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Biological and clinical advances in the understanding of tumor immunology suggest that immuneresponsiveness of human tumors is a complex biological phenomenon that could be best studied by a real-timecomparison of tumor/host interactions in the tumor microenvironment through a high-throughputdiscovery-driven approach.This conclusion is derived from our recognition that too many hypotheses or,inother words,no solid single hypothesis exist,based on experimental results,to further drive experimentation inhuman subjects.Functional genomic studies entertained during the last few years consolidated the belief that inhumans the interactions between tumor and immune cells are too complex to be approached exclusively with ahypothesis driven method.We believe that immune cells suit cancer cells in a Yin and Yang balance byopposing and yet mutually depending on each other.Indeed,immune infiltration in tumors may play a dualrole modulating in different circumstances cancer cell growth or destruction through a physiologicalmodulation of inflammation.It is reasonable to question what induces inflammation at the tumor site.Wehypothesize that inflammation is primarily driven by the phenotype of tumor cells that can modulate theirmicroenvironment through cell-to-cell interactions or the secretion of soluble factors.Thus,in analogy theobservation of immune cells within tumors parallels the presence of paramedics,police and firemen at thescene of an accident,which is reactive to and not causative of the occurrence.In this review we will explore thishypothesis by reporting and summarizing most of our recent work in the frame of available literature on thesubject.Cellular & Molecular Immunology.2004;1(4):256-265.
Biological and clinical advances in the understanding of tumor immunology suggest that immuneresponsiveness of human tumors is a complex biological phenomenon that could be best studied by a real-timecomparison of tumor / host interactions in the tumor microenvironment through a high-throughput discovery-driven approach. conclusion is derived from our recognition that too many hypotheses or, inother words, no solid single hypothesis exist, based on experimental results, to further drive experimentation in human subjects. Functional genomic studies entertained during the last few years consolidated the belief that inhumans the interactions between tumor and immune cells are too complex to be approached exclusively with ahypothesis driven method. We believe that immune cells suit cancer cells in a Yin and Yang balance byopposing and yet mutually depending on each other .dede, immune infiltration in tumors may play a dualrole modulating in different circumstances cancer cell growth or destructi on through a physiological modulation of inflammation. It is reasonable to question what induces inflammation at the tumor site. Wehypothesize that inflammation is primarily driven by the phenotype of tumor cells that can modulate their microenvironment through cell-to-cell interactions or the secretion of soluble factors. Thus, in analogy theobservation of immune cells within tumors parallels the presence of paramedics, police and firemen at thescene of an accident, which is reactive to and not causative of the the occurrence.In this review we will explore this hypothetical by reporting and summarizing most of our recent work in the frame of available literature on the subject. Cellular & Molecular Immunology. 2004; 1 (4): 256-265.