Persistent inflammation predisposes to some forms of cancer and the host response to malignant illness exhibits a number of parallels with inflammation and wound healing. The cells involved in inflammation are detected in a variety of widespread 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 might enhance malignant potential. Certain chemokines are likely to subvert antitumour immunity by favouring improvement of ineffective Kind 2 responses. Tumour cells could even utilize chemokine receptors in homing to lymph nodes and different organs. Thus, the cells, cytokines and chemokines found in tumours usually tend to contribute to tumour progress, progression and immunosuppression than they're to mount an efficient host antitumour response.
This book attracts collectively contributions from an international group of scientists and clinicians from diverse disciplines, ranging from epidemiology to immunology, cell biology, molecular oncology, molecular medication and pharmacology to debate these and related issues. Subjects covered include the epidemiological links between most cancers and inflammation, the parallels between inflammation and cancer, the function of irritation in most cancers, inflammatory genes as risk components for cancer initiation and progression, irritation and most cancers angiogenesis, and preventative and therapeutic strategies.
Associated Novartis Basis symposia:
252 Technology and Effector Capabilities of Regulatory Lymphocytes
Chair: Jean-Fran?ois Bach
254 Immunoinformatics: Bioinformatic Strategies for Higher Understanding of Immune Perform
Chair: Hans-Georg Rammensee
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