Tumour-cord parameters in two rat hepatomas that differ in their radiobiological oxygenation status

Abstract

Tumour cords have been examined quantitatively in two rat hepatomas, 3924A and H-4-II-E, that differ in their radiobiological oxygenation status (oxygen enhancement ratio for growth delay [tumour clamped: tumor 'in air'] was 1.35 for 3924A and only 1.08 for H-4-II-E). The average thickness of tumour cords in 3924A was 118 microns and only 69 microns in H-4-II-E. The migration rates across the cords of the two tumours were approximately the same (1.7 and 1.4 micron X h-1) but for any given distance from the subtending blood vessel, the proportion of histologically-dead cells within the cord was always higher for H-4-II-E. Volume for volume, H-4-II-E contained four times as much vascular space as 3924A but it is suggested that the poor quality of this vasculature in H-4-II-E contributed to its relative radioresistance.

Tumour cords in 52 human bronchial and cervical squamous cell carcinomas: Inferences for their cellular kinetics and radiobiology

“…while values of cord radius, MI and NI in 2 rat hepatomas accord qualitatively with their relative oxygenation status, radiobiologically -defined (Moore et al, 1984). The cord model as proposed by Thomlinson and Gray (1955) represents a unique synthesis of tumour pathology, physiology and radiobiology, and it is perhaps surprising that more attempts have not been made over the years to test its predictions for the behaviour of irradiated cells within organised tumours in their mammalian hosts.…”

“…Tannock, 1968;Hirst et al, 1982;Moore et al, 1984). The tumour cell population next to the vessel is the ultimate source of this flow (although it is sustained by all mitoses) and is characterised by a high proportion of cells in cell cycle (mean growth fraction, i.e.…”

“…3924A hepatoma, 10. H-4-1I-E hepatoma (Moore et al, 1984); 11. AH109A hepatoma (Yamaura & Matsuzawa, 1979); 12.…”

Cell Kinetics in a Tumour Cord

“…The mean thickness of the cords (i.e. the distance between the vessel wall and the "rst layer of necrotic cells) in di!erent tumours has been found to be 60}120 m, whereas the mean radius of the central vessel has been found to be 10}40 m. The decreasing value along the cord radius of the fraction of cells in S phase, which is given by the labelling index measured a short time after a pulse injection of tritiated thymidine, shows that cell proliferation within the cord slows down moving towards the periphery (Tannock, 1968;Hirst & Denekamp, 1979;Moore et al, 1984). This slowing of the proliferation could be related to the decrease of the concentration of some critical chemical (s).…”

“…However, in some tumours, the tumour architecture shows a certain degree of regularity. Malignant cells proliferate around fairly straight blood vessels, forming cylindrical arrangements of viable tumour cells named tumour cords (Tannock, 1968;Hirst & Denekamp, 1979;Hirst et al, 1982;1991;Moore et al, 1984Moore et al, , 1985Falkvoll, 1990). Oxygen tension and the concentration of nutrients, such as glucose, decay radially within the cord and, when they fall below some critical values, cell death occurs, so the cords are surrounded by regions of necrosis.…”