Chronic inflammation predisposes to some forms of cancer and the host response to malignant disease shows several parallels with inflammation and wound healing. The cells involved in inflammation are detected in a range of common cancers, together with the inflammatory cytokines and members of the chemokine ligand/receptor systems. Neutralization or deletion of the gene for some inflammatory cytokines confers resistance to tumour induction and experimental metastasis. Over-expression of such cytokines in tumour cells may enhance malignant potential. Certain chemokines are likely to subvert antitumour immunity by favouring development of ineffective Type 2 responses. Tumour cells may even utilize chemokine receptors in homing to lymph nodes and other organs. Thus, the cells, cytokines and chemokines found in tumours are more likely to contribute to tumour growth, progression and immunosuppression than they are to mount an effective host antitumour response. This book draws together contributions from an international group of scientists and clinicians from diverse disciplines, ranging from epidemiology to immunology, cell biology, molecular oncology, molecular medicine and pharmacology to debate these and related issues. Topics covered include the epidemiological links between cancer and inflammation, the parallels between inflammation and cancer, the role of inflammation in cancer, inflammatory genes as risk factors for cancer initiation and progression, inflammation and cancer angiogenesis, and preventative and therapeutic strategies. Related Novartis Foundation symposia: 252 Generation and Effector Functions of Regulatory Lymphocytes Chair: Jean-Fran ois Bach 254 Immunoinformatics: Bioinformatic Strategies for Better Understanding of Immune Function Chair: Hans-Georg Rammensee

Chronic inflammation predisposes to some forms of cancer and thehost response to malignant disease shows several parallels withinflammation and wound healing. The cells involved in inflammationare detected in a range of common cancers, together with theinflammatory cytokines and members of the chemokine ligand/receptorsystems.Neutralization or deletion of the gene for some inflammatorycytokines confers resistance to tumour induction and experimentalmetastasis. Over-expression of such cytokines in tumour cells mayenhance malignant potential. Certain chemokines are likely tosubvert antitumour immunity by favouring development of ineffectiveType 2 responses. Tumour cells may even utilize chemokine receptorsin homing to lymph nodes and other organs. Thus, the cellscytokines and chemokines found in tumours are more likely tocontribute to tumour growth, progression and immunosuppression thanthey are to mount an effective host antitumour response.This book draws together contributions from an international groupof scientists and clinicians from diverse disciplines, ranging fromepidemiology to immunology, cell biology, molecular oncologymolecular medicine and pharmacology to debate these and relatedissues. Topics covered include the epidemiological links betweencancer and inflammation, the parallels between inflammation andcancer, the role of inflammation in cancer, inflammatory genes asrisk factors for cancer initiation and progression, inflammationand cancer angiogenesis, and preventative and therapeuticstrategies.Related Novartis Foundation symposia:252 Generation and Effector Functions of RegulatoryLymphocytesChair: Jean-François Bach254 Immunoinformatics: Bioinformatic Strategies for BetterUnderstanding of Immune FunctionChair: Hans-Georg Rammensee

Chair's Introduction (S. Gordon).Inflammation and cancer: an epidemiological perspective (M.Thun, et al.).Chemokine-based pathogenetic mechanisms in cancer (I. Conti, etal.).General Discussion I.Anti-TNF therapy of rheumatoid arthritis: what can we learnabout chronic disease? (M. Feldmann, et al.).How do chemokine/chemokine receptor activations affecttumorigenesis? (A. Richmond, et al.).Proinflammatory cytokines, immune response and tumourprogression (M. Spadaro and G. Forni).General discussion II.Lymphangiogenesis and tumour metastasis (J. Tille, et al.).Infiltration of tumours by macrophages and dendritic cells:tumour-associated macrophages as a paradigm for polarized M2mononuclear phagocytes (A. Mantovani, et al.).The influence of CD25¯+ cells on the generationof immunity to tumour cell-lines in mice (E. Jones, et al.).Macrophages: modulators of breast cancer progression (E. Lin andJ. Pollard).Chemokines: angiogenesis and metastases in lung cancer (R.Strieter, et al.).Macrophage infiltration and angiogenesis in human malignancy (H.Knowles, et al.).The role of inflammation for tumour growth and tumoursuppression (T. Blankenstein).Cyclooxygenase 2: from inflammation to carcinogenesis (A.Ristimäki).The inflammatory cytokine network of epithelial cancer:therapeutic implications (P. Szlosarek and F. Balkwill).In vivo manipulation of DC migration and activation toelicit anti-tumour immunity (A. Vicari, et al.).Final general discussion.Concluding remarks (S. Gordon).Index of contributors.Subject Index.