Abstract

It is well established that an intimate connection exists between inflammation and neoplasia. Indeed, particular chronic infections and autoimmune processes giving rise to prolonged site-specific inflammation are known to increase the probability of the development of specific cancers. Molecular characterisation of these processes has revealed profound similarities in the specific molecules involved in persistence of inflammation and in both the primary induction of neoplastic processes and in specification of the preferred anatomic sites of metastatic spread. The therapeutic importance of these findings is underscored by the remarkable success in the treatment of autoimmune pathology using medications initially developed for use in oncology and this arena is one of considerable therapeutic promise for rheumatologists.

Highlights

  • It is well established that an intimate connection exists between inflammation and neoplasia

  • Numerous autoimmune diseases are associated with neoplasia, with an elevated risk of lymphoma in Sjögren’s syndrome [1] and rheumatoid arthritis [2], and gastrointestinal inflammation in Crohn’s disease and ulcerative colitis is likewise associated with increased risk of intestinal neoplasia [3]

  • For example, are required for tumour growth in a model of pancreatic cancer [7] and macrophages promote invasive, metastatic behaviour in murine mammary cancer [8]. The importance of these cellular similarities is underscored by the observation that inhibition of tyrosine kinase activity with imatinib is an established therapeutic strategy in systemic mastocytosis [9] and chronic myeloid leukaemia [10], but has been reported to be effective in rheumatoid arthritis [11,12,13]

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Summary

Introduction

It is well established that an intimate connection exists between inflammation and neoplasia. One of the most fundamental biological similarities between inflammation and cancer is the presence of similar inflammatory cells in these processes, and on occasions these immune cells have been demonstrated to be essential for tumour progression.

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Conclusion
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