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      Association between Cysticercosis and Neoplasia: A Study Based on Autopsy Findings

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          Chronic infections including the cysticercosis induce inflammatory cells to produce free radicals and synthesize carcinogenic toxins. The cells with genetic mutations proliferate in a disorganized manner, leading to the development of neoplasia. The aim of the present study was to demonstrate the relation between cysticercosis and neoplasia. Patients autopsied were divided into 4 groups: patients with neoplasia and cysticercosis (NC), patients with neoplasia only (NN), patients with cysticercosis only (CC), and patients without neoplasia or cysticercosis (WW). Of 2012 autopsy reports analyzed, 0.4 showed NC. In groups CC and NC, the most common location of the parasite was the brain. There was a predominance of three or more cysticerci in groups NC and CC. In the NC group, all had malignant neoplasms, and was predominance of benign neoplasm in NN group. The digestive system was the most frequent neoplasia. By calculating odds ratio, rate of neoplasia in patients with cysticercosis was 0.74. In conclusion, the demographic profile of patients with cysticercosis and neoplasia is similar to that of patients with cysticercosis alone. The incidence of cysticercosis and neoplasia was greater in older patients suggesting that immunosenescence may contribute to development of neoplasia promoted by cysticercosis.

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          Most cited references 36

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          Chronic infections and inflammatory processes as cancer risk factors: possible role of nitric oxide in carcinogenesis.

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          Infection by bacteria, parasites or viruses and tissue inflammation such as gastritis, hepatitis and colitis are recognized risk factors for human cancers at various sites. Nitric oxide (NO) and other oxygen radicals produced in infected and inflamed tissues could contribute to the process of carcinogenesis by different mechanisms, which are discussed on the basis of authors' studies on liver fluke infection and cholangiocarcinoma development. A similar mechanism could apply to other suspected and known cancer-causing agents including Helicobacter pylori infection (stomach cancer) or asbestos exposure (lung mesothelioma). Studies on the type of tissue and DNA damage produced by NO and by other reactive oxygen species are shedding new light on the molecular mechanisms by which chronic inflammatory processes may initiate or enhance carcinogenesis in humans.
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            Neurocysticercosis: updates on epidemiology, pathogenesis, diagnosis, and management.

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            Neurocysticercosis is now recognized as a common cause of neurologic disease in developing countries and the United States. The pathogenesis and clinical manifestations vary with the site of infection and accompanying host response. Inactive infection should be treated symptomatically. Active parenchymal infection results from an inflammatory reaction to the degenerating cysticercus and will also respond to symptomatic treatment. Controlled trials have not demonstrated a clinical benefit for antiparasitic drugs. Ventricular neurocysticercosis often causes obstructive hydrocephalus. Surgical intervention, especially cerebrospinal fluid diversion, is the key to management of hydrocephalus. Shunt failure may be less frequent when patients are treated with prednisone and/or antiparasitic drugs. Subarachnoid cysticercosis is associated with arachnoiditis. The arachnoiditis may result in meningitis, vasculitis with stroke, or hydrocephalus. Patients should be treated with corticosteroids, antiparasitic drugs, and shunting if hydrocephalus is present.
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              Involvement of inflammatory reactions and elevated cell proliferation in the development of bladder cancer in schistosomiasis patients.

              Schistosoma haematobium infection is strongly associated with urinary bladder cancer. Although numerous explanations have been proposed for this association, the nature of this relationship remains unresolved. This paper explores the hypothesis that inflammation and elevated cell proliferation play a major role in the development of bladder cancer in infected patients, possibly by increasing the level of genetic instability in the urothelium. The paper details in vivo and in vitro studies being done in our laboratories to test this hypothesis. These studies include population studies in which chromosomal breakage in the bladder of infected individuals is assayed using the micronucleus (MN) test on exfoliated urothelial cells. The approach also includes parallel studies in Vancouver with patients with long-term catheter drainage, a population with many similarities to schistosomiasis patients. In the in vitro studies we are co-incubating bladder cells with activated neutrophils or experimental conditions simulating inflammation. These studies show that inflammatory cells when activated can induce micronuclei in bladder cells and that this response is associated with loci on chromosome 11, a chromosome commonly altered during bladder carcinogenesis. A final approach being used is to assay chromosomal change (MN frequencies and numerical chromosome alterations) and level of proliferation (expression of proliferating cell nuclear antigen) in archival biopsies from schistosomiasis patients. Preliminary results show that a dysregulation of cell proliferation is occurring during cystitis in these patients. The extent to which this alteration affects the level of chromosomal breakage is yet to be determined.

                Author and article information

                The Scientific World Journal
                Hindawi Publishing Corporation
                29 October 2013
                : 2013
                Biological and Natural Science Institute, General Pathology Discipline, Triângulo Mineiro Federal University, Disciplina de Patologia Geral, Rua Frei Paulino No. 30, Bairro Abadia, 38025-180 Uberaba, MG, Brazil
                Author notes
                *Camila Lourencini Cavellani: camila@

                Academic Editors: T. T. Chye, M. C. Botelho, M. Gnanasekar, and N. Rout

                Copyright © 2013 Camila Lourencini Cavellani et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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