15 results match your criteria: "European Cancer and Environment Research Institute (ECERI)[Affiliation]"

Background: A fundamental property of cancer cells is their metabolic reprogramming, allowing them to increase glucose uptake and glycolysis. Using a rat colon adenocarcinoma model, we previously showed that blood levels of free methylglyoxal (MG), a side-product of glycolysis, remained normal in animals grafted with a non-growing tumor cell clone, while MG levels were significantly increased and positively correlated with tumor growth in animals grafted with a tumorigenic cell clone issued from the same tumor.

Methods: We measured free MG in the blood of cancerous non-diabetic patients and compared the results to healthy subjects and non-cancerous diabetic patients.

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From a cohort of 2018 evaluable consecutive cases issued from the European Clinical Trial Database, we describe the complete clinical symptomatic presentation of electrohypersensitivity (EHS) and multiple chemical sensitivity (MCS) and their association in the framework of a unique, sensitivity-related environmental neurologic syndrome. Eligibility criteria are those of the Atlanta consensus meeting for MCS, and those of WHO for EHS. There were 1428 EHS, 85 MCS and 505 EHS/MCS evaluable cases, so EHS was associated with MCS in 25%.

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Article Synopsis
  • Environmental stressors during pregnancy, such as pollutants and metals, can affect DNA methylation, influencing the risk of chronic diseases later in life.
  • The study investigated how these exposures relate to DNA methylation in placental, maternal, and neonatal cells by analyzing 28 mother-infant pairs and utilizing artificial neural networks.
  • Results indicated that factors like suboptimal birth weight and maternal stress during pregnancy are linked to specific DNA methylation changes, suggesting that maternal exposure to environmental toxins can have significant implications for fetal development and health.*
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Much of the controversy over the cause of electrohypersensitivity (EHS) lies in the absence of recognized clinical and biological criteria for a widely accepted diagnosis. However, there are presently sufficient data for EHS to be acknowledged as a distinctly well-defined and objectively characterized neurologic pathological disorder. Because we have shown that 1) EHS is frequently associated with multiple chemical sensitivity (MCS) in EHS patients, and 2) that both individualized disorders share a common pathophysiological mechanism for symptom occurrence; it appears that EHS and MCS can be identified as a unique neurologic syndrome, regardless their causal origin.

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Clinical research aiming at objectively identifying and characterizing diseases via clinical observations and biological and radiological findings is a critical initial research step when establishing objective diagnostic criteria and treatments. Failure to first define such diagnostic criteria may lead research on pathogenesis and etiology to serious confounding biases and erroneous medical interpretations. This is particularly the case for electrohypersensitivity (EHS) and more particularly for the so-called "provocation tests", which do not investigate the causal origin of EHS but rather the EHS-associated particular environmental intolerance state with hypersensitivity to man-made electromagnetic fields (EMF).

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Electrohypersensitivity as a Newly Identified and Characterized Neurologic Pathological Disorder: How to Diagnose, Treat, and Prevent It.

Int J Mol Sci

March 2020

Association for Research Against Cancer (ARTAC), 57/59 rue de la Convention, 75015 Paris, France.

Since 2009, we built up a database which presently includes more than 2000 electrohypersensitivity (EHS) and/or multiple chemical sensitivity (MCS) self-reported cases. This database shows that EHS is associated in 30% of the cases with MCS, and that MCS precedes the occurrence of EHS in 37% of these EHS/MCS-associated cases. EHS and MCS can be characterized clinically by a similar symptomatic picture, and biologically by low-grade inflammation and an autoimmune response involving autoantibodies against O-myelin.

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The dominant pathogenic model, somatic mutation theory (SMT), considers carcinogenesis as a 'genetic accident' due to the accumulation of 'stochastic' DNA mutations. This model was proposed and accepted by the scientific community when cancer mainly affected the elderly, but it does not explain the epidemiological observation of the continuous increase in cancer incidence among children and young adults. Somatic mutation theory has been proposed for a revision based on the emerging experimental evidence, as it does not fully address some issues that have proven to be crucial for carcinogenesis, namely: the inflammatory context of cancer; the key role played by the stroma, microenvironment, endothelial cells, activated macrophages, and surrounding tissues; and the distorted developmental course followed by the neoplastic tissue.

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A letter to the IJERPH Editor was submitted by Terracini B. et al. as a comment to our latest paper "Hospitalizations in Pediatric and Adult Patients for all Cancer Type in Italy:[.

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: Cancer Registries (CRs) remain the gold standard for providing official epidemiological estimations. However, due to CRs' partial population coverage, hospitalization records might represent a valuable tool to provide additional information on cancer occurrence and expenditures at national/regional level for research purposes. The Epidemiology of Cancer in Italy (EPIKIT) study group has been built up, within the framework of the Civic Observers for Health and Environment: Initiative of Responsibility and Sustainability (COHEIRS) project under the auspices of the Europe for Citizens Program, to assess population health indicators.

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Epigenetics of Obesity.

Prog Mol Biol Transl Sci

June 2017

Department of Translational Research and New Technologies in Medicine and Surgery, Medical Genetics Laboratories, University of Pisa, Pisa, Italy. Electronic address:

Obesity is a metabolic disease, which is becoming an epidemic health problem: it has been recently defined in terms of Global Pandemic. Over the years, the approaches through family, twins and adoption studies led to the identification of some causal genes in monogenic forms of obesity but the origins of the pandemic of obesity cannot be considered essentially due to genetic factors, because human genome is not likely to change in just a few years. Epigenetic studies have offered in recent years valuable tools for the understanding of the worldwide spread of the pandemic of obesity.

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Replicative random mutations as an unproven cause of cancer: A technical comment.

Mol Clin Oncol

April 2016

Cancer Research Center, Association for Research and Treatments Against Cancer (ARTAC), F-75015 Paris, France; European Cancer and Environment Research Institute (ECERI), B-1000 Brussels, Belgium.

Article Synopsis
  • * Instead of the two groups of cancer types proposed by the original study, this reanalysis introduces a three-group model, which offers a better understanding of cancer risk factors.
  • * This new model significantly decreases the percentage of cancer cases that could be linked to random mutations, suggesting that other factors may play a more crucial role in cancer etiology.
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For at least 30 years cancer has been defined as a genetic disease and explained by the so-called somatic mutation theory (SMT), which has dominated the carcinogenesis field. Criticism of the SMT has recently greatly increased, although still not enough to force all SMT supporters to recognize its limits. Various researchers point out that cancer appears to be a complex process concerning a whole tissue; and that genomic mutations, although variably deleterious and unpredictably important in determining the establishment of the neoplastic phenotype, are not the primary origin for a malignant neoplasia.

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Obesity is becoming an epidemic health problem. During the last years not only genetic but also, and primarily, environmental factors have been supposed to contribute to the susceptibility to weight gain or to develop complications such as type 2 diabetes. In spite of the intense efforts to identify genetic predisposing variants, progress has been slow and success limited, and the common obesity susceptibility variants identified only explains a small part of the individual variation in risk.

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