| Summary: | HYPOTHESIS
The hypothesis of the present work is that tumor cells express on their surface tumorassociated
antigens that have the potential to activate the complement system. At the
same time, tumor cells have developed mechanisms that make them resistant to
complement cytotoxic effects. The subsequent effects of complement activation on
complement-resistant cancer cells play a pivotal role in the development of malignant
features, ending in tumor progression.
OBJECTIVES
1. To study complement activation by the alternative and classical pathways on
non-small cell lung cancer (NSCLC) cells and normal bronchial epithelial cells.
2. To study the expression, at the mRNA and protein levels, of the main
complement inhibitory proteins in NSCLC and normal bronchial epithelial cells.
3. To study the role of complement in a syngeneic mouse model of lung cancer,
with special interest in tumor-associated characteristics of the microenvironment such as
angiogenesis and immunosuppression.
4. To evaluate the tumor-promoting effects of complement on NSCLC cells.
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