Cancer and Inflammation - No. 256 / Edition 1

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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.

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Editorial Reviews

From the Publisher
"This book…is highly informative, very up-to-date, and demonstrates the complex biochemical events that may result in carcinogenesis." (Doody's Electronic Journal)

“…a useful guide to the considered thoughts of those within their field.” (The Newsletter of the British Society of Cell Biology, Summer 2005)

Doody's Review Service
Reviewer: Christiane Querfeld, MD (Northwestern University Feinberg School of Medicine)
Description: This is an excellent comprehensive compendium of presentations and discussions by internationally recognized experts from the symposium on Cancer and Inflammation, held at the Novartis Foundation in London in November 2002.
Purpose: Recent data have documented the concept that inflammation is a crucial component of carcinogenesis. This book provides an update of the current state of knowledge on host response mechanisms such as signaling molecules of the innate immune system, such as chemokines and their receptors contributing to tumor invasion, migration, and metastasis as well as tumor inhibition, and outlines possible targets for inhibition of these processes.
Audience: For scientists working in the research-cancer area it provides a stimulating, useful, and comprehensive outline in this area. For others unfamiliar with this subject area, it provides an extremely good overview of current understanding of the molecular basis of inflammation-associated neoplasia and of potential targets for drugs.
Features: The book starts with an epidemiological outline of chronic inflammation and cancer. A second topic covers the role of inflammatory cytokines, chemokines and their chemokine ligand/receptor system and discusses their potential role in tumorgenesis and progression as well as in tumor angiogenesis. The following topic covers immunologically activated cells such as dendritic cells, macrophages, and regulatory T-cells involved in antitumor response and tumor growth and progression with therapeutic implications leading to antitumor immunity. Finally, anticytokine therapies including anti-TNF á established in autoimmune disorders are discussed as potential new treatment modalities.
Assessment: This book of 15 reviews followed by discussion sections is highly informative, very up-to-date, and demonstrates the complex biochemical events that may result in carcinogenesis.

3 Stars from Doody
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Product Details

  • ISBN-13: 9780470855102
  • Publisher: Wiley
  • Publication date: 3/5/2004
  • Series: Novartis Foundation Symposia Series, #144
  • Edition number: 1
  • Pages: 290
  • Product dimensions: 6.28 (w) x 9.33 (h) x 0.71 (d)

Meet the Author

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

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Read an Excerpt

Cancer and Inflammation, No. 256

John Wiley & Sons

ISBN: 0-470-85510-X

Chapter One

Inflammation and cancer: an epidemiological perspective

Michael J. Thun, S. Jane Henley and Ted Gansler

American Cancer Society, 1599 Clifton Road, Atlanta, GA, 30329-4251, USA

Abstract. Many chronic inflammatory conditions increase the risk of cancer in affected tissues. Clinical conditions that involve both inflammation and increased cancer risk include a broad range of immunological disorders, infections (bacterial, helminthic, viral), and chronic chemical and mechanical irritation. For example, the inflammatory bowel diseases, ulcerative colitis and Crohn's disease, predispose to the development of cancers of the large bowel and/or terminal ileum; chronic infection with the bacterium Helicobacter pylori causes atrophic gastritis, dysplasia, adenocarcinoma and an unusual form of gastric lymphoma; and parasitic infection with schistosomes and other trematodes cause cancers of the urinary bladder and the intrahepatic and extrahepatic biliary tract. Chronic reflux of gastric acid and bile into the distal oesophagus causes chemical injury, Barrett's oesophagus and oesophageal adenocarcinoma. Chronic cholecystitis and gallstones predispose to cancer of the gallbladder. Besides these clinical syndromes, subclinical inflammation may promote the development of certain tumours. The expression of COX-2 and lipid mediators of inflammation increases during the multistage progression of these tumours. Non-steroidalanti-inflammatory drugs (NSAIDs), which inhibit COX-2 activity and tumour development in many experimental and clinical settings, are inversely associated with certain cancers in epidemiological studies. Despite their promise, however, anti-inflammatory drugs are not yet recommended for the prevention or treatment of any cancers. Numerous questions must be resolved concerning their molecular and cellular targets of action, efficacy, safety, treatment regimen, indications, and the balance of risks and benefits from treatment in designated patient populations.

2004 Cancer and inflammation. Wiley, Chichester (Novartis Foundation Symposium 256) p 6-28

The hypothesis that chronic irritation or injury may predispose to the development of certain cancers was raised by Virchow in the mid-19th century (Parsonnet 1999). He theorized that chronic irritation may establish the setting in which cells grow abnormally, as exemplified by bladder cancer occurring in patients from North Africa infected with Schistosoma haematobium (Parsonnet 1999). Numerous case reports and clinical series have described carcinomas of the skin arising as a complication of burns and scars, chronic sinus tracts, fistulas (Kaplan 1987, Scotto et al 1996) and ulcers (Parsonnet 1999). Lung carcinomas have been reported at the site of scar tissue in patients with previous tuberculosis (Auerbach et al 1979) and sarcomas can occur as a complication of surgical implants and foreign bodies (IARC 1999). However, the evidence implicating many of these chronic inflammatory conditions with cancer is limited. Much of the information derives from case reports. Scar tissue that adjoins a carcinoma may be a consequence rather than a cause of tumour growth (Blot & Fraumeni 1996). In any event, the great majority of cancers that occur arise in patients and tissues with no obvious chronic inflammatory disease.

A more contemporary version of Virchow's hypothesis is that the inflammatory processes induced by chronic injury contribute to the multistage development of cancer and that these, rather than the specific cause of the injury, account for the carcinogenicity in the majority of settings listed above. Inflammation involves a complex of host responses that, in the context of acute injury, promote wound healing and tissue regeneration. These responses include recruitment of specific types of cells, release of inflammatory mediators and interactions among chemokine ligand/receptor systems. Leukocytes (neutrophils, monocytes, macrophages, and eosinophils) generate reactive oxygen and nitrogen species that can directly damage the genes that control cell growth (Christen et al 1999). Cells that mediate the inflammatory response release autocrine and paracrine factors that stimulate cell proliferation, inhibit apoptosis, induce angiogenesis, and impair certain immune responses. Collectively, these factors can accelerate mutagenesis, promote the survival and clonal proliferation of mutated cells, and increase the probability that a particular clone of cells will acquire the requisite genetic mutations to become an invasive and metastatic cancer.

Even in the absence of overt inflammation, many of the same factors that mediate the acute inflammatory response are also produced by solid tumours at various stages of their development. For example, factors that stimulate cell proliferation, inhibit apoptosis and induce angiogenesis are involved in both wound healing and carcinogenesis. Enzymes like the inducible form of cyclooxygenase (COX-2) are expressed during wound healing and certain stages of neoplasia and increase production of inflammatory mediators. Much of the ongoing research on inflammation and cancer now focuses on the potential role of subclinical inflammatory mediators on the development of a wide range of cancers rather than on clinical inflammatory conditions known to predispose to specific cancers.

This overview considers three lines of evidence that are relevant to the hypothesis that chronic inflammation promotes the development of certain cancers. First it describes the broad spectrum of clinical disorders that involve both chronic inflammation and increased cancer risk. These include chronic inflammation from certain immunological conditions (ulcerative colitis, Crohn's disease, etc.), from chemical or mechanical irritation (reflux oesophagitis, gall stones), and from selected infections (bacterial, helminthic and viral) (Shacter & Weitzman 2002). Next it considers the increased expression of various inflammatory mediators that occurs during the development of various tumours. Finally, it considers the epidemiological, clinical and experimental evidence that non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the occurrence or progression of certain cancers (Thun et al 2002).

Clinical conditions that involve chronic inflammation and cancer

Clinicians have long been aware that a wide variety of chronic inflammatory disorders predispose to malignancy in the affected organ(s). Table 1, modified from Shacter & Weitzman (2002), lists examples of chronic inflammatory diseases that give rise to carcinomas and/or sarcomas. The only haematopoeitic cancer mentioned in Table 1 is the mucosa-associated lymphoid tumour (MALT), an unusual lymphoma that, like gastric adenocarcinoma, can be induced by chronic infection with Helicobacter pylori. Other conditions that predispose to lymphoma through chronic immune stimulation, and viral agents thought to induce cancer through direct interactions with host DNA, are not included in Table 1.

Idiopathic immunologically mediated conditions

Inflammatory bowel disease (IBD). Ulcerative colitis and Crohn's disease are related but clinically and histologically distinct inflammatory diseases of the bowel that predispose to adenocarcinomas of the large bowel, terminal ileum, and in some cases extraintestinal sites including the biliary tract (Podolsky 2002). Tumours often occur at the site of chronic inflammation (Fenkel 2002). In ulcerative colitis the intestinal inflammation is limited to the colon and rectum, whereas in Crohn's disease, two-thirds of patients have inflammation and increased risk of cancer in the terminal ileum. Inflammation is thought to result from a combination of genetic susceptibility and inappropriate activation of the mucosal immune system by normal luminal flora (Podolsky 2002). The absolute risk of developing colorectal cancer is high when extensive disease begins at a young age. Forty percent of patients diagnosed with pancolitis from ulcerative colitis before age 15 years developed colon cancer during 20-years of follow-up in a population-based linkage study in Sweden (Ekbom et al 1990). Numerous specific and non-specific inflammatory factors are expressed in patients with these conditions. These include phagocytic products (oxygen metabolites, nitric oxide, collagenases, etc.), toxic lymphocyte products, cytokines (including chemokines), neuropeptides and various components of plasma proteolytic cascades (Podolsky 2002).

Other immunological diseases. Various other idiopathic immunologically-mediated conditions that predispose to certain cancers are listed in Table 1. These include primary sclerosing cholangitis, lichen sclerosis, oral lichen planus and autoimmune gastritis. The list is not intended to be inclusive. Not mentioned are Hashimotos's thyroiditis or Sjogren's syndrome, which are associated with lymphomas but not solid cancers (Ron 1996). Lymphomas may arise from chronic polyclonal stimulation of immune cells leading to monoclonal proliferation rather than from more general inflammatory processes.

Chemical andmechanical irritation

Gastroesophageal reflux. Chronic reflux of gastric acid and bile from the stomach into the distal oesophagus causes chemical inflammation and histological abnormalities known as Barrett oesophagus (Shaheen & Ransohoff 2002). Damaged squamous cell epithelium of the lower oesophagus is replaced by metaplastic intestinal-type columnar epithelium that in some patients progresses to high-grade dysplasia. The risk of developing adenocarcinoma is estimated to be 0.5% per year among all patients with Barrett oesophagus, but 25% among those with high-grade dysplasia (Shaheen & Ransohoff 2002). Aggressive treatment with proton pump inhibitors has not been shown to induce regression of the histological abnormalities. The incidence of oesophageal adenocarcinoma has increased more rapidly than that of any other cancer in the USA since the mid- 1970s (Devesa et al 1998).

Familial pancreatitis, sporadic chronic pancreatitis and haemachromatosis all cause chemically induced chronic inflammation with increased risk of cancer in the affected organ.

Gallstones. Chronic cholecystitis from recurrent or persistent gallstones predisposes to biliary tract cancer. The risk of gallbladder cancer is reportedly 4-5 times higher in patients with than without gallstones (Lowenfels et al 1999). Factors that predispose to gallstone formation are also risk factors for biliary tract cancer. These include obesity, multiple pregnancies and a genetic disorder of cholesterol metabolism prevalent among indigenous populations of North and South America.

Pneumoconioses. Asbestos fibres deposited in the lung and pleura cause chronic inflammation, asbestosis (pleural plaques and interstitial fibrosis), and increased risk of both mesothelioma and lung cancer (IARC 1977). Exposure to crystalline silica causes both pulmonary fibrosis and increased risk of lung cancer (IARC 1997).

Surgical implants. Metal nails and implants, as in hip replacement, are occasionally associated with cancers of the bone and other adjacent tissues at the site of the implant (IARC 1999). This literature consists largely of case-reports rather than systematic epidemiological studies.

Infectious conditions

Bacterial-Helicobacterpylori. Clinical, epidemiological, and experimental studies have established that the bacterium H. pylori is the principal cause of both gastric adenocarcinoma and of an uncommon mucosa-associated lymphoid tissue (MALT) lymphoma of the stomach (IARC 1994a, Suerbaum & Michetti 2002). H. pylori is a Gram-negative, spiral bacteria that colonizes the mucus layer of the stomach. Its pathogenicity is greatest when colonization begins in childhood and involves more virulent strains that express the CagA (a 128 kDa cytotoxin associated gene A-positive) protein. Adverse effects are also modified by host factors such as diet and genetic susceptibility (Yamaguchi & Kakizoe 2001). Persistent infection causes the development of chronic atrophic gastritis, achlorhydria, intestinal metaplasia, dysplasia and adenocarcinoma in susceptible persons. Similar findings are seen in experimental studies of ferrets and rhesus monkeys infected with other species of Helicobacter (Nightingale & Gruber 1994). Premalignant gastric lesions (Correa et al 2000) and low grade B cell gastric lymphomas (Wotherspoon et al 1993) may regress following successful eradication of the infection. Inflamed gastric epithelium is a rich source of interleukin 8 (IL8) and epithelial-cell-derived neutrophil-activating peptide 78 (Suerbaum & Michetti 2002). Cytotoxic strains of H. pylori that produce CagA+ induce greater production of IL8 from gastric epithelial cells.

Bacterial other. Other examples of chronic bacterial infection that may increase cancer risk include chronic osteomyelitis (predisposing to cancers of the skin and bone), chronic draining fistulas (causing local squamous cell carcinomas of the skin), chronic indwelling catheters (causing cystitis and bladder cancer) and cervicitis from Chlamydia.

Helminth infections-Schistosoma haematobium. Chronic infection with Schistosoma haematobium accounts for a substantial fraction of cancers of the urinary bladder in Egypt, where bladder cancer comprises approximately one-third of all cancers in men (Ferlay et al 2000). Many of the severe pathological manifestations of schistosomiasis such as ulcers, bladder polyps, fistulae, and strictures result from the physical and immunological response of the host to the eggs rather than direct effects of the organism (Rosin & Hofsath 1999). The eggs from S. haematobium are deposited largely in the terminal ureters and bladder (IARC1994a). Egg deposition stimulates the activation and recruitment of monocytes and other leukocytes, which contribute to chronic ulceration. Egg remnants have been demonstrated in 82% of patients with urinary bladder cancer from S. haematobium in one large case series in Egypt (El-Biokany et al 1981). The bladder tumours associated with S. haematobium are typically squamous cell rather than transitional carcinomas. There is some evidence implicating another species of schistosome, S. japonicum in colorectal cancer (Rosin & Hofseth 1999), although the International Agency for Research on Cancer (IARC) has classified this evidence as 'limited' (IARC 1994a).

Infection with other trematodes. Three species of liver fluke infest the intrahepatic bile ducts of people who consume raw fish in parts of Southeast Asia (Opisthorchis viverrini), China and neighbouring countries (Clonorchis sinensis), and the former Soviet Union and Eastern Europe (O. felineus).


Excerpted from Cancer and Inflammation, No. 256 Excerpted by permission.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

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Table of Contents

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.

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