An upregulation of anti-ROS defences in cancer cells may explain why tumour cell lines in vitro are extremely resistant to cytolysis by hydrogen peroxide [ 20].
The additive effect of these mechanisms, more intensive and prolonged exposure to platinum in the setting of defective double-strand break repair, may explain why tumour cells with low expression of BRCA1 will be more sensitive to IP chemotherapy.
This may explain why tumours with high EZH2 respond poorly to therapy, in contrast to tumours with high BMI1.
Additional functions beyond the involvement in proteolysis may explain the tumour-promoting role of PAI-1 (Bajou et al, 1998).
This hypothesis may explain why tumours develop more rapidly following asbestos exposure in TAg expressing compared to wild type mice and why the rate and incidence of tumour development reflects the TAg transgene dose.
Whole mount preparations for these tumours revealed striking differences in the vasculature between the parental and IL-12-expressing B16 tumours that may explain the altered tumour growth observed.
41 The generation of low-molecular-weight HA fragments (including oligosaccharides) in large quantities from intratumoral HA could antagonise existing HA CD44 interactions 15 42 and may explain for the tumour specificity of PEGPH20-induced hyperpermeability.
The cancer stem cell (CSC) hypothesis, which suggests that the variety between functionally important properties of individual cells arises from differences in their differentiation status, may explain the intra-tumour heterogeneity seen in breast tumours (Campbell and Polyak, 2007; Shackleton et al, 2009).
Several of these activating events are blocked by BP-1, which may explain its anti-tumour activity.
Conventional cancer treatments may eradicate the tumour bulk but spare these cells, which may explain why an initial tumour regression does not necessarily translate to an improved patient survival in many clinical trials for advanced cancers (Wicha et al, 2006).
