Infections as a major preventable cause of human cancer

Kuper, Hannah; Adami, Hans Olov; Trichopoulos, D.

doi:10.1046/j.1365-2796.2000.00742.x

Cited by 665 publications

(368 citation statements)

References 87 publications

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“…The link between unresolved inflammation and cancer has been well established with estimates that 15% of cancer deaths are inflammation-related [4]. Evidence for this link includes the following: a) some inflammatory diseases are associated with increased risk of cancer development; b) inflammatory mediators are present surrounding and within most tumors [5]; c) overexpression of inflammatory cytokines increases cancer development and progression in murine studies; d) inhibition of inflammatory mediators decreases cancer development and progression; and e) the use of nonsteroidal anti-inflammatory drugs (NSAIDs) has been found to decrease cancer incidence and delay progression in patients with breast, prostate, lung and colorectal cancers [6,7].…”

Section: Introductionmentioning

confidence: 99%

The Inflammatory Tumor Microenvironment, Epithelial Mesenchymal Transition and Lung Carcinogenesis

Heinrich

Walser

Krysan

et al. 2011

Cancer Microenvironment

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The inflammatory tumor microenvironment (TME) has many roles in tumor progression and metastasis, including creation of a hypoxic environment, increased angiogenesis and invasion, changes in expression of microRNAs (miRNAs) and an increase in a stem cell phenotype. Each of these has an impact on epithelial mesenchymal transition (EMT), particularly through the downregulation of E-cadherin. Here we review seminal work and recent findings linking the role of inflammation in the TME, EMT and lung cancer initiation, progression and metastasis.Finally, we discuss the potential of targeting aspects of inflammation and EMT in cancer prevention and treatment.

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Section: Introductionmentioning

confidence: 99%

The Inflammatory Tumor Microenvironment, Epithelial Mesenchymal Transition and Lung Carcinogenesis

Heinrich

Walser

Krysan

et al. 2011

Cancer Microenvironment

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“…Varicella zoster virus remains in a dormant state until the cellmediated immune system is depressed and allows the virus to multiply. There is some evidence that infections may promote certain types of cancers (Kuper et al, 2000). It has also been suggested that herpes zoster has a direct carcinogenic effect (Rogers and Tindall, 1971).…”

Section: Discussionmentioning

confidence: 99%

The risk and prognosis of cancer after hospitalisation for herpes zoster: a population-based follow-up study

et al. 2004

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We examined the risk of cancer and survival in a cohort of patients hospitalised with herpes zoster between 1977 and 1996, drawn from the Danish National Registry of Patients. Through linkage with the Danish Cancer Registry, we compared the observed number of cancers with the expected number on the basis of national age-, gender-, and site-specific incidence rates. The survival of herpes zoster patients with cancer was compared with that of non-herpes zoster patients with cancer. Among the 10 588 patients hospitalised with herpes zoster whom we identified, 1427 cancers were observed compared with 1239 expected (relative risk ¼ 1.2, 95% confidence interval 1.1 -1.2). The risk was substantially elevated during the first year of follow-up, mainly for haematological cancer. Patients with cancer within 1 year of follow-up had a higher prevalence of distant metastases than controls, although the mortality was similar. For those with haematological cancer, however, the mortality was higher for herpes zoster patients than for controls. Haematological cancer following hospitalisation for herpes zoster has a poorer prognosis than in non-herpes zoster patients.

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“…In fact, although the first connection between inflammation and cancer was made as early as 1983, the concept is still (but progressively) gaining ground [30]. It has become evident that many malignancies originate in areas of infection and inflammation, as a result of normal host response [31], which induces chronic inflammation. Immune cells generate reactive oxygen species (ROS) and nitrogen species to fight infection leading to DNA damage in proliferating cells, which, when occurring repeatedly, induces permanent genomic alterations that promote cancer.…”

Section: Cancer Development At Inflammation Sitesmentioning

confidence: 99%

Targeting Inflammation to Improve Tumor Drug Delivery

2017

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Inefficient delivery of drugs is a main cause of chemotherapy failure in hypo-perfused tumors. To enhance perfusion and drug delivery in these tumors, two strategies have been developed: vascular normalization, aiming at normalizing tumor vasculature and blood vessel leakiness; and stress alleviation, aiming at decompressing tumor vessels. Vascular normalization is based on antiangiogenic drugs, whereas stress alleviation on stroma-depleting agents. Here, an alternatively approach to normalize vessels is presented, considering that malignant tumors tend to develop at chronic inflammation sites. Similarly to tumor vessel leakiness, inflammation is also characterized by vascular hyper-permeability. Therefore, testing the ability of anti-inflammatory agents, such as non-steroidal anti-inflammatory drugs or inflammation resolution mediators, as an alternative way to increase tumor drug delivery, might prove promising.Keywords stress alleviation; vascular normalization; tumor perfusion; anti-inflammatory agents; inflammation resolution The Tumor microenvironment and drug deliveryTumors are complex tissues consisting of cancer cells and their microenvironment [1,2], which includes structural and cellular components. Structural components of the tumor microenvironment comprise tumor blood and lymphatic vessels, and the extracellular matrix (ECM) (see Glossary); while the stromal cell constituents [3] include angiogenic vascular cells (endothelial cells and pericytes), infiltrating immune cells, and cancer-associated fibroblasts (CAFs). Naturally, interactions between cancer cells and the various components of tumor microenvironment affect fundamental cancer cell properties such as proliferation, apoptosis, migration and invasion.It has been postulated that components and features of the tumor microenvironment may also set certain barriers with regard to the effective delivery of therapeutic agents, resulting in compromised therapeutic outcomes and decreased survival [4]. Chemotherapeutic drugs are, without a doubt, potent cytotoxic agents. However, they often fail to cure cancer due to the fact that they are unable to reach cancer cells within the tumor in sufficient amounts [5,6]. Hence, the discovery of more efficient approaches to enhance tumor drug delivery is imperative. Here, the main obstacles in drug delivery to the tumor are presented along with the approaches currently used to overcome them. Furthermore, the use of anti-inflammatory agents is proposed as a promising alternative approach to normalize vessels and improve therapy. Europe PMC Funders Group Causes of insufficient drug delivery to tumorsInefficient drug delivery may arise due to barriers posed by abnormal structure and function of tumor stroma, known as desmoplasia. Desmoplastic tumors are characterized by a dense ECM, containing increased levels of total fibrillar collagen, hyaluronan, fibronectin, proteoglycans and tenascin C [4], which also provides the tumor with a reservoir of growth factors eventually promoting its growth. The dense ...

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Infections as a major preventable cause of human cancer

Cited by 665 publications

References 87 publications

The Inflammatory Tumor Microenvironment, Epithelial Mesenchymal Transition and Lung Carcinogenesis

The Inflammatory Tumor Microenvironment, Epithelial Mesenchymal Transition and Lung Carcinogenesis

The risk and prognosis of cancer after hospitalisation for herpes zoster: a population-based follow-up study

Targeting Inflammation to Improve Tumor Drug Delivery

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