The epithelial component of normal and noninvasive breast tumor tissue is physically separated from the stroma by both the myoepithelial cells and the basement membrane (BM). Myoepithelial cells are joined by intermediate or gap junctions and a number of intercellular adhesion molecules, forming a continuous sheet or belt that encircles the epithelial cells (except at the terminal ductal-lobular unit, within which about 20% of the epithelial cells are reported to be in direct contact with the BM) BM = basement membrane; DCIS = ductal carcinoma in situ; ER = estrogen receptor; H & E = hematoxylin and eosin; LOH = loss of heterozygosity; MI = microsatellite instability; PCR = polymerase chain reaction; SMA = smooth muscle actin. AbstractIntroduction Our previous studies detected focal disruptions in myoepithelial cell layers of several ducts with carcinoma in situ. The cell cluster overlying each of the myoepithelial disruptions showed a marked reduction in or a total loss of immunoreactivity for the estrogen receptor (ER). This is in contrast to the adjacent cells within the same duct, which were strongly immunoreactive for the ER. The current study attempts to confirm and expand previous observations on a larger scale.

The epithelial component of normal and non-invasive breast tissues is normally surrounded by a layer of myoepithelial (ME) cells, whose absence or disruption is an absolute prerequisite for tumor invasion and metastasis [1]. ME cells are not easily identifiable in hematoxylin/eosin (H&E)-stained breast tissue sections, as they are often indistinguishable from subjacent myofibroblastic cells in the stroma. Immunohistochemical staining for smooth muscle actin (SMA) has been routinely used to assist in the identification of ME cells [2]. However, we and others have repeatedly noted that about 4-6% of morphologically recognizable ME cells in H&E-stained sections fail to display SMA immunoreactivity [3,4]. We attempted to assess whether these SMA-negative cells also lack the expression of eight additional markers that are supposed to present exclusively or preferentially at ME cells. Materials and methods Case selectionFormalin-fixed, paraffin-embedded tissue blocks from female patients with breast lesions were retrieved from files of the Armed Forces Institute of Pathology. Consecutive sections at 4-5 µm thickness were cut and placed on CK = cytokeratin; ER = estrogen receptor; H&E = hematoxylin/eosin; ME = myoepithelial; SMA = smooth muscle actin; SM-MHC = smooth muscle myosin heavy chain; WT-1 = Wilms' tumor-1. (Print ISSN 1465-5411; Online ISSN 1465-542X). This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. AbstractIntroduction: Immunostaining for smooth muscle actin (SMA) is commonly used to elucidate mammary myoepithelial (ME) cells, whose presence or absence is a reliable criterion for differentiating in situ and invasive carcinomas. However, some morphologically distinct ME cells fail to stain for SMA. This study intended to assess whether these SMA-negative cells also lack the expression of other ME cell markers.

A case of pathologically proven extraskeletal osteochondroma is presented with magnetic resonance imaging (MRI), computed tomography (CT), bone scan and radiographic findings. The diagnosis of extraskeletal osteochondroma should be considered when a discrete, ossified mass is localized in the soft tissues of the distal extremities. Nomenclature surrounding this entity is controversial and is discussed.

No abstract

Goblet cell carcinoid (GCC) is a rare but distinctive neoplasm with features of both adenocarcinoma and carcinoid tumor. Most cases described in the literature have occurred in the appendix. An additional well-defined location is the ovary, and these tumors have been associated with a mature teratoma of the ovary. GCC arising within a mature teratoma of the mediastinum has not been described in the English-language literature. We report a case of this previously undescribed entity and provide a review of the literature on mediastinal teratomas with malignant transformation. The histologic findings included uniform, smooth-bordered glandular nests lined by goblet cells and admixed endocrine and Paneth cells. Occasional tubular glands were present, as were transitional type glands with both goblet cell and tubular features. Cytologic atypia was minimal, and mitotic activity was rare. Immunohistochemical studies showed positive staining of GCC tumor cells with chromogranin, cytokeratin, neuron-specific enolase, serotonin (focal), and Leu-7 (focal). The GCC component was entirely contained within the mature teratoma.