Cancer and Inflammation

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-François Bach

254 Immunoinformatics: Bioinformatic Strategies for Better
Understanding of Immune Function

Chair: Hans-Georg Rammensee

Auteur
The Novartis Foundation is an international scientific and educational charity which promotes the study and general knowledge of science and in particular encourages international co-operation in scientific research. Chair: SIAMON GORDON, Sir William Dunn School of Pathology, University of Oxford, UK

Texte du rabat
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-François Bach

1. Immunoinformatics: bioinformatic strategies for better understanding of immune function
   Chair: Hans-Georg Rammensee

Contenu
Chair's Introduction (S. Gordon). Inflammation and cancer: an epidemiological perspective (M. Thun, et al.).

Chemokine-based pathogenetic mechanisms in cancer (I. Conti, et al.).

General Discussion I.

Anti-TNF therapy of rheumatoid arthritis: what can we learn about chronic disease? (M. Feldmann, et al.).

How do chemokine/chemokine receptor activations affect tumorigenesis? (A. Richmond, et al.).

Proinflammatory cytokines, immune response and tumour progression (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 M2 mononuclear phagocytes (A. Mantovani, et al.).

The influence of CD25+ cells on the generation of immunity to tumour cell-lines in mice (E. Jones, et al.).

Macrophages: modulators of breast cancer progression (E. Lin and J. 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 tumour suppression (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 to elicit anti-tumour immunity (A. Vicari, et al.).

Final general discussion.

Concluding remarks (S. Gordon).

Index of contributors.

Subject Index.