The Fine Structure of the Basement Membrane in Epidermal Tumors

Frei, J

doi:10.1083/jcb.15.2.335

Cited by 86 publications

(24 citation statements)

References 32 publications

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“…The most likely mechanism for the destruction at this junction still seems to be enzymatic, but the precise nature of this important alteration awaits elucidation. Pseudopodia have been described previously in premalignant and malignant lesions (Frei, 1962;Tarin, 1967;Frithiof, 1969;Woods & Smith, 1969Gould et al, 1975;White & Gohari, 1981b;Smith, 1981) and it has been suggested that they may have some role in the release of enzymes which may be responsible for the destruction of the underlying connective tissue. We have described the presence of small electrondense vacuoles which resemble lysosomal dense bodies (White & Gohari, 1981b;White et al, 1981) and these structures may provide the mechanism for these lytic processes.…”

Section: Discussionmentioning

confidence: 99%

Quantitative studies of hemidesmosomes during progressive DMBA carcinogenesis in hamster cheek-pouch mucosa

White¹,

Gohari²

1981

Br J Cancer

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Section: Discussionmentioning

confidence: 99%

Quantitative studies of hemidesmosomes during progressive DMBA carcinogenesis in hamster cheek-pouch mucosa

White¹,

Gohari²

1981

Br J Cancer

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“…Abnormal bulging pseudopodia have been observed in vitro on human colon cancer cells (17) and on astrocytes that have been transformed by Rous sarcoma virus (25), but neither of these studies related the surface protrusions to the distribution of alpha filaments. In vivo, pseudopodial protrusions from the cancer cell surface have been observed in squamous cell carcinomas (9,18,42,46) and adenocarcinomas (14). These pseudopodia have often been considered as the earliest indication of malignant invasion (9,46).…”

Section: Discussionmentioning

confidence: 99%

“…Stoker (44) has reported that multiple pseudopodia appear on cells within 18 h after infection with a transforming virus. Pseudopodia also appear early in chemical carcinogenesis (18,49). However, pseudopod formation is not restricted to malignancy since other studies show that regenerating stratified squamous epithelia also have large pseudopodia (33,40,41).…”

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confidence: 99%

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Contact-Inhibited Revertant Cell Lines Isolated From Sv40-Transformed Cells

McNutt

Culp

Black

1973

The Journal of Cell Biology

158

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A comparison is made of the ultrastructure of the cell periphery in three cloned cell lines: untransformed Balb/c 3T3 cells, SV40-transformed Balb/c 3T3 cells, and revertant cells obtained from the transformed cell line by a selection technique utilizing concanavalin A. Both thin-section and surface replication techniques are used for in situ examination of the cell lines. Microfilaments, 70 Å in diameter (called alpha filaments), are abundant in untransformed and revertant cell lines, particularly in the anterior expansions of the cells, which tend to have many microvilli and small pseudopodia. Alpha filaments are diminished in the anterior expansions of transformed cells, which contain large blunt pseudopodia and relatively few microvilli. Surface replicas confirm the impression gained from thin sections that transformed cells have a greater proportion of their cell surface involved in bulging pseudopodia than either untransformed or revertant cells. Since alpha filaments are shown to bind heavy meromyosin and are similar to F-actin, these filaments are thought to be important in cell motility. These observations suggest that a close relationship exists between decreased alpha filaments, bulging pseudopodia, and loss of contact inhibition of movement in transformed cells.

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“…1983. The mor phology of BMs in invasive carcinomas has been studied for more than sixty years [Broders, 1932;Frei, 1962;Vracko, I974;Abrahamson. I986: Van Den Hooff.…”

Section: Introductionmentioning

confidence: 99%

The Basement Membrane and Its Involvement in Carcinoma Cell Invasion

Flug

Köpf-Maier²

1995

Cells Tissues Organs

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During the development of invasive cancer, carcinoma cells have to penetrate the extracellular matrix including the basement membrane (BM). This is a usually continuous layer composed of a dense meshwork of collagens, glycoproteins and proteoglycans. It normally underlies epithelia and lacks any pores large enough to allow epithelial cells to pass through them. In consequence, the invasion of carcinoma cells through the BM must be either an active process effected by the carcinoma cells themselves or is mediated by structural alterations of the BM occurring during carcinogenesis and cancer progression. It was supposed by many authors that invading and metastasizing carcinoma cells are able to degrade actively the continuous, uninterrupted BM by secreting type IV collagenase and other proteolytic enzymes. Although there is a wealth of experimental evidence which fits the concept that the active degradation of the BM is an essential requirement for carcinoma cell invasion and metastasis, certain data do not agree with this hypothesis. Thus, it is still doubtful whether active lysis of the BM by carcinoma cells is actually a prerequisite for invasion and metastasis or whether there are alternative and/or additional mechanisms favoring the invasion of carcinoma cells.

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The Fine Structure of the Basement Membrane in Epidermal Tumors

Cited by 86 publications

References 32 publications

Quantitative studies of hemidesmosomes during progressive DMBA carcinogenesis in hamster cheek-pouch mucosa

Quantitative studies of hemidesmosomes during progressive DMBA carcinogenesis in hamster cheek-pouch mucosa

Contact-Inhibited Revertant Cell Lines Isolated From Sv40-Transformed Cells

The Basement Membrane and Its Involvement in Carcinoma Cell Invasion

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