Immunohistochemical staining patterns of tenascin in invasive breast carcinomas

Abstract

Eighty-two cases of primary invasive breast carcinoma and adjacent "normal" mammary glands were examined immunohistochemically for tenascin expression and distribution. Formalin-fixed tissues pretreated with actinase were processed by the avidin-biotin complex method using anti-human tenascin monoclonal antibody (RBC1). In normal mammary glands, tenascin was distributed around the ducts and ductules but not around the acini. In carcinomas, a high incidence of tenascin-positive cases (greater than 67%) was seen with various histological appearances, with the exception of lobular carcinoma where a low incidence was found (25%). Although intense staining was seen around cancerous foci when compared with normal mammary glands, tenascin was often expressed at cancer-mesenchymal junctions with dense fibrotic stroma, but not at junctions with active inflammatory change and a loose fibrotic stroma. Tenascin, expression is not an all-or-none marker for mammary malignancy and the staining pattern suggests either a role in stimulating cancer cells or a host defence mechanism accompanied by a desmoplastic response to them.

The borderline: Basement membranes and the transition from premalignant to malignant neoplasia

“…No consistent differences in tenascin localization were found among different types of carcinoma in various tissues. Tumors that exerted a desmoplastic reaction, however, showed more tenascin staining, as was also observed by Shoji et al (1992), whereas the reverse was observed in tumors with scanty stroma, such as carcinoids. In pleomorphic adenomas of the salivary gland, Soini et al (1992) observed tenascin staining in the stromal compartment, especially in dense stroma and in chondroid areas.…”

Tenascin expression in inflammatory, dysplastic and neoplastic lesions of the human stomach

“…In advanced tumours of both DGCA and IGCA, Tn immunoreactivity in the stroma was markedly increased. These findings are in keeping with previous data on invasive tumours [16,22,26]. Metastatic islets and cell lines of DGCA and IGCA differed in their immunoreactions for Tn.…”

Ets transcription factors cooperate with Sp1 to activate the human Tenascin-C promoter

“…TN-C is generally found at low levels in the normal adult tissues, but is upregulated in some physiological and pathological conditions including wound healing, in¯ammatory lesions, ®brosis and in cancer tissues (ChiquetEhrismann et al, 1995;Crossin, 1996;Mackie, 1997). Studies have demonstrated elevated TN-C expression in various human cancers, including breast (Shoji et al, 1992;Yoshida et al, 1997), lung (Kusagawa et al, 1998), colon (Sakai et al, 1993;Hanamura et al, 1997), and liver (Yamada et al, 1992). TN-C is expressed in both cancer and stromal cells, suggesting a possible role in invasive properties of the cancer cells themselves as well as in the remodeling of cancer stroma.…”