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I Buckley

Publications and source records attributed to I Buckley.

6 recordsLinked to original sources
PubMed1985

The phenotypic nature of malignancy--an hypothesis.

Malignant cells exhibit two constant behavioural features which together determine lethality: cell proliferation and invasion. Since proliferation alone produces only benign tumours, invasion is the key to malignancy. All tissue cells are inherently motile, so it is argued that invasion will occur in vivo whenever cell movement is not under control. From embryological studies it is understood that movement is normally controlled by interacting sets of cell surface recognition molecules. Accordingly it is hypothesized that the prime phenotypic defect in malignancy is loss (or masking) of the malignant cells' recognition molecules. It is believed that malignant transformation occurs in stem cells at critical differentiation "switching" steps involving changes in surface phenotype. A cell recognition defect could arise therefore if cell surface marker deletion is not followed by full expression of a complete set of new markers. Investigation of such a possibility could test the hypothesis.

Animals↗
PubMed1983

Ciliary but not saltatory movements are inhibited by vanadate microinjected into living cultured cells.

To test the idea that saltatory organelle movements of nonmuscle cells might be driven by microtubule-dynein interactions, we microinjected vanadate into several different types of cultured cell. Solutions of sodium metavanadate made up in a simple buffered salt solution were pressure microinjected into fully spread cells in an open-topped culture chamber placed on the stage of an inverted microscope. The cells were observed by oil-immersion phase-contrast optics and results were recorded on movie film. Vanadate, at 10(-5)-10(-2) M, microinjected into cultured chick embryo fibroblasts, failed to inhibit organelle movements. To test the effectiveness of vanadate's inhibitory action under living cell conditions, ciliated epithelial cells were microinjected. In these cells even the smallest microinjection of 5 X 10(-5) M vanadate caused an immediate cessation of ciliary beating. Moreover, in cells that were well spread it was found that whereas vanadate, at 5 X 10(-5)-5 X 10(-3) M, inhibited ciliary motion, it failed to inhibit organelle saltations in the same cell. To determine whether vanadate would inhibit a living actin-myosin system, myocardial cells were also microinjected. Following microinjection of 5 X 10(-5) and 5 X 10(-4) M vanadate a temporary tonic contraction (which also occurred following microinjection of buffer alone) was followed by regular beating. Taken together these results demonstrate that in living cell systems microtubule-dynein interactions are as sensitive to vanadate inhibition as they are in demembranated model systems, and that a working actin-myosin system in a living muscle cell does not share this great sensitivity. In light of the pronounced differential inhibitory effects of vanadate on the movements of cilia and organelles, our results suggest that saltatory organelle movements in chick embryo fibroblasts and rabbit oviduct epithelial cells are unlikely to be brought about by microtubule-dynein interactions.

Adenosine Triphosphatases↗