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Primary and metastatic carcinomas have a reactive stroma characterized by many myofibroblasts. These cells have also been documented in nonepithelial malignancies, such as sarcomas, malignant melanoma, and lymphoid tumors but in generally far fewer numbers. In non-Hodgkin's lymphoma, Hodgkin's disease, and leukemia, myofibroblasts are rather rarely documented. In particular, there appear to be no reports of myofibroblasts in either primary bone-marrow/peripheral blood leukemia or secondary deposits of leukemia. In this paper, a case of a relapsed chronic myeloid leukemia appearing in an inguinal lymph node is described, containing many myofibroblasts. The case is detailed and presented with a discussion on the role of myofibroblasts in the progression of nonepithelial cancers. [ABSTRACT FROM AUTHOR]

The fibronexus is recognized as a characteristic marker of the myofibroblast. However, it is not completely specific for this cell, having been seen in aortic smooth muscle (in attenuated form) and endothelium in experimental animals. This paper documents fibronexus junctions in human in vivo endothelium. Ultrastructural observations were made on the vasculature of a desmoplastic and focally neurotropic malignant melanoma. Cross-sectioned fibronectin fibrils were seen outside the stromal surface of the endothelial plasmalemma. Often, they were positioned directly opposite the actin-filament bundles in the peripheral cytoplasm. Neoplastic and in vitro cultured cells apart, endothelium is the only nonmyofibroblastic cell type to show well-developed fibronexus junctions. Mostly, they have been documented in aortic endothelium in experimental animals, where they possibly constitute an adaptation to hemodynamic stress, and where they might more securely anchor endothelium on to subjacent connective tissue. They might also function as mechanotransducers of extracellular stress in the extracellular milieu. The present observations constitute a further, rare example of endothelium-associated fibronexuses in reactive human vessels. [ABSTRACT FROM AUTHOR]

Cellular transformations, reflecting phenotypic plasticity. characterize embryonic life, would-repair, physiological adaptation, and neoplasia. Fibroblastic tumors show a range of cellular differentiation, which can be rationalized in terms of phenotypic plasticity of the "normal" fibroblast. In this paper. the various kinds of fibroblast transformation are discussed, and some insights provided into the molecular mechanisms involved. Comparable molecular events may take place in neoplastic fibroblasts to produce the heterogeneous tumors nevertheless identified as fibroblastic. The following transformations are discussed: histiocytic, and fibrohistiocytic tumors; adipocytic, and lipogenic tumors; myofibroblastic, and myofibroblastic tumors. A definition of the fibroblast is required. This consists of spindle-cell morphology, vimentin- staining, and abundant rough endoplasmic reticulum. Transformation to histiocytic, lipogenic and myofibroblastic phenotypes requires the development of lysosomes, lipid droplets and lamina, and peripheral myofilaments and fibronexuses respectively. These occur in non-malignant transforming (transdifferentiating) fibroblasts, and also in tumors identified as fibrohistiocytic, lipogenic and myofibroblastic. The molecular basis of the myofibroblast transformation is probably the best studied. It is driven primarily by transforming growth factor ft Investigations into the mechanisms of differentiation in normal fibroblasts could prove fertile ground for defining comparable differentiation in tumors. In this respect, there are very few publications on the presence of growth factors in tumors or tumor like lesions. There is, however, increasing investigation into gene expression and gene products in tumors, which bear on the differentiation process. Ultimately, our understanding of the molecular events controlling differentiation in cancer will lead to control, cure and prevention. [ABSTRACT FROM AUTHOR]

Some interpretational problems associated with the myofibroblast, which affect how this cell is identified, are discussed. Questions addressed include distinguishing between "external" lamina ("basement membrane") and the fibronectin fibril of the fibronexus; the nature of stress fibers (bundles of smooth-muscle myofilaments with focal densities); the utility of some of these features to distinguish between myofibroblastic and smooth-muscle cell surfaces; and cytoskeletal immunophenotype. The following points are emphasized. Myofibroblasts have a surface characterized by prominent fibronectin fibrils and fibronexus junctions, which are distinct from lamina ("basement membrane"). This can permit a distinction to be made between smooth-muscle and myofibroblastic lesions and tumors. Myofibroblasts are typically positive for vimentin and α-smooth-muscle actin, but desmin is not a useful discriminant between smooth-muscle and myofibroblastic lesions. The main features for defining the myofibroblast are abundant rough endoplasmic reticulum; modestly developed peripheral myofilaments with focal densities (stressfibers); fibronexus junctions; vimentin and smooth-muscle actin immunostaining. Other features include a Golgi apparatus and collagen secretion granules, gap junctions, and actin-associated nondesmosomal junctions. Illustrations of the usefulness of these criteria in the diagnosis of soft-tissue lesions (myofibrosarcoma, so-called myofibroblastoma) are given. [ABSTRACT FROM AUTHOR]

The article reports on the structural characterization of myofibroblasts in the bladder by researchers from Manchester, England. The cellular physiology of the lower urinary tract is in an exciting phase thanks to the identification of a novel cell type, present in the bladder within the detrusor and in the suburothelial space. Such cells might have the potential to intercede in several fundamental processes, including processing of sensory information, pacemaking, and modulating contractile function.

To clarify the characteristics and origin of the cellular components in atherosclerosis, carotid atherosclerotic plaques (CAPs) of four patients were studied by light microscopy using hematoxylin-eosin, Congo red and alpha-smooth-muscle actin stains, and by transmission electron microscopy of different regions of CAPs. By light microscopy, CAPs were composed of 1) a fibrous cap; 2) an atherosclerotic core presenting focal fibrosis, neovascularization, hemorrhage, necrosis, chondrification and ossification; and 3) a basal band composed of a hyperplasic pseudo-media and affected tunica media. Ultrastructurally, the CAPs contained a diversity of cells including fibroblasts, myofibroblasts, osteochondrocytes, vascular smooth-muscle cells, foam cells and other myoid cells characterized by varied features of the above mentioned cells. The results indicated that CAPs were derived from a proliferation of multipotential mesenchymal stem cells, leading to the presence of degenerated foam cells and lipid-laden cells. [ABSTRACT FROM AUTHOR]