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Salud Publica de Mexico 2019To perform a systematic review of the main epigenetic aberrations involved in non-small cell lung carcinomas' (NSCLC) diagnosis, progression, and therapeutics.
OBJECTIVE
To perform a systematic review of the main epigenetic aberrations involved in non-small cell lung carcinomas' (NSCLC) diagnosis, progression, and therapeutics.
MATERIALS AND METHODS
We performed a systematic review of the scientific literature on lung cancer epigenetics, focusing on NSCLC.
RESULTS
Several advances in the molecular study of classical epigenetic mechanisms and massive studies of lung cancer epigenome have contributed relevant new evidence revealing that various molecular complexes are functionally influencing genetic-epigenetic and transcriptional mechanisms that promote lung tumorigenesis (initiation, promotion, and progression), and are also involved in NSCLC therapyresistance mechanisms.
CONCLUSIONS
Several epigenetic complexes and mechanisms must be analyzed and considered for the design of new and efficient therapies, which could be fundamental to develop an integrated knowledge to achieve a comprehensive lung cancer personalized medicine.
Topics: Carcinoma, Non-Small-Cell Lung; DNA Methylation; Disease Progression; Epigenesis, Genetic; Histones; Humans; Lung Neoplasms
PubMed: 31276346
DOI: 10.21149/10089 -
Frontiers in Public Health 2023Cervical cancer (CC) is the fourth most common neoplasia affecting women worldwide. Female sex workers (FSWs) are among those at highest risk of developing and...
BACKGROUND
Cervical cancer (CC) is the fourth most common neoplasia affecting women worldwide. Female sex workers (FSWs) are among those at highest risk of developing and succumbing to CC. Yet, they are often overlooked in CC screening programs and have limited access to CC healthcare globally. The development of CC screening programs for this high-risk target population is necessary to reduce the global burden of this disease and to reach the World Health Organization's objective of accelerating the elimination of CC.
OBJECTIVE
This review summarizes findings on CC screening programs for FSWs that have been implemented worldwide, and assesses their effectiveness and sustainability.
METHODS
A scoping review was conducted using the Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR). A literature search was performed on PubMed, Swisscovery, and Google Scholar for studies describing and assessing CC screening programs for FSWs. In addition, targeted searching online Non-Governmental and International Organizations websites identified grey literature. A single reviewer screened titles and abstracts, and extracted data from the research findings.
RESULTS
The search identified 13 articles published from 1989 to 2021. All implemented programs successfully reached FSWs and provided them with CC screening during the study period. The most effective and sustainable strategies were the Screen and Treat approach, introducing CC screening into existing STI services in drop-in or outreach clinics, HPV-DNA self-sampling, and integrating sex-workers-specific services in public health facilities. Follow-up was deemed the main challenge in providing and enhancing CC healthcare to FSWs with rates of loss to follow-up ranging from 35 to 60%.
CONCLUSION
FSWs are often omitted in national CC screening programs. The further development and improvement of CC healthcare, including follow-up systems, for this high-priority target population are imperative.
Topics: Humans; Female; Early Detection of Cancer; Uterine Cervical Neoplasms; Sex Workers; Ambulatory Care Facilities; Mass Screening
PubMed: 37841741
DOI: 10.3389/fpubh.2023.1226779 -
Water Research Nov 2014Globally, denitrification is commonly employed in biological nitrogen removal processes to enhance water quality. However, substantial knowledge gaps remain concerning... (Review)
Review
Globally, denitrification is commonly employed in biological nitrogen removal processes to enhance water quality. However, substantial knowledge gaps remain concerning the overall community structure, population dynamics and metabolism of different organic carbon sources. This systematic review provides a summary of current findings pertaining to the microbial ecology of denitrification in biological wastewater treatment processes. DNA fingerprinting-based analysis has revealed a high level of microbial diversity in denitrification reactors and highlighted the impacts of carbon sources in determining overall denitrifying community composition. Stable isotope probing, fluorescence in situ hybridization, microarrays and meta-omics further link community structure with function by identifying the functional populations and their gene regulatory patterns at the transcriptional and translational levels. This review stresses the need to integrate microbial ecology information into conventional denitrification design and operation at full-scale. Some emerging questions, from physiological mechanisms to practical solutions, for example, eliminating nitrous oxide emissions and supplementing more sustainable carbon sources than methanol, are also discussed. A combination of high-throughput approaches is next in line for thorough assessment of wastewater denitrifying community structure and function. Though denitrification is used as an example here, this synergy between microbial ecology and process engineering is applicable to other biological wastewater treatment processes.
Topics: Bacteria; DNA, Bacterial; Denitrification; Environmental Microbiology; In Situ Hybridization, Fluorescence; Nitrogen; Sewage; Waste Disposal, Fluid
PubMed: 25078442
DOI: 10.1016/j.watres.2014.06.042 -
Evidence-based Complementary and... 2015Objective. To evaluate the efficacy and safety of Kushenin (KS) combined with nucleoside analogues (NAs) for chronic hepatitis B (CHB). Methods. Randomized controlled... (Review)
Review
Objective. To evaluate the efficacy and safety of Kushenin (KS) combined with nucleoside analogues (NAs) for chronic hepatitis B (CHB). Methods. Randomized controlled trials (RCTs) of KS combined with NAs for CHB were identified through 7 databases. Frequencies of loss of serum HBeAg, HBeAg seroconversion, undetectable serum HBV-DNA, ALT normalization, and adverse events at 48 weeks were abstracted by two reviewers. The Cochrane software was performed to assess the risk of bias in the included trials. Data were analyzed with Review Manager 5.3 software. Results. 18 RCTs involving 1684 subjects with CHB were included in the analysis. KS combined with NAs including lamivudine (LAM), entecavir (ETV), adefovir dipivoxil (ADV), and telbivudine (TLV) showed different degree of improvement in CHB indices. KS combined with NAs increased the frequency of loss of serum HBeAg, HBeAg seroconversion, undetectable HBV-DNA levels, and ALT normalization compared with single agents. It also decreased serum ALT and AST level after one-year treatment. However, KS combined with TLV did not show a significant difference in CHB indices. The side-effects of KS combined with NAs were light and of low frequency. Conclusion. KS combined with NAs improves the efficacy of NAs in CHB.
PubMed: 26347789
DOI: 10.1155/2015/529636 -
Complex Psychiatry 2023Posttraumatic stress disorder (PTSD) is a complex multifactorial disorder influenced by the interaction of genetic and environmental factors. Analyses of epigenomic and... (Review)
Review
INTRODUCTION
Posttraumatic stress disorder (PTSD) is a complex multifactorial disorder influenced by the interaction of genetic and environmental factors. Analyses of epigenomic and transcriptomic modifications may help to dissect the biological factors underlying the gene-environment interplay in PTSD. To date, most human PTSD epigenetics studies have used peripheral tissue, and these findings have complex and poorly understood relationships to brain alterations. Studies examining brain tissue may help characterize the brain-specific transcriptomic and epigenomic profiles of PTSD. In this review, we compiled and integrated brain-specific molecular findings of PTSD from humans and animals.
METHODS
A systematic literature search according to the PRISMA criteria was performed to identify transcriptomic and epigenomic studies of PTSD, focusing on brain tissue from human postmortem samples or animal-stress paradigms.
RESULTS
Gene- and pathway-level convergence analyses revealed PTSD-dysregulated genes and biological pathways across brain regions and species. A total of 243 genes converged across species, with 17 of them significantly enriched for PTSD. Chemical synaptic transmission and signaling by G-protein-coupled receptors were consistently enriched across omics and species.
DISCUSSION
Our findings point out dysregulated genes highly replicated across PTSD studies in humans and animal models and suggest a potential role for the corticotropin-releasing hormone/orexin pathway in PTSD's pathophysiology. Further, we highlight current knowledge gaps and limitations and recommend future directions to address them.
PubMed: 37404872
DOI: 10.1159/000529536 -
Antioxidants (Basel, Switzerland) Dec 2021Physical activity may benefit health by modulating oxidative stress and inflammation. However, the selection of suitable exercise-induced oxidative stress biomarkers is... (Review)
Review
Physical activity may benefit health by modulating oxidative stress and inflammation. However, the selection of suitable exercise-induced oxidative stress biomarkers is still challenging. This study aimed at systematically summarizing the available evidence on exercise-induced oxidative stress measured in urine and/or saliva. Two meta-analyses including the most frequently quantified biomarkers of oxidative stress, namely, urinary isoprostane and DNA oxidation products, were performed. Three electronic databases (PubMed, EMBASE and Cochrane CENTRAL) were interrogated. Among 4479 records, 43 original articles were included in the systematic review and 11 articles were included in meta-analysis I and II, respectively. We observed a pooled trend of increase of urinary isoprostanes in response to physical activity (+0.95, 95% CI: -0.18; 2.09). In comparison with aerobic exercise, anaerobic training determined a greater induction of isoprostanes (+5.21, 95% CI: 2.76; 7.66, < 0.0001), which were markedly increased after vigorous physical activity (+6.01, 95% CI: 1.18; 10.84, < 0.001) and slightly decreased in response to exercise interventions protracted over time (e.g., months) (-1.19, 95% CI: -2.25; -0.12, < 0.001). We recommend the most integrative approach of oxidative stress multi-marker panels in response to physical activity instead of selecting one preferential biomarker to quantify physical activity-induced oxidative stress in humans.
PubMed: 34943111
DOI: 10.3390/antiox10122008 -
Toxics Dec 2023A growing body of literature has attempted to characterize how traffic-related air pollution (TRAP) affects molecular and subclinical biological processes in ways that... (Review)
Review
Methylomic, Proteomic, and Metabolomic Correlates of Traffic-Related Air Pollution in the Context of Cardiorespiratory Health: A Systematic Review, Pathway Analysis, and Network Analysis.
A growing body of literature has attempted to characterize how traffic-related air pollution (TRAP) affects molecular and subclinical biological processes in ways that could lead to cardiorespiratory disease. To provide a streamlined synthesis of what is known about the multiple mechanisms through which TRAP could lead to cardiorespiratory pathology, we conducted a systematic review of the epidemiological literature relating TRAP exposure to methylomic, proteomic, and metabolomic biomarkers in adult populations. Using the 139 papers that met our inclusion criteria, we identified the omic biomarkers significantly associated with short- or long-term TRAP and used these biomarkers to conduct pathway and network analyses. We considered the evidence for TRAP-related associations with biological pathways involving lipid metabolism, cellular energy production, amino acid metabolism, inflammation and immunity, coagulation, endothelial function, and oxidative stress. Our analysis suggests that an integrated multi-omics approach may provide critical new insights into the ways TRAP could lead to adverse clinical outcomes. We advocate for efforts to build a more unified approach for characterizing the dynamic and complex biological processes linking TRAP exposure and subclinical and clinical disease and highlight contemporary challenges and opportunities associated with such efforts.
PubMed: 38133415
DOI: 10.3390/toxics11121014 -
Mutation Research. Reviews in Mutation... 2016Accumulating evidence suggests that epigenetic alterations play an important role in chemically-induced carcinogenesis. Although the epigenome and genome may be equally... (Review)
Review
Accumulating evidence suggests that epigenetic alterations play an important role in chemically-induced carcinogenesis. Although the epigenome and genome may be equally important in carcinogenicity, the genotoxicity of chemical agents and exposure-related transcriptomic responses have been more thoroughly studied and characterized. To better understand the evidence for epigenetic alterations of human carcinogens, and the potential association with genotoxic endpoints, we conducted a systematic review of published studies of genotoxic carcinogens that reported epigenetic endpoints. Specifically, we searched for publications reporting epigenetic effects for the 28 agents and occupations included in Monograph Volume 100F of the International Agency for the Research on Cancer (IARC) that were classified as "carcinogenic to humans" (Group 1) with strong evidence of genotoxic mechanisms of carcinogenesis. We identified a total of 158 studies that evaluated epigenetic alterations for 12 of these 28 carcinogenic agents and occupations (1,3-butadiene, 4-aminobiphenyl, aflatoxins, benzene, benzidine, benzo[a]pyrene, coke production, formaldehyde, occupational exposure as a painter, sulfur mustard, and vinyl chloride). Aberrant DNA methylation was most commonly studied, followed by altered expression of non-coding RNAs and histone changes (totaling 85, 59 and 25 studies, respectively). For 3 carcinogens (aflatoxins, benzene and benzo[a]pyrene), 10 or more studies reported epigenetic effects. However, epigenetic studies were sparse for the remaining 9 carcinogens; for 4 agents, only 1 or 2 published reports were identified. While further research is needed to better identify carcinogenesis-associated epigenetic perturbations for many potential carcinogens, published reports on specific epigenetic endpoints can be systematically identified and increasingly incorporated in cancer hazard assessments.
Topics: Animals; Carcinogenicity Tests; Carcinogens; Environmental Exposure; Epigenesis, Genetic; Gene Expression Regulation; Genetic Association Studies; Genetic Predisposition to Disease; Genetic Variation; Humans; Mutagenicity Tests; Mutagens; Occupational Exposure
PubMed: 27234561
DOI: 10.1016/j.mrrev.2016.03.004 -
Biomedicine & Pharmacotherapy =... Jul 2024The intricate crosstalk between long noncoding RNAs (lncRNAs) and epigenetic modifications such as chromatin/histone methylation and acetylation offer new perspectives... (Review)
Review
The intricate crosstalk between long noncoding RNAs (lncRNAs) and epigenetic modifications such as chromatin/histone methylation and acetylation offer new perspectives on the pathogenesis and treatment of kidney diseases. lncRNAs, a class of transcripts longer than 200 nucleotides with no protein-coding potential, are now recognized as key regulatory molecules influencing gene expression through diverse mechanisms. They modulate the epigenetic modifications by recruiting or blocking enzymes responsible for adding or removing methyl or acetyl groups, such as DNA, N6-methyladenosine (m6A) and histone methylation and acetylation, subsequently altering chromatin structure and accessibility. In kidney diseases such as acute kidney injury (AKI), chronic kidney disease (CKD), diabetic nephropathy (DN), glomerulonephritis (GN), and renal cell carcinoma (RCC), aberrant patterns of DNA/RNA/histone methylation and acetylation have been associated with disease onset and progression, revealing a complex interplay with lncRNA dynamics. Recent studies have highlighted how lncRNAs can impact renal pathology by affecting the expression and function of key genes involved in cell cycle control, fibrosis, and inflammatory responses. This review will separately address the roles of lncRNAs and epigenetic modifications in renal diseases, with a particular emphasis on elucidating the bidirectional regulatory effects and underlying mechanisms of lncRNAs in conjunction with DNA/RNA/histone methylation and acetylation, in addition to the potential exacerbating or renoprotective effects in renal pathologies. Understanding the reciprocal relationships between lncRNAs and epigenetic modifications will not only shed light on the molecular underpinnings of renal pathologies but also present new avenues for therapeutic interventions and biomarker development, advancing precision medicine in nephrology.
Topics: RNA, Long Noncoding; Humans; Epigenesis, Genetic; Histones; Acetylation; DNA Methylation; Kidney Diseases; Chromatin; Animals
PubMed: 38870627
DOI: 10.1016/j.biopha.2024.116922 -
Environmental Toxicology and... Dec 2017Silica nanoparticles (SiNPs) have been found to pass through biological barriers and get distributed in the human body. They induce cell apoptosis via various mechanisms... (Review)
Review
Silica nanoparticles (SiNPs) have been found to pass through biological barriers and get distributed in the human body. They induce cell apoptosis via various mechanisms in body organs. To understand these mechanisms, we carried out systematic review of in vitro studies on SiNPs-induced cell apoptosis. Office of Health Assessment and Translation approach for Systematic Review and Evidence Integration was used to identify 14 studies dating from the year 2000 to current. Four studies showed an increase in DNA damage, cell cycle arrest, proapoptotic factors and decrease in antiapoptotic factors resulting to apoptosis. Eight studies showed induction of mitochondrial dysfunction, Bax upregulation, Bcl-2 downregulation, and caspase-3, -7, -9 activities increase. Increase in FADD, TNFR1 and Bid proteins was observed in one study, while the other NO production and caspase-3 activity was increased. These studies found the potency of SiNPs to induce cell apoptosis through DNA damage, mitochondrial, tumor necrosis factor, and nitric oxide related pathways.
Topics: Animals; Apoptosis; Apoptosis Regulatory Proteins; Cell Cycle Checkpoints; DNA Damage; Down-Regulation; Humans; In Vitro Techniques; Mitochondria; Nanoparticles; Signal Transduction; Silicon Dioxide
PubMed: 28957724
DOI: 10.1016/j.etap.2017.09.012