We believe that this subtle retention reflects binding in the tumours.
Over the whole tumour sections, specific ETB receptor binding in the P22 tumour was 1.7 fmol mg−1 (Table 2) compared to 0.7 fmol mg−1 for the HSN tumour (Bell et al, 1998).
Distribution of ETB binding in the P22 tumour suggested ETB receptor localisation on tumour cells as well as on the vasculature, which may also be significant for tumour growth.
However, the heterogeneous binding in the HSN tumour suggests that specific binding on the blood vessels of this tumour may be considerably higher than the average value suggests.
TACs in microPET indicated a progesterone-mediated decrease of C-SA4503 binding in the C6 tumour (by 36%), but not in the brain (Fig. 4).
Pretreatment of animals with progesterone caused a 31% decrease of sigma ligand binding in the C6 tumour, but did not significantly affect tracer uptake in any other organ or in plasma (Table 1).
ETB receptor binding in the rat HSN tumour was concentrated in small regions of intense binding (Bell et al, 1998), which suggested specific vascular localisation.
These activated PMN produced reactive oxygen species (ROS) which are found to play an important role in the observed enhanced locoregional tumour recurrence in which binding of the tumour cells to the mesothelium is an essential step (van Rossen et al, 1999, 2000).
The pro-proliferative effects of mortalin in cancer cells have been assigned, at least in part, to its binding with the tumour suppressor protein, p53 that results in its retention in the cytoplasm and inhibition of its transcriptional activation and control of centrosome duplication function [ 17– 17].
This humanised bsMAb may be employed in two phase radioimmunotherapy, binding to the tumour via the anti-CEA arm and localising a radiolabelled chelate with the other arm, without inducing a strong immune response observed sometimes with murine MAbs.
