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Cancer stem cells have been unequivocally identified in some tumour systems and are important because if they are not eradicated, no matter how many tumour cells are killed by therapy, the tumour will come back.
The efficacy of LTBI is believed to stem from three mechanisms, namely; immune-enhancement, induction of apoptosis, and the intrinsic hypersensitivity to low-radiation doses demonstrated in many cell lines and tumour systems.
The specific involvement of the CXCR4/CXCL12 axis in cell proliferation, and organ-specific metastasis has been partially addressed and remains controversial in some tumour systems, including NB [13].
In both tumour systems, significant anti-tumour effects of aprotinin were observed.
Furthermore, in some experimental tumour systems, increased MMP production did not correlate with increased metastasis [ 22].
These studies were all carried out in allogeneic tumour systems or by artificially influencing the immunization process.
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The anti-tumour effect of local injection of C. parvum, unlike that of systemic injection in this particular tumour system, thus appears to be T-cell dependent.
Good immunoprotection was afforded by A9/SEWA somatic hybrid cells in the C3H mouse/C3H Py tumour system, confirming results previously obtained in the A.SW mouse/SEWA tumour system.
Tumour histopathology was classified according to the World Health Organization Classification of Tumour system.
This resemblance justifies drug resistance studies in this experimental in vivo human tumour system.
Various procedures for immunoprotection in the A-SW mouse SEWA tumour system were compared.
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