The development of a technique for the morphometric analysis of invasion in cancer

Suh, Okhee; Weiss, Leonard

doi:10.1016/s0022-5193(84)80132-0

Cited by 34 publications

(7 citation statements)

References 13 publications

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“…This is indicated by the fact that larger clusters with less nutrient depletion move faster (Figs 13 and 16). As such, this supports the notion that, if cell metabolism comes into play within the aforementioned r r range, both key features of a tumor system, proliferation and invasion, are likely required to drive and direct spatio-temporal expansion of the tumor system (Deisboeck et al, 2001;Suh & Weiss, 1984). Furthermore, Fig.…”

Section: Y Mansury Et Alsupporting

confidence: 79%

Emerging Patterns in Tumor Systems: Simulating the Dynamics of Multicellular Clusters with an Agent-based Spatial Agglomeration Model

Mansury

Kimura

Lobo

et al. 2002

Journal of Theoretical Biology

116

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Section: Y Mansury Et Alsupporting

confidence: 79%

Emerging Patterns in Tumor Systems: Simulating the Dynamics of Multicellular Clusters with an Agent-based Spatial Agglomeration Model

Mansury

Kimura

Lobo

et al. 2002

Journal of Theoretical Biology

116

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“…A technique has now been developed in which from statistical analyses of cancer cell density counts made on tumor sections, differentiation may be made between the density patterns associated with diffusive (active) cancer cell movement and the more abrupt growth patterns. Tests made on sections of human melanomas confirm the validity of the analytical technique and indicate that, in the material examined, a zone of actively moving melanoma cells approximately 500-/tm wide precedes the main growing body (62). Although other types of human tumors have yet to be examined, on the basis of this and the other work it seems probable that active movements of cancer cells play a role in various invasion and metastasis-related phenomena.…”

Section: ) Cell Detachment and Cell Locomotionsupporting

confidence: 58%

Cell detachment and metastasis

1983

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Cancer cell detachment in three distinct and critical parts of the metastatic cascade is discussed. The detachment of cancer cells from their parent tumors is an initial early event in metastasis. The site of detachment with respect to proximity to blood vessels may determine the initial dissemination route. Many factors affect cell detachment; we specifically consider the effects of growth-rate, necrosis, enzyme activity, and stress on cell release in terms of metastasis-promoting mechanisms. Detachment is also discussed in relation to active cancer cell locomotion, where localized detachment from the substratum is a prerequisite for translatory movement. The importance of active cell movement in tissue invasion has only recently been assessed, and, in the case of at least some human malignant melanomas, a zone of actively moving cancer cells is believed to precede the growing body of the tumor. The secondary release of cancer cells from temporary arrest sites at the vascular endothelium consequent upon intravascular dissemination is also a major area of investigation. Circulating cancer cells arrest at vascular endothelium or are impacted in small vessels, however, most are released into the circulation and subsequently perish. The blood stream is a hostile environment, and it is probable that cancer cells are sufficiently damaged in translocation by hemodynamic trauma and humoral factors such that they easily detach or are 'sheared-off' the vascular endothelium by blood flow. Another possibility is that in some cases they are processed by 'first organ encounters' and perish before or shortly after arriving in a second organ. Animal studies have shown that, following intravenous injection, 60-100% of the injected dose of viable cancer cells are initially arrested in the lungs, but very few remain after 24 hr. As it is only those retained cells which produce tumors, the mechanisms involved in this secondary release, which occurs in all organs so far examined, are critical to any understanding of the metastatic cascade and metastatic inefficiency. The arrest of cancer cells at the vascular endothelium and their subsequent release have been associated with the presence of platelets, and the deposition of fibrin and manipulation of platelet-aggregating mechanisms and fibrinolysis are discussed in terms of their antimetastatic effects. The role of the reticuloendothelial system, natural killer cells, and polymorphs is discussed in relation to cancer cell clearance from blood vessels and also to inherent cancer cell properties which may act to inhibit their metastasis. Although detachment of cancer cells from a primary tumor may be regarded as metastasis promoting, secondary release of cancer cells may be associated with inhibition of metastasis.

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“…It is therefore of interest that a morphometric analysis of invasive (vertical phase) melanomas indicated that an initial phase of invasion was associated with the active migration of melanoma cells towards the subcutis, and that after migrating several hundred micrometers, active cancer ceil movement temporarily ceased the gaps between the cancer cells were 'filled-in' by proliferation. Invasion progressed by repetitive cycles of migration and proliferation [16].…”

Section: Lnvasion/intravasationmentioning

confidence: 99%

Biomechanical interactions of cancer cells with the microvasculature during hematogenous metastasis

Weiss

1992

Cancer Metast Rev

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Different aspects of hematogenous metastasis are discussed from the viewpoint of biomechanics. The processes considered include the role of primary tumor pressure, cell locomotor forces and degradation, in invasion of tissues and intravasation by cancer cells. Consideration of the fluid dynamics of cancer cell movement along capillaries lead to the view that in vivo, arrest is primarily due to mechanical trapping of cancer cells, and that the pathobiologic role of so-called adhesion molecules is not mainly in the arrest and adhesion of cancer cells, but rather in stimulating their proliferation by signal induction. As a consequence of deformation from spherical-to-cylindrical shape in the microvasculature, demands for increased surface membrane area leads to increases in surface membrane tension above critical levels for rupture, and the cancer cells are rapidly and lethally damaged. The possibility is briefly discussed of increasing the susceptibility of circulating cancer cells to mechanical trauma, as a form of anti-metastatic therapy.

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The development of a technique for the morphometric analysis of invasion in cancer

Cited by 34 publications

References 13 publications

Emerging Patterns in Tumor Systems: Simulating the Dynamics of Multicellular Clusters with an Agent-based Spatial Agglomeration Model

Emerging Patterns in Tumor Systems: Simulating the Dynamics of Multicellular Clusters with an Agent-based Spatial Agglomeration Model

Cell detachment and metastasis

Biomechanical interactions of cancer cells with the microvasculature during hematogenous metastasis

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