Topical Collection "Occupational and Environmental Carcinogenesis"

A topical collection in Cancers (ISSN 2072-6694). This collection belongs to the section "Cancer Epidemiology and Prevention".

Editors

Topical Collection Information

Dear Colleagues,

Carcinogenesis is a complex, multistep process, involving the accumulation of genetic and epigenetic alterations that confer growth and/or survival advantages, through which cells gradually achieve unchecked growth and eventually become fully malignant and invasive. There are numerous sources of physical, chemical, and biological exposures that stem from endogenous and exogenous sources—including occupational and environmental settings—that can induce such genetic and epigenetic alterations. This damage is repaired through a high-fidelity DNA repair process that operates through multiple pathways, although the system is imperfect and varies by repair mechanism, potentially resulting in the incorporation of DNA damage and epigenetic alterations.

Any substance that causes cancer is referred to as a carcinogen. If allowed to accumulate in the body for an extended period of time, there is a greater likelihood your cells will become damaged, which results in the growth of cancer cells.

Some of these changes in our cells may be caused by genetics, while others may be caused by environmental and occupational factors. Environmental and occupational factors can include a wide range of exposures, such as the following:

  • Lifestyle factors (nutrition, tobacco use, physical activity)
  • Natural occurring exposures (ultraviolet light, radon gas, infectious agents)
  • Medical treatments (radiation and medicine)
  • Workplace and household exposures
  • Pollution
  • Asbestos
  • Formaldehyde
  • Radon
  • Wood dust

Furthermore, it is relevant to study the epidemiology of probable/possible carcinogens in order to clarify the real effects on health.

In conclusion, the objective of this Special Issue is to clarify aspects related to carcinogenesis and occupational and/or environmental exposure.
Therefore in silico, in vitro, ex vivo, epidemiological studies and reviews are welcome.

Prof. Dr. Caterina Ledda
Prof. Dr. Venerando Rapisarda
Collection Editors

Manuscript Submission Information

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Keywords

  • occupational
  • environmental
  • exposure
  • workplace
  • epigenetics

Published Papers (6 papers)

2021

Jump to: 2020

Article
Oxidative Stress Biomarkers in Urine of Metal Carpentry Workers Can Be Diagnostic for Occupational Exposure to Low Level of Welding Fumes from Associated Metals
Cancers 2021, 13(13), 3167; https://doi.org/10.3390/cancers13133167 (registering DOI) - 24 Jun 2021
Abstract
Urinary concentrations of 16 different exposure biomarkers to metals were determined at the beginning and at the end of a working shift on a group of workers in the metal carpentry industry. Five different oxidative stress biomarkers were also measured, such as the [...] Read more.
Urinary concentrations of 16 different exposure biomarkers to metals were determined at the beginning and at the end of a working shift on a group of workers in the metal carpentry industry. Five different oxidative stress biomarkers were also measured, such as the oxidation products of RNA and DNA metabolized and excreted in the urine. The results of workers exposed to metals were compared to those of a control group. The metal concentrations found in these workers were well below the occupational exposure limit values and exceeded the mean concentrations of the same metals in the urine of the control group by a factor of four at maximum. Barium (Ba), mercury (Hg), lead (Pb) and strontium (Sr) were correlated with the RNA oxidative stress biomarker, 8-oxo-7, 8-dihydroguanosine (8-oxoGuo), which was found able to discriminate exposed workers from controls with a high level of specificity and sensitivity. The power of this early diagnostic technique was assessed by means of the ROC curve. Ba, rubidium (Rb), Sr, tellurium (Te), and vanadium (V) were correlated with the level of the protein oxidation biomarker 3-Nitrotyrosine (3-NO2Tyr), and Ba, beryllium (Be), copper (Cu), and Rb with 5-methylcytidine (5-MeCyt), an epigenetic marker of RNA damage. These effect biomarkers can help in identifying those workers that can be defined as “occupationally exposed” even at low exposure levels, and they can provide information about the impact that such doses have on their health. Full article
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Graphical abstract

Review
Cadmium-Associated Molecular Signatures in Cancer Cell Models
Cancers 2021, 13(11), 2823; https://doi.org/10.3390/cancers13112823 - 05 Jun 2021
Viewed by 381
Abstract
The exposure of cancer cells to cadmium and its compounds is often associated with the development of more malignant phenotypes, thereby contributing to the acceleration of tumor progression. It is known that cadmium is a transcriptional regulator that induces molecular reprogramming, and therefore [...] Read more.
The exposure of cancer cells to cadmium and its compounds is often associated with the development of more malignant phenotypes, thereby contributing to the acceleration of tumor progression. It is known that cadmium is a transcriptional regulator that induces molecular reprogramming, and therefore the study of differentially expressed genes has enabled the identification and classification of molecular signatures inherent in human neoplastic cells upon cadmium exposure as useful biomarkers that are potentially transferable to clinical research. This review recapitulates selected studies that report the detection of cadmium-associated signatures in breast, gastric, colon, liver, lung, and nasopharyngeal tumor cell models, as specifically demonstrated by individual gene or whole genome expression profiling. Where available, the molecular, biochemical, and/or physiological aspects associated with the targeted gene activation or silencing in the discussed cell models are also outlined. Full article
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Review
Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression
Cancers 2021, 13(10), 2392; https://doi.org/10.3390/cancers13102392 - 14 May 2021
Viewed by 404
Abstract
Benzene carcinogenic ability has been reported, and chronic exposure to benzene can be one of the risk elements for solid cancers and hematological neoplasms. Benzene is acknowledged as a myelotoxin, and it is able to augment the risk for the onset of acute [...] Read more.
Benzene carcinogenic ability has been reported, and chronic exposure to benzene can be one of the risk elements for solid cancers and hematological neoplasms. Benzene is acknowledged as a myelotoxin, and it is able to augment the risk for the onset of acute myeloid leukemia, myelodysplastic syndromes, aplastic anemia, and lymphomas. Possible mechanisms of benzene initiation of hematological tumors have been identified, as a genotoxic effect, an action on oxidative stress and inflammation and the provocation of immunosuppression. However, it is becoming evident that genetic alterations and the other causes are insufficient to fully justify several phenomena that influence the onset of hematologic malignancies. Acquired epigenetic alterations may participate with benzene leukemogenesis, as benzene may affect nuclear receptors, and provoke post-translational alterations at the protein level, thereby touching the function of regulatory proteins, comprising oncoproteins and tumor suppressor proteins. DNA hypomethylation correlates with stimulation of oncogenes, while the hypermethylation of CpG islands in promoter regions of specific tumor suppressor genes inhibits their transcription and stimulates the onset of tumors. The discovery of the systems of epigenetic induction of benzene-caused hematological tumors has allowed the possibility to operate with pharmacological interventions able of stopping or overturning the negative effects of benzene. Full article
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Article
Increased Hospitalization and Mortality from COVID-19 in Prostate Cancer Patients
Cancers 2021, 13(7), 1630; https://doi.org/10.3390/cancers13071630 - 01 Apr 2021
Viewed by 418
Abstract
Background: Cancer patients with COVID-19 have a poor disease course. Among tumor types, prostate cancer and COVID-19 share several risk factors, and the interaction of prostate cancer and COVID-19 is purported to have an adverse outcome. Methods: This was a single-institution retrospective study [...] Read more.
Background: Cancer patients with COVID-19 have a poor disease course. Among tumor types, prostate cancer and COVID-19 share several risk factors, and the interaction of prostate cancer and COVID-19 is purported to have an adverse outcome. Methods: This was a single-institution retrospective study on 286,609 patients who underwent the COVID-19 test at Mount Sinai Hospital system from March 2020 to December 2020. Chi-square/Fisher’s exact tests were used to summarize baseline characteristics of categorical data, and Mann–Whitney U test was used for continuous variables. Univariable logistic regression analysis to compare the hospitalization and mortality rates and the strength of association was obtained by the odds ratio and confidence interval. Results: This study aimed to compare hospitalization and mortality rates between men with COVID-19 and prostate cancer and those who were COVID-19-positive with non-prostate genitourinary malignancy or any solid cancer, and with breast cancer patients. We also compared our studies to others that reported the incidence and severity of COVID-19 in prostate cancer patients. Our studies highlight that patients with prostate cancer had higher susceptibility to COVID-19-related pathogenesis, resulting in higher mortality and hospitalization rates. Hospitalization and mortality rates were higher in prostate cancer patients with COVID-19 when compared with COVID-19 patients with non-prostate genitourinary (GU) malignancies. Full article
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2020

Jump to: 2021

Review
Thyroid Cancer and Circadian Clock Disruption
Cancers 2020, 12(11), 3109; https://doi.org/10.3390/cancers12113109 - 24 Oct 2020
Cited by 3 | Viewed by 1077
Abstract
Thyroid cancer (TC) represents the most common malignancy of the endocrine system, with an increased incidence across continents attributable to both improvement of diagnostic procedures and environmental factors. Among the modifiable risk factors, insulin resistance might influence the development of TC. A relationship [...] Read more.
Thyroid cancer (TC) represents the most common malignancy of the endocrine system, with an increased incidence across continents attributable to both improvement of diagnostic procedures and environmental factors. Among the modifiable risk factors, insulin resistance might influence the development of TC. A relationship between circadian clock machinery disfunction and TC has recently been proposed. The circadian clock machinery comprises a set of rhythmically expressed genes responsible for circadian rhythms. Perturbation of this system contributes to the development of pathological states such as cancer. Several clock genes have been found deregulated upon thyroid nodule malignant transformation. The molecular mechanisms linking circadian clock disruption and TC are still unknown but could include insulin resistance. Circadian misalignment occurring during shift work, jet lag, high fat food intake, is associated with increased insulin resistance. This metabolic alteration, in turn, is associated with a well-known risk factor for TC i.e., hyperthyrotropinemia, which could also be induced by sleep disturbances. In this review, we describe the mechanisms controlling the circadian clock function and its involvement in the cell cycle, stemness and cancer. Moreover, we discuss the evidence supporting the link between circadian clockwork disruption and TC development/progression, highlighting its potential implications for TC prevention, diagnosis and therapy. Full article
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Editorial
Occupational and Environmental Carcinogenesis
Cancers 2020, 12(9), 2547; https://doi.org/10.3390/cancers12092547 - 08 Sep 2020
Cited by 4 | Viewed by 858
Abstract
Occupational carcinogens have been shown to cause a considerable disease burden at a national and global level [...] Full article
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