2/3 complex; under these conditions, cell-cell adhesion is high and cell migration/membrane dynamics are low. [47,51,86,[107][108][109][110][111][112][113][114][115][116][117][118][119] Histological type and growth [51], grade [47,112,117], stage [47], metastasis [47], survival [47,111] Survival [47], reduced more frequently in diffuse tumors [51] …”

Identification of a claudin‐4 and E‐cadherin score to predict prognosis in breast cancer

“…(5) Studies evaluating the expression of E-cadherin report the loss of these molecules in approximately 80% of lobular carcinomas. (6)(7)(8)(9)(10) Claudin (CLDN) tight junction molecules were originally described by Furuse et al in 1998. (11) In the past decade, there have been multiple attempts to evaluate their expression in several pathological states and organs.…”

Wnt Signaling Pathway in Invasive Ductal Carcinoma of the Breast: Relationship between β-Catenin, Disheveled and Cyclin D1 Expression

“…The role of β-catenin in the linkage between α-catenin and E-cadherin in the cadherin/catenin complex is probably regulated by epidermal growth factor-mediated tyrosine phosphorylation of β-catenin [11, 12]. The components of the cadherin/catenin complex are implicated in differentiation and tumor progression, as their reduced expression is not only frequent in poorly differentiated tumors, but might also produce loss of adhesiveness and increased invasive and metastatic potential [13,14,15]. In the absence of a Wnt signal, β-catenin levels are kept low through interactions with glycogen synthase kinase-3β (GSK3β), casein kinase-1α (CK1α), APC and axin [16,17,18].…”