scholarly journals Lost opportunities for cancer prevention: historical evidence on early warnings with emphasis on radiofrequency radiation

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Lennart Hardell ◽  
Michael Carlberg
Keyword(s):  
Brain Tumors ◽  
Human Cancer ◽  
Latency Period ◽  
Negative Consequences ◽  
Case Control Studies ◽  
Fifth Generation ◽  
Heating Effects ◽  
Wireless Phones ◽  
Unbiased Risk ◽  
Early Warnings

Abstract Some historical aspects on late lessons from early warnings on cancer risks with lost time for prevention are discussed. One current example is the cancer-causing effect from radiofrequency (RF) radiation. Studies since decades have shown increased human cancer risk. The fifth generation, 5G, for wireless communication is about to be implemented world-wide despite no comprehensive investigations of potential risks to human health and the environment. This has created debate on this technology among concerned people in many countries. In an appeal to EU in September 2017, currently endorsed by more than 400 scientists and medical doctors, a moratorium on the 5G deployment was required until proper scientific evaluation of negative consequences has been made (www.5Gappeal.eu). That request has not been taken seriously by EU. Lack of proper unbiased risk evaluation of the 5G technology makes adverse effects impossible to be foreseen. This disregard is exemplified by the recent report from the International Commission on non-ionizing radiation protection (ICNIRP) whereby only thermal (heating) effects from RF radiation are acknowledged despite a large number of reported non-thermal effects. Thus, no health effects are acknowledged by ICNIRP for non-thermal RF electromagnetic fields in the range of 100 kHz–300 GHz. Based on results in three case-control studies on use of wireless phones we present preventable fraction for brain tumors. Numbers of brain tumors of not defined type were found to increase in Sweden, especially in the age group 20–39 years in both genders, based on the Swedish Inpatient Register. This may be caused by the high prevalence of wireless phone use among children and in adolescence taking a reasonable latency period and the higher vulnerability to RF radiation among young persons.

scholarly journals Increasing Evidence for Involvement of SV40 in Human Cancer

2001 ◽  
Vol 17 (3) ◽  
pp. 167-172 ◽  
Author(s):  
Janet S. Butel
Keyword(s):  
Brain Tumors ◽  
Functional Role ◽  
Human Cancer ◽  
Tumor Development ◽  
Human Tumor ◽  
Dna Virus ◽  
Oncogenic Potential ◽  
Tumor Virus ◽  
Human Infections

SV40, a small DNA virus, is known to possess strong oncogenic potential. Millions of people were exposed to SV40 as an unknown contaminant of some early poliovaccines. This article briefly summarizes the increasing evidence of the association of SV40 with certain types of human cancer, including mesotheliomas and brain tumors. Unanswered questions pertaining to the pathogenesis of human infections by SV40 and the functional role of the virus in tumor development are noted. It is concluded that SV40 should be considered a candidate human tumor virus and that vigorous efforts to clarify the role of the virus in human disease should be supported.

TP53 Mutations in Canine Brain Tumors

2011 ◽  
Vol 49 (5) ◽  
pp. 796-801 ◽  
Author(s):  
D. York ◽  
R. J. Higgins ◽  
R. A. LeCouteur ◽  
A. N. Wolfe ◽  
R. Grahn ◽  
...  
Keyword(s):  
Brain Tumors ◽  
Human Cancer ◽  
Gene Mutations ◽  
Tp53 Gene ◽  
Suppressor Gene ◽  
Cancer Mutation ◽  
Canine Brain ◽  
Gene Tp53 ◽  
Altered Gene ◽  
P53 Inactivation

The p53 tumor suppressor gene ( TP53) is the most frequently altered gene in human cancer. Mutation of the gene has been shown to be an important mechanism of p53 pathway inactivation in a variety of human brain tumors, particularly those of astrocytic origin. Genomic DNA from a series of 37 glial and 51 nonglial canine brain tumors was sequenced to determine the frequency of TP53 gene mutations involving exons 3–9. Exonic mutations were found in 3 of 88 tumors (3.4%) and specifically in 1 of 18 astrocytic tumors (5.5%). This is markedly lower than that reported in comparable human tumors, suggesting that alternative mechanisms of p53 inactivation are likely to be present if p53 function contributes significantly to oncogenesis in canine brain tumors.

scholarly journals Eruptive Seborrheic Keratoses Are Associated With a Co-Occurring Malignancy in the Majority of Reported Cases: A Systematic Review

2021 ◽  
pp. 120347542110351
Author(s):  
Sara Mirali ◽  
Asfandyar Mufti ◽  
Rafael Paolo Lansang ◽  
Muskaan Sachdeva ◽  
Jensen Yeung
Keyword(s):  
Systematic Review ◽  
Medical Condition ◽  
Case Reports ◽  
Healthcare Providers ◽  
Case Series ◽  
Latency Period ◽  
Skin Condition ◽  
Case Control Studies ◽  
Drug Induced ◽  
Seborrheic Keratoses

Background Eruptive seborrheic keratoses (ESK) is a benign skin condition that has been associated with malignant and nonmalignant diseases. We conducted a systematic review of reported cases of ESK to identify and summarize associated comorbidities. Methods MEDLINE and Embase were searched from database inception (1946) to July 31, 2020 for original articles describing ESK with or without a co-occurring condition. Subject demographics, as well as details of ESK and associated diagnoses were extracted from 76 articles (70 case reports, 3 case series, 3 case control studies) representing 92 patients. Results In total, 76.1% ( n = 70/92) of patients with ESK had a co-occurring malignancy, 4.3% ( n = 4/92) presented with a nonmalignant condition, 9.8% ( n = 9/92) experienced ESK as an adverse drug reaction, and 9.8% ( n = 9/92) did not report any underlying medical condition. ESK preceded a cancer diagnosis in 76.1% ( n = 70/92) of patients with a mean latency period of 4.0 months (range: 0.25-9 months). The most common malignancies associated with ESK were cutaneous T-cell lymphoma ( n = 10/70, 14.3%) and gastrointestinal adenocarcinoma ( n = 9/70, 12.9%). ESK preceded nonmalignant conditions or no disease in 14.1% ( n = 13/92) of patients with a mean latency period of 3.1 months (range: 0.75-6 months). Drug-induced ESK occurred in 9.8% ( n = 9/92) of patients with a mean latency period of 7.1 weeks after changing medication. Conclusion Although the role of ESK as a paraneoplastic cutaneous marker is debated, healthcare providers should consider screening for underlying malignancy in patients presenting with ESK. Larger studies are needed to confirm its role as a marker for disease.

EXTH-69. FUNCTIONAL GENOMICS UNCOVER GENETIC DEPENDENCIES IN ATRTS

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi179-vi179
Author(s):  
Daniel Merk ◽  
Sophie Hirsch ◽  
Foteini Tsiami ◽  
Bianca Walter ◽  
Lara Haeusser ◽  
...  
Keyword(s):  
Brain Tumors ◽  
Small Molecule ◽  
Human Cancer ◽  
Human Cancer Cell Lines ◽  
Drug Assays ◽  
Atypical Teratoid ◽  
Embryonal Brain ◽  
Atypical Teratoid Rhabdoid Tumors ◽  
Rhabdoid Tumors ◽  
Context Specific

Abstract Brain tumors are the leading cause of cancer-related deaths in children. Embryonal brain tumors including medulloblastoma and atypical teratoid rhabdoid tumors (ATRTs) account for 15% of all primary brain and CNS tumors under the age of 14 years, with ATRTs being most prevalent in infants. Despite intensive research efforts, survival estimates for ATRT patients stay relatively low as compared to other tumor entities with a median survival of around 17 months. We here describe genome-wide CRISPR/Cas9 knockout screens in combination with small-molecule drug assays to identify targetable vulnerabilities in ATRTs. Based on functional genomic screening revealing ATRT context-specific genetic vulnerabilities (n = 671 genes), we successfully generated a small-molecule library that shows preferential activity in ATRT cells as compared to a broad selection of other human cancer cell lines. Of note, none of these drugs differentially affect ATRT cells from distinct molecular subgroups, suggesting that top candidate inhibitors might serve as pan-ATRT therapeutic avenues. CDK4/6 inhibitors, among the most potent drugs in our library, are capable of inhibiting tumor growth due to mutual exclusive dependency of ATRTs on either CDK4 or CDK6. Our approach might serve as a blueprint for fostering the identification of functionally-instructed therapeutic strategies in other incurable diseases beyond ATRT, whose genomic profiles also lack actionable alterations so far.

Risk Assessment

2002 ◽  
Keyword(s):  
Risk Assessment ◽  
Human Health ◽  
Large Scale ◽  
Human Cancer ◽  
Food Additives ◽  
Latency Period ◽  
Epidemiological Studies ◽  
Preliminary Evaluation ◽  
Active Ingredients ◽  
Daily Lives

The purpose of risk assessment is estimation of the severity of harmful effects to human health and the environment that may result from exposure to chemicals present in the environment. The Environmental Protection Agency (EPA) procedure of risk assessment, whether related to human health or to the environment, involves four steps: 1. hazard assessment 2. dose–response assessment 3. exposure assessment 4. risk characterization The quantity of chemicals in use today is staggering. According to the data compiled by Hodgson and Guthrie in 1980 (1), there were then 1500 active ingredients of pesticides, 4000 active ingredients of therapeutic drugs, 2000 drug additives to improve stability, 2500 food additives with nutritional value, 3000 food additives to promote product life, and 50,000 additional chemicals in common use. Considering the growth of the chemical and pharmaceutical industries, these amounts must now be considerably larger. Past experience has shown that some of these chemicals, although not toxic unless ingested in large quantities, may be mutagenic and carcinogenic with chronic exposure to minute doses, or may interfere with the reproductive or immune systems of humans and animals. To protect human health it is necessary to determine that compounds to which people are exposed daily or periodically in their daily lives (such as cosmetics, foods, and pesticides) will not cause harm upon long-term exposure. The discussion in this chapter will focus primarly on carcinogenicity and mutagenicity, but also endocrine disrupters will be considered. The carcinogenicity of some chemicals was established through epidemiological studies. However, because of the long latency period of cancer, epidemiological studies require many years before any conclusions can be reached. In addition, they are very expensive. Another method that could be used is bioassay in animals. Such bioassays, although quite useful in predicting human cancer hazard, may take as long as 2 years or more and require at least 600 animals per assay. This method is also too costly in terms of time and money to be considered for large-scale screening. For these reasons an inexpensive, short-term assay system is needed for preliminary evaluation of potential mutagens and carcinogens.

scholarly journals Periodontitis as a potential risk factor for premature delivery

2021 ◽  
Vol 8 (1) ◽  
pp. 27-33
Author(s):  
Ana Turcu-Duminică ◽  
Anca Dumitriu ◽  
Stana Paunica ◽  
Corina Gică ◽  
Radu Botezatu ◽  
...  
Keyword(s):  
Birth Weight ◽  
Periodontal Disease ◽  
Premature Birth ◽  
Premature Delivery ◽  
Negative Consequences ◽  
Case Control Studies ◽  
Natural Evolution ◽  
Prospective Cohort Studies ◽  
The Subject ◽  
The Impact

Pregnancy is a particular period of time for a woman, so that it is important to accurately determine the impact of adjacent pathologies on the natural evolution of the nine months of pregnancy. Although there is still much to debate on the association between periodontal disease and pregnancy, the conclusion seems to remain the same: untreated periodontal pathology in pregnancy could have adverse consequences such as premature birth or low birth weight fetuses. Periodontopathies are introduced as risk factors, the novelty of the subject being the association between untreated periodontal pathology and the evolution of pregnancy. The affected periodontal tissue has the potential of releasing microorganisms that could colonize the placenta, ultimately having adverse consequences on the evolution of pregnancy, consequences such as premature birth or inadequate birth weight. The purpose of this review is to assess the association between periodontal disease and the negative consequences on pregnancy. Using databases such as PubMed, more than 1,500 articles were screened, including systematic reviews, case-control studies and prospective cohort studies assessing the association between periodontitis and pregnancy. Only 54 from the abovementioned papers were included in the final review.

scholarly journals Evaluation of Mobile Phone and Cordless Phone Use and Glioma Risk Using the Bradford Hill Viewpoints from 1965 on Association or Causation

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Michael Carlberg ◽  
Lennart Hardell
Keyword(s):  
Animal Studies ◽  
Meta Analysis ◽  
Low Frequency ◽  
Cumulative Exposure ◽  
Malignant Schwannoma ◽  
Case Control Studies ◽  
Cordless Phone ◽  
Increased Risk ◽  
Wireless Phones ◽  
Glioma Risk

Objective.Bradford Hill’s viewpoints from 1965 on association or causation were used on glioma risk and use of mobile or cordless phones.Methods.All nine viewpoints were evaluated based on epidemiology and laboratory studies.Results.Strength: meta-analysis of case-control studies gave odds ratio (OR) = 1.90, 95% confidence interval (CI) = 1.31–2.76 with highest cumulative exposure. Consistency: the risk increased with latency, meta-analysis gave in the 10+ years’ latency group OR = 1.62, 95% CI = 1.20–2.19. Specificity: increased risk for glioma was in the temporal lobe. Using meningioma cases as comparison group still increased the risk. Temporality: highest risk was in the 20+ years’ latency group, OR = 2.01, 95% CI =1.41–2.88, for wireless phones. Biological gradient: cumulative use of wireless phones increased the risk. Plausibility: animal studies showed an increased incidence of glioma and malignant schwannoma in rats exposed to radiofrequency (RF) radiation. There is increased production of reactive oxygen species (ROS) from RF radiation. Coherence: there is a change in the natural history of glioma and increasing incidence. Experiment: antioxidants reduced ROS production from RF radiation. Analogy: there is an increased risk in subjects exposed to extremely low-frequency electromagnetic fields.Conclusion.RF radiation should be regarded as a human carcinogen causing glioma.

scholarly journals The influence of LncRNA H19 polymorphic variants on susceptibility to cancer: A systematic review and updated meta-analysis of 28 case-control studies

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0254943
Author(s):  
Kunpeng Wang ◽  
Zheng Zhu ◽  
Yiqiu Wang ◽  
Dayuan Zong ◽  
Peng Xue ◽  
...  
Keyword(s):  
Systematic Review ◽  
Subgroup Analysis ◽  
Sequential Analysis ◽  
Cancer Susceptibility ◽  
Human Cancer ◽  
Meta Analysis ◽  
Trial Sequential Analysis ◽  
Control Group ◽  
Case Control Studies ◽  
Polymorphic Variants

Objective Although myriad researches upon the associations between LncRNA H19 polymorphic variants (rs2839698 G>A, rs217727 G>A, rs2107425 C>T, rs2735971 A>G and rs3024270 C>G) and the susceptibility to cancer have been conducted, these results remained contradictory and perplexing. Basing on that, a systematic review and updated meta-analysis was performed to anticipate a fairly precise assessment about such associations. Methods We retrieved the electronic databases EMBASE, PubMed and Web of Science for valuable academic studies before February 28, 2021. Ultimately, 28 of which were encompassed after screening in this meta-analysis, and the available data was extracted and integrated. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) was used to evaluate such associations. For multi-level investigation, subgroup analysis derived from source of controls together with genotypic method was preformed. Results Eventually, 28 articles altogether embodying 57 studies were included in this meta-analysis. The results illuminated that LncRNA H19 polymorphisms mentioned above were all irrelevant to cancer susceptibility. Nevertheless, crucial results were found concentrated in population-based control group when subgroup analysis by source of controls were performed in H19 mutation rs2839698 and rs2735971. Meanwhile, in the stratification analysis by genotypic method, apparent cancer risks were discovered by TaqMan method in H19 mutation rs2107425 and rs3024270. Then, trial sequential analysis demonstrated that the results about such associations were firm evidence of effect. Conclusion Therefore, this meta-analysis indicated that LncRNA H19 polymorphisms were not associated with the susceptibility to human cancer. However, after the stratification analysis, inconsistent results still existed in different genotypic method and source of control. Thus, more high-quality studies on cancer patients of different factors were needed to confirm these findings.

scholarly journals Hypothesis Tests for Neyman's Bias in Case-Control Studies

2016 ◽  
Author(s):  
David Swanson ◽  
Rebecca Betensky ◽  
Chris Anderson
Keyword(s):  
Atrial Fibrillation ◽  
Brain Tumors ◽  
Odds Ratio ◽  
Case Control ◽  
Data Sets ◽  
Stroke Mortality ◽  
Hypothesis Tests ◽  
Case Control Studies

Survival bias is a long-recognized problem in case-control studies, and many varieties of bias can come under this umbrella term. We focus on one of them, termed Neyman's bias or "prevalence-incidence bias." It occurs in case-control studies when exposure affects both disease and disease-induced mortality, and we give a formula for the observed, biased odds ratio under such conditions. We compare our result with previous investigations into this phenomenon and consider models under which this bias may or may not be important. Finally, we propose three hypothesis tests to identify when Neyman's bias may be present in case-control studies. We apply these tests to three data sets, one of stroke mortality, another of brain tumors, and the last of atrial fibrillation, and find some evidence of Neyman's bias in the former two cases, but not the last case. Keywords: odds ratio; survival bias; truncation.

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