Phototherapy and childhood cancer: Shared risk factors.
Ontology highlight
ABSTRACT:
SUBMITTER: Heck JE
PROVIDER: S-EPMC7017910 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:BackgroundNeonatal phototherapy (NNPT) has long been used as an effective and relatively safe method of treating neonatal hyperbilirubinemia. Considering the subsequent evidence of long-term impacts of NNPT such as malignancies, this study was conducted to evaluate the relationship between NNPT and childhood cancers.MethodsThis case-control study assessed 116 children up to 4 years old with every kind of cancer referred to the Oncology department of Afzalipour hospital, Kerman, Iran, from 2011 to 18. Moreover, 116 pediatric patients without cancer hospitalized at the same Center were included after sex and age matching as the control group. The history of phototherapy and its duration were evaluated in these two groups.ResultsWe found no association between the NNPT and malignancies in children. However, high intensive phototherapy was higher historically among affected cancerous patients than in non-cancerous cases without any statistically significant difference (25% vs 19%; P = 0.26). Maternal educational level and history of maternal infection during pregnancy, which initially appeared to be two factors associated with malignancy in single variable regression analyses, were not significant based on the adjusted models.ConclusionsThe results did not show a positive correlation between NNPT and childhood cancers, which may partly be due to the relatively small sample size of the study. However, some other evidence is worrisome enough that NNPT should not be considered risk-free. Additional multi-centric studies should be undertaken to specify that phototherapy is really safe.
| S-EPMC9215034 | biostudies-literature
Project description:Cancer and cardiovascular diseases (CVD) account for approximately 27.5 million deaths every year. While they share some common environmental risk factors, their shared genetic risk factors are not yet fully understood. The aim of the present study was to aggregate genetic risk factors associated with the comorbidity of cancer and CVDs. For this purpose, we: (1) created a catalog of genes associated with cancer and CVDs, (2) visualized retrieved data as a gene-disease network, and (3) performed a pathway enrichment analysis. We performed screening of PubMed database for literature reporting genetic risk factors in patients with both cancer and CVD. The gene-disease network was visualized using Cytoscape and the enrichment analysis was conducted using Enrichr software. We manually reviewed the 181 articles fitting the search criteria and included 13 articles in the study. Data visualization revealed a highly interconnected network containing a single subnetwork with 56 nodes and 146 edges. Genes in the network with the highest number of disease interactions were JAK2, TTN, TET2, and ATM. The pathway enrichment analysis revealed that genes included in the study were significantly enriched in DNA damage repair (DDR) pathways, such as homologous recombination. The role of DDR mechanisms in the development of CVDs has been studied in previously published research; however, additional functional studies are required to elucidate their contribution to the pathophysiology to CVDs.
| S-EPMC9300967 | biostudies-literature
Project description:BackgroundIdentifying modifiable risk factors for child victimisation and polyvictimisation (exposure to multiple types of victimisation) is critical for informing prevention efforts, yet little evidence is available in low- and middle-income countries. The authors aimed to estimate the prevalence of child victimisation and polyvictimisation, and examine unique and shared risk factors in a population-based cohort in Southern Brazil.MethodsLifetime child victimisation was based on maternal report when children were aged 4 years old (N∼3900) and included five types of victimisation (conventional crime, child maltreatment, peer/sibling victimisation, sexual victimisation, and witnessing/indirect victimisation) and polyvictimisation. Based on a socioecological model, possible risk factors were examined in four levels: community, maternal and family, parent, and child.FindingsConventional crime and peer/sibling victimisation were the most common types of victimisation (46.0 and 46.5%, respectively), followed by witnessing/indirect victimisation (27.0%), and child maltreatment (11.3%). Sexual victimisation had the lowest prevalence (1.4%). One in 10 (10.1%) children experienced polyvictimisation. In general, boys had higher victimisation rates than girls. There were few risk factors related only to specific types of victimisation (e.g., child disability was uniquely associated with child maltreatment and peer/sibling victimisation). Instead, most risk factors were shared across nearly all victimisation types and also associated with polyvictimisation. These shared risk factors were: violent neighbourhood and low social cohesion, maternal adverse childhood experiences, younger maternal age, parental antisocial behaviour, intimate partner violence against mothers, and maternal depression.InterpretationThese findings reveal a general pattern of accumulative risk effects for different types of victimisation and polyvictimisation, rather than unique risk profiles in children aged four year Prevention efforts should target risk factors at multiple levels (e.g.,: community, maternal and family and parent) during early childhood.FundingWellcome Trust grant 10735_Z_18_Z.
| S-EPMC10950884 | biostudies-literature
Project description:BackgroundChildhood-onset and adult-onset asthma differ with respect to severity and comorbidities. Whether they also differ with respect to genetic risk factors has not been previously investigated in large samples. The goals of this study were to identify shared and distinct genetic risk loci for childhood-onset and adult-onset asthma, and to identify the genes that might mediate the effects of associated variation.MethodsWe did genome-wide and transcriptome-wide studies, using data from the UK Biobank, in individuals with asthma, including adults with childhood-onset asthma (onset before 12 years of age), adults with adult-onset asthma (onset between 26 and 65 years of age), and adults without asthma (controls; aged older than 38 years). We did genome-wide association studies (GWAS) for childhood-onset asthma and adult-onset asthma each compared with shared controls, and for age of asthma onset in all asthma cases, with a genome-wide significance threshold of p<5 × 10-8. Enrichment studies determined the tissues in which genes at GWAS loci were most highly expressed, and PrediXcan, a transcriptome-wide gene-based test, was used to identify candidate risk genes.FindingsOf 376 358 British white individuals from the UK Biobank, we included 37 846 with self-reports of doctor-diagnosed asthma: 9433 adults with childhood-onset asthma; 21 564 adults with adult-onset asthma; and an additional 6849 young adults with asthma with onset between 12 and 25 years of age. For the first and second GWAS analyses, 318 237 individuals older than 38 years without asthma were used as controls. We detected 61 independent asthma loci: 23 were childhood-onset specific, one was adult-onset specific, and 37 were shared. 19 loci were associated with age of asthma onset. The most significant asthma-associated locus was at 17q12 (odds ratio 1·406, 95% CI 1·365-1·448; p=1·45 × 10-111) in the childhood-onset GWAS. Genes at the childhood onset-specific loci were most highly expressed in skin, blood, and small intestine; genes at the adult onset-specific loci were most highly expressed in lung, blood, small intestine, and spleen. PrediXcan identified 113 unique candidate genes at 22 of the 61 GWAS loci. Single-nucleotide polymorphism-based heritability estimates were more than three times larger for childhood-onset asthma (0·327) than for adult-onset disease (0·098). The onset of disease in childhood was associated with additional genes with relatively large effect sizes, with the largest odds ratio observed at the FLG locus at 1q21.3 (1·970, 95% CI 1·823-2·129).InterpretationGenetic risk factors for adult-onset asthma are largely a subset of the genetic risk for childhood-onset asthma but with overall smaller effects, suggesting a greater role for non-genetic risk factors in adult-onset asthma. Combined with gene expression and tissue enrichment patterns, we suggest that the establishment of disease in children is driven more by dysregulated allergy and epithelial barrier function genes, whereas the cause of adult-onset asthma is more lung-centred and environmentally determined, but with immune-mediated mechanisms driving disease progression in both children and adults.FundingUS National Institutes of Health.
| S-EPMC6534440 | biostudies-literature
Project description:Childhood cancer survivors are at increased risk of cardiovascular disease (CVD), which may be associated with traditional CVD risk factors. We used CVD risk aggregation instruments to describe survivor cardiometabolic health and compared their results with sibling controls.Traditional CVD risk factors measured in 110 survivors and 31 sibling controls between 15 and 39 years old were aggregated using Pathobiological Determinants of Atherosclerosis in Youth (PDAY) scores and the Framingham Risk Calculator (FRC) and expressed as ratios. The PDAY odds ratio represents the increased odds of currently having an advanced coronary artery lesion, and the FRC risk ratio represents the increased risk of having a myocardial infarction, stroke, or coronary death in the next 30 years. Ratios are relative to an individual of similar age and sex without CVD risk factors.The median PDAY odds ratio for survivors was 2.2 (interquartile range 1.3-3.3), with 17% >4. The median FRC risk ratio was 1.7 (interquartile range 1.0-2.0), with 12% >4. Survivors and siblings had similar mean PDAY odds ratios (2.33 vs 2.29, P = .86) and FRC risk ratios (1.72 vs 1.53, P = .24). Cancer type and treatments were not associated with cardiometabolic health. There was a suggested association for physical inactivity with PDAY odds ratios (r = 0.17, P = .10) and FRC risk ratios (r = 0.19, P = .12).Cardiometabolic health is poor in childhood cancer survivors but not different than that of their siblings, highlighting the importance of managing traditional CVD risk factors and considering novel exposures in survivors.
| S-EPMC3374397 | biostudies-literature
Project description:To investigate maternal and perinatal risk factors for childhood cancer.Case-control analysis of linked records from the Aberdeen Maternity and Neonatal Databank with the Scottish Cancer Registry and the General Registry of Births and Deaths in Scotland was carried out.Aberdeen, Scotland.Cases (n=176) comprised children diagnosed with cancer under 15 years or recorded as having died of cancer. Four controls per case were matched by age and gender.Maternal age, body mass index, social class, marital status and smoking as well as pre-eclampsia, antepartum haemorrhage and previous miscarriage, gestational age, birth weight and Apgar scores were compared between groups to test for association with cancer. ORs with 95% CIs were calculated using conditional logistic regression in univariable and multivariable models.Of the maternal characteristics tested, mother's age at delivery (cases mean 28.9 (SD 5.6) years vs controls mean 30.2 (SD 4.6), p=0.002) and smoking status (38.6% smokers among cases, 29.7% among controls, p=0.034) were found to be different between groups. Of the perinatal factors tested, low Apgar score at 5 min (adjusted OR (AOR) 4.59, 95% CI 1.52 to 13.87) and delivery by caesarean section (AOR 1.95, 95% CI 1.30 to 2.92) showed statistically significant associations with childhood cancer in the multivariable model.Younger maternal age, maternal smoking, delivery by caesarean section and low Apgar score at 5 min were independently associated with increased risk of childhood cancer. These general findings should be interpreted with caution as this study did not have the power to detect any association with individual diagnostic categories of childhood cancer.
| S-EPMC3902197 | biostudies-literature
Project description:PurposeAlthough studies regarding dental developmental disturbances after childhood cancer treatment have increased, they have many limitations. Studies analyzing the significance of independent clinical risk factors with regard to the dental health status are also rare. We aimed to investigate the risk factors for dental developmental disturbances, particularly severe disturbances, in childhood cancer survivors (CCS).Materials and methodsOral examinations and retrospective reviews of medical and panoramic radiographs were performed for 196 CCS (mean age, 15.6 years). Cancer type, age at diagnosis, treatment modality, type and accumulated dose of administered drugs, and dose and site of radiation were recorded. Dental developmental disturbances were diagnosed using panoramic radiographs and graded for severity according to the Modified Dental Defect Index (MDDI). Descriptive statistics and multivariate analyseswere performed to determine the association between dental abnormalities and clinical factors.ResultsIn total, 109 CCS (55.6%) exhibited at least one dental anomaly, and the median value of MDDI was 2.5. Microdontia (30.6%) was the most prevalent anomaly, followed by tooth agenesis (20.4%), V-shaped roots (14.8%), and taurodontism (10.2%). Multivariate analysis revealed that a young age at diagnosis (≤ 3 years), a history of hematopoietic stem cell transplantation, the use of multiple classes of chemotherapeutic agents (≥ 4 classes), and the use of heavy metal agents were significant risk factors for severe dental disturbances.ConclusionCCS with any of the above risk factors for severe developmental disturbances should be comprehensively followed up to minimize adverse consequences to their dental development and preserve their future dental health.
| S-EPMC6056986 | biostudies-literature
Project description:IntroductionChildhood cancer (CC) is a leading cause of death among children aged 0-19 years worldwide. Each year, 400,000 new cases of CC are diagnosed globally. Given the between-country differences in CC incidence rates, types and trends, this study aimed to identify possible risk factors for CC in Armenia.MethodsWe used a case-control study design and enrolled participants from the only specialized pediatric hematology and oncology center in Armenia. Cases included patients ≤ 14 years old diagnosed and treated with a malignant disease between 2017 and 2020 in the centre. Controls included patients diagnosed and treated in the center during the same period for a non-malignant disease. We conducted telephone interviews with mothers of cases and controls. Independent risk factors of cancer were identified using multivariable logistic regression analysis.ResultsOverall, 234 participants (117 cases, 117 controls) were included in the study. Based on the fitted model, maternal usage of folic acid during pregnancy was protective against CC, almost twice decreasing its odds (OR = 0.54; 95% CI: 0.31-0.94). On the contrary, experiencing horrifying/terrifying event(s) during pregnancy (OR = 2.19; 95% CI: 1.18-4.07) and having induced abortions before getting pregnant with the given child (OR = 2.94; 95% CI: 1.45-5.96) were associated with higher odds for a child to develop cancer.ConclusionDespite the limited sample size of the study, significant modifiable risk factors for CC in Armenia were identified, all of which were linked to the period of pregnancy. The data from this study adds to the limited information available from etiological CC research throughout the world, and it will increase understanding of CC risk factors in settings with small populations and low resources. Although these findings may be helpful for future research, they should be taken with caution unless validated from further larger-scale studies.
| S-EPMC9873390 | biostudies-literature
Project description:PurposeChildhood cancer survivors have an increased risk of secondary sarcomas. To better identify those at risk, the relationship between therapeutic dose of chemotherapy and radiation and secondary sarcoma should be quantified.Methods and materialsWe conducted a nested case-control study of secondary sarcomas (105 cases, 422 matched controls) in a cohort of 14,372 childhood cancer survivors. Radiation dose at the second malignant neoplasm (SMN) site and use of chemotherapy were estimated from detailed review of medical records. Odds ratios (ORs) and 95% confidence intervals were estimated by conditional logistic regression. Excess odds ratio (EOR) was modeled as a function of radiation dose, chemotherapy, and host factors.ResultsSarcomas occurred a median of 11.8 years (range, 5.3-31.3 years) from original diagnosis. Any exposure to radiation was associated with increased risk of secondary sarcoma (OR = 4.1, 95% CI = 1.8-9.5). A dose-response relation was observed, with elevated risks at doses between 10 and 29.9 Gy (OR = 15.6, 95% CI = 4.5-53.9), 30-49.9 Gy (OR = 16.0, 95% CI 3.8-67.8) and >50 Gy (OR = 114.1, 95% CI 13.5-964.8). Anthracycline exposure was associated with sarcoma risk (OR = 3.5, 95% CI = 1.6-7.7) adjusting for radiation dose, other chemotherapy, and primary cancer. Adjusting for treatment, survivors with a first diagnosis of Hodgkin lymphoma (OR = 10.7, 95% CI = 3.1-37.4) or primary sarcoma (OR = 8.4, 95% CI = 3.2-22.3) were more likely to develop a sarcoma.ConclusionsOf the risk factors evaluated, radiation exposure was the most important for secondary sarcoma development in childhood cancer survivors; anthracycline chemotherapy exposure was also associated with increased risk.
| S-EPMC3423483 | biostudies-literature
Project description:Early childhood caries (ECC) is major oral health problem, mainly in socially disadvantaged populations. ECC affects infants and preschool children worldwide. The prevalence of ECC differs according to the group examined, and a prevalence of up to 85% has been reported for disadvantaged groups. ECC is the presence of one or more decayed, missing, or filled primary teeth in children aged 71 months (5 years) or younger. It begins with white-spot lesions in the upper primary incisors along the margin of the gingiva. If the disease continues, caries can progress, leading to complete destruction of the crown. The main risk factors in the development of ECC can be categorized as microbiological, dietary, and environmental risk factors. Even though it is largely a preventable condition, ECC remains one of the most common childhood diseases. The major contributing factors for the for the high prevalence of ECC are improper feeding practices, familial socioeconomic background, lack of parental education, and lack of access to dental care. Oral health plays an important role in children to maintain the oral functions and is required for eating, speech development, and a positive self-image. The review will focus on the prevalence, risk factors, and preventive strategies and the management of ECC.
| S-EPMC5514393 | biostudies-other