scholarly journals O6B.2 Cancer risk by ore type in a mixed miners cohort

2019 ◽  
Vol 76 (Suppl 1) ◽  
pp. A53.2-A53
Author(s):  
Paul A Demers ◽  
Colin Berriault ◽  
Avinash Ramkissoon ◽  
Minh T Do ◽  
Nancy Lightfoot ◽  
...  

Background and objectivesMining may involve exposure to many carcinogens, including respirable crystalline silica (RSC), diesel engine exhaust (DEE), nickel (Ni), chromium (Cr), radon (Rn), and arsenic (As), which vary by ore being mined. The province of Ontario, Canada has a diverse mining sector with associated exposures including gold (RSC/DEE/As/Cr), uranium (RSC/DEE/Rn), and nickel-copper (DEE/Ni), and other ores (RSC/DEE). The study aim was to examine the risk of cancer by ore type in a mixed mining cohort.MethodsFrom 1928–1987 workers in the Ontario minerals industry were required to undergo an annual physical examination and chest x-ray, as well as record their mining work history in order to receive certification. Data from these exams was used to create the Mining Master File (MMF) cohort. Cancers were identified through linkage of the MMF with the Ontario Cancer Registry (1964–2017). Cancer risk among miners was compared to provincial rates using Standardized Incidence Ratios (SIR); internal analyses were conducted using Poisson regression.ResultsIndividuals who died or were lost before 1964, had missing or invalid data, or employment of less than two weeks were excluded. Too few women (n=161) were available for analysis. In total, 61 397 men were included in the analysis. Gold miners had excesses of lung (SIR=1.30, 95%CI=1.23–1.38) and nasopharyngeal cancer (SIR=2.34, 95%CI=1.39–3.70). Uranium miners had excesses of lung (SIR=1.57, 95%CI=1.45–1.70), bladder (SIR=1.20, 95%CI=1.02–1.40), and bone (SIR=2.45, 95%CI=1.30–4.19) cancers. Nickel-copper miners had excesses of lung (SIR=1.13, 95%CI=1.08–1.19), bone (SIR=2.02, 95%CI=1.32–2.96), and sinonasal cancer (SIR=1.73, 95%CI=1.12–2.56).ConclusionsIncreased risks for specific cancers were observed among people who mined many different ore types. Most of the associations were as expected, but several (e.g., bone cancers) will undergo further investigation. Future analyses will examine the impact of combined exposures among miners of multiple ore types.

2021 ◽  
Author(s):  
Antonio Bandala-Jacques ◽  
Kevin Daniel Castellanos Esquivel ◽  
Fernanda Pérez-Hurtado ◽  
Cristobal Hernández-Silva ◽  
Nancy Reynoso-Noverón

BACKGROUND Screening for prostate cancer has long been a debated, complex topic. The use of risk calculators for prostate cancer is recommended for determining patients’ individual risk of cancer and the subsequent need for a prostate biopsy. These tools could lead to a better discrimination of patients in need of invasive diagnostic procedures and for optimized allocation of healthcare resources OBJECTIVE To systematically review available literature on current prostate cancer risk calculators’ performance in healthy population, by comparing the impact factor of individual items on different cohorts, and the models’ overall performance. METHODS We performed a systematic review of available prostate cancer risk calculators targeted at healthy population. We included studies published from January 2000 to March 2021 in English, Spanish, French, Portuguese or German. Two reviewers independently decided for or against inclusion based on abstracts. A third reviewer intervened in case of disagreements. From the selected titles, we extracted information regarding the purpose of the manuscript, the analyzed calculators, the population for which it was calibrated, the included risk factors, and the model’s overall accuracy. RESULTS We included a total of 18 calculators across 53 different manuscripts. The most commonly analyzed ones were they PCPT and ERSPC risk calculators, developed from North American and European cohorts, respectively. Both calculators provided high precision for the diagnosis of aggressive prostate cancer (AUC as high as 0.798 for PCPT and 0.91 for ERSPC). We found 9 calculators developed from scratch for specific populations, which reached diagnostic precisions as high as 0.938. The most commonly included risk factors in the calculators were age, PSA levels and digital rectal examination findings. Additional calculators included race and detailed personal and family history CONCLUSIONS Both the PCPR and the ERSPC risk calculators have been successfully adapted for cohorts other than the ones they were originally created for with no loss of diagnostic accuracy. Furthermore, designing calculators from scratch considering each population’s sociocultural differences has resulted in risk tools that can be well adapted to be valid in more patients. The best risk calculator for prostate cancer will be that which was has been calibrated for its intended population and can be easily reproduced and implemented CLINICALTRIAL CRD42021242110


J ◽  
2019 ◽  
Vol 2 (4) ◽  
pp. 430-448
Author(s):  
Manuela Chiavarini ◽  
Andrea Ostorero ◽  
Giulia Naldini ◽  
Roberto Fabiani

Many studies have investigated the relationship between medically assisted reproduction (MAR) and health outcomes, particularly cancer, in the offspring. This meta-analysis investigated the association between MAR and childhood cancer. Data sources were PubMed, Scopus, and Web of Science up until June 2018. From the selected studies, we extracted the cancer risk estimates of the exposure of interest (MAR, assisted reproductive technology—ART, and in fitro fertilization—IVF). We conducted the meta-analysis using a random effects model. The outcomes of interest were childhood cancers, classified according to the international classification of childhood cancer (ICCC-3). In our meta-analysis (18 cohort and 15 case-control studies) the overall cancer risk was significantly increased in children conceived by MAR, ART, or IVF. MAR and ART significantly increased the risk for hematological tumors, hepatic tumors, and sarcomas (odds ratio (OR) 1.54; 95% CI 1.18–2.02 and OR 1.92; 95% CI 1.34–2.74, respectively). MAR increased acute myeloid leukemia risk (OR 1.41; 95% CI 1.02–1.95) and ART increased neural cancer risk (OR 1.21; 95% CI 1.01–1.46). Our results suggest an increased risk of cancer in children conceived by MAR. Further studies are needed to investigate the impact of fertility treatments, parental subfertility status, and their association on health outcomes in the offspring.


2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 20063-20063
Author(s):  
D. Serraino ◽  
P. Piselli ◽  
G. Busnach ◽  
F. Citterio ◽  
L. Fratino ◽  
...  

20063 Background: Acquired immunesuppression due to HIV-infection or to anti-rejection therapies following organ transplantation is a well known risk factor for cancer. This increased risk has been well documented for young adults, whereas few data are available on older persons. In this study, we assessed the impact of cancer in HIV-positive persons (HIV+) and in transplant persons (TRP) who were 50 years of age or older. Methods: Data from a multi-cohort study conducted in Italy and France were analysed. Individuals ≥50 years of age were selected from the original study group constituted by 2002 HIV+ seroconverters from Italy, 6072 HIV+ from France and 2755 Italian TRP (1844 kidney, 702 heart, 159 liver and 50 lung TRP). Sex- and age-standardized incidence ratios (SIR) and 95% confidence intervals (CI) were computed to quantify the cancer risk as compared to the general population. Among HIV+, the risk of cancer was also assessed according to treatment with highly active antiretroviral therapies (HAART). Results: This analysis was based on 94 cancers diagnosed in 833 HIV+, and on 154 cancers diagnosed in 1558 TRP ≥50 years of age. The SIRs for all cancers decreased with ageing, ranging from 5.1 (95% CI: 4.0–6.5) in HIV+ aged 50–59 to 2.1 (95% CI: 1.4–3.1) in HIV+ aged 60 or older. In TRP, the SIRs for all cancer were 2.5 (95% CI:2.0–3.1) and 1.6 (95% CI: 1.2–2.0), respectively. In HIV+, the protective effect of HAART was more evident in those aged 50–59 (SIR = 6.8 in never treated and SIR = 2.4 in ever treated) than in HIV+ aged ≥60 (SIR = 2.8 and SIR = 1.6, respectively). This pattern of cancer occurrence was peculiar to virus-related cancers (e.g., Kaposi’s sarcoma, non-Hodgkin’s lymphoma, liver cancer). SIRs for lung cancer in both groups were significantly increased but did not significantly differ according to HAART and/or age. The survival of both HIV+ and TRP was significantly reduced by the diagnosis of cancer, but the difference in survival was not associated with ageing (p = 0.20). Conclusions: Aged individuals with acquired immunesuppression have a cancer pattern similar to younger persons with immunosuppression, but the burden of cancer will increase in absolute terms because of the increasing proportion of older individuals among both HIV+ and TRP. No significant financial relationships to disclose.


Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1150 ◽  
Author(s):  
Mohammad Hashemi ◽  
Shima Karami ◽  
Sahel Sarabandi ◽  
Abdolkarim Moazeni-Roodi ◽  
Andrzej Małecki ◽  
...  

A number of case-control studies regarding the association of the polymorphisms in the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) genes with the risk of cancer have yielded inconsistent findings. Therefore, we have conducted a comprehensive, updated meta-analysis study to identify the impact of PD-1 and PD-L1 polymorphisms on overall cancer susceptibility. The findings revealed that PD-1 rs2227981 and rs11568821 polymorphisms significantly decreased the overall cancer risk (Odds Ratio (OR) = 0.82, 95% CI = 0.68–0.99, p = 0.04, TT vs. CT+CC; OR = 0.79, 95% CI = 0.67–0.94, p = 0.006, AG vs. GG, and OR = 0.82, 95% CI = 0.70–0.96, p = 0.020, AG+AA vs. GG, respectively), while PD-1 rs7421861 polymorphism significantly increased the risk of developing cancer (OR = 1.16, 95% CI = 1.02–1.33, p = 0.03, CT vs. TT). The PD-L1 rs4143815 variant significantly decreased the risk of cancer in homozygous (OR = 0.62, 95% CI = 0.41–0.94, p = 0.02), dominant (OR = 0.70, 95% CI = 0.50–0.97, p = 0.03), recessive (OR = 0.76, 95% CI = 0.60–0.96, p = 0.02), and allele (OR = 0.78, 95% CI = 0.63–0.96, p = 0.02) genetic models. No significant association between rs2227982, rs36084323, rs10204525, and rs2890658 polymorphisms and overall cancer risk has been found. In conclusions, the results of this meta-analysis have revealed an association between PD-1 rs2227981, rs11568821, rs7421861, as well as PD-L1 rs4143815 polymorphisms and overall cancer susceptibility.


BMJ Open ◽  
2017 ◽  
Vol 7 (10) ◽  
pp. e016905 ◽  
Author(s):  
Jorma Sormunen ◽  
Melina Arnold ◽  
Isabelle Soerjomataram ◽  
Eero Pukkala

PurposeThe cohort was set up to study the impact of lifestyle factors in early adulthood on disease outcomes, with a focus on assessing the influence of body composition and physical performance in early adulthood on subsequent cancer risk.ParticipantsMen born in 1958 who performed their military service between the ages of 17 and 30 years were included in this study (n=31 158). They were eligible for military service if they were healthy or had only minor health problems diagnosed at the beginning of their service. Men with chronic illnesses requiring regular medication or treatment were not eligible for service. Comprehensive health data including diagnosed illnesses, anthropometric measures and health behaviour were collected at the beginning and at the end of military service, including data from medical check-ups.Findings to dateDuring the follow-up, 1124 new cancer cases were diagnosed between baseline (ie, end of the military service for each individual) and end of the year 2014. In the end of the follow-up, 91% of the study participants were still alive. Overweight (body mass index (BMI) ≥25 kg/m2) and obesity (BMI ≥30 kg/m2) were associated with an overall increased risk of cancer. A good or excellent physical condition significantly reduced cancer risk.Future plansThe dataset offers the possibility of linkage with other databases, such as the Finnish Cancer Registry (eg, primary site of the tumour, morphology, time of detection, spreading and primary treatment), vital statistics (date of emigration or deaths), censuses (socioeconomic indicators), hospital discharge data (comorbidity) and population surveys (life habits).


2016 ◽  
Vol 58 (3) ◽  
pp. 323-330 ◽  
Author(s):  
Thomas Nyheim ◽  
Lars E Staxrud ◽  
Jørgen J Jørgensen ◽  
Kristin Jensen ◽  
Hilde M Olerud ◽  
...  

Background Endovascular aneurysm repair (EVAR) is becoming the mainstay treatment of abdominal aortic aneurisms (AAA). The postoperative follow-up regime includes a lifelong series of CT angiograms (CTAs) at different intervals in addition to EVAR, which will confer significant cumulative radiation exposure over time. Purpose To examine the impact of age and follow-up regime over time on cumulative radiation exposure and attributable cancer risk after EVAR. Material and Methods We calculated a mean effective dose (ED) for the EVAR procedure, CTA, and plain abdominal X-rays (PAX). Cumulative ED was calculated for standard, complex, and simplified surveillance over 5, 10, and 15 years for different age groups. Results For EVAR, the mean ED was 34 mSv (range, 12–75 mSv) per procedure. For PAX, the ED was 1.1 mSv (range, 0.3–4.4 mSv), and for CTA it was 8.0 mSv (range, 2–20 mSv). For a 55-year-old man, an attributable cancer risk (ACR) in standard surveillance at 5 and 15 years of follow-up was 0.35% and 0.65%, respectively. The corresponding values were 0.22% and 0.37% for a 75-year-old man. When using a simplified follow-up, the ACRs for a 55-year-old at 5 and 15 years were 0.30% and 0.37%, respectively. These values were 0.18% and 0.21% for a 75-year-old man. A complex follow-up with half-yearly CTA over similar age and time span doubled the ACR. Conclusion Treating younger patients with EVAR poses a low ACR of 0.65% (15-year standard surveillance) compared to a lifetime cancer risk of 44%. A simplified surveillance should be used if treating younger patients, which will halve the ACR over 15 years.


2018 ◽  
Author(s):  
Michael Meyer-Hermann

AbstractIn recent years the transfer of blood from young to old individuals was shown to bear the potential of rejuvenation of stem cell activity. While this process might increase life expectancy by prolonging functionality of organs, higher cell replication rates bear also the risk of cancer. The extent of this risk is not known.While it is difficult to evaluate this cancer risk in experiments, this is possible with a mathematical model for tissue homeostasis by stem cell replication and associated cancer risk. The model suggests that young blood treatments can induce a substantial delay of organ failure with only minor increase in cancer risk. The benefit of rejuvenation therapy as well as the impact on cancer risk depend on the biological age at the time of treatment and on the overall cell turnover rate of the organs. Different organs have to be considered separately in the planning of the systemic treatment. In particular, the model predicts that the treatment schedules successfully applied in mice are not directly transferable to humans and guidelines for successful protocols are proposed. The model presented here may be used as a guidance for the development of treatment protocols.Additional informationThere is NO competing interests.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Yasmin Bylstra ◽  
Weng Khong Lim ◽  
Sylvia Kam ◽  
Koei Wan Tham ◽  
R. Ryanne Wu ◽  
...  

Abstract Background Family history has traditionally been an essential part of clinical care to assess health risks. However, declining sequencing costs have precipitated a shift towards genomics-first approaches in population screening programs rendering the value of family history unknown. We evaluated the utility of incorporating family history information for genomic sequencing selection. Methods To ascertain the relationship between family histories on such population-level initiatives, we analysed whole genome sequences of 1750 research participants with no known pre-existing conditions, of which half received comprehensive family history assessment of up to four generations, focusing on 95 cancer genes. Results Amongst the 1750 participants, 866 (49.5%) had high-quality standardised family history available. Within this group, 73 (8.4%) participants had an increased family history risk of cancer (increased FH risk cohort) and 1 in 7 participants (n = 10/73) carried a clinically actionable variant inferring a sixfold increase compared with 1 in 47 participants (n = 17/793) assessed at average family history cancer risk (average FH risk cohort) (p = 0.00001) and a sevenfold increase compared to 1 in 52 participants (n = 17/884) where family history was not available (FH not available cohort) (p = 0.00001). The enrichment was further pronounced (up to 18-fold) when assessing only the 25 cancer genes in the American College of Medical Genetics (ACMG) Secondary Findings (SF) genes. Furthermore, 63 (7.3%) participants had an increased family history cancer risk in the absence of an apparent clinically actionable variant. Conclusions These findings demonstrate that the collection and analysis of comprehensive family history and genomic data are complementary and in combination can prioritise individuals for genomic analysis. Thus, family history remains a critical component of health risk assessment, providing important actionable data when implementing genomics screening programs. Trial registration ClinicalTrials.gov NCT02791152. Retrospectively registered on May 31, 2016.


2021 ◽  
Vol 10 (1) ◽  
pp. 153
Author(s):  
Hong Jin Yoon ◽  
Jie-Hyun Kim ◽  
Gi Hyeon Seo ◽  
Hyojin Park

N-nitrosodimethylamine (NDMA), a known carcinogenic agent, was recently detected in some products of ranitidine. Several studies have investigated the detectability of NDMA, in drugs and their risks. However, only a few epidemiological studies have evaluated cancer risk from the use of such individual drugs. This study investigates the risk of cancer in ranitidine users. We conducted an observational population-based cohort study using the Health Insurance Review and Assessment databases, which contain information about the use of medicines in South Korea. The primary study cohort consisted of ranitidine users (n = 88,416). For controls, we enrolled users of famotidine, another H2-receptor antagonist in which no NDMA has been detected. A 4:1 matched cohort was constructed to compare cancer outcomes of the two groups. Our matched cohort comprised of 40,488 ranitidine users and 10,122 famotidine users. There was no statistical difference in the overall cancer risk between the ranitidine and famotidine groups (7.45% vs. 7.56%, HR 0.99, 95% CI 0.91–1.07, p = 0.716). Additionally, no significant differences were observed in the analysis of 11 single cancer outcomes. We found no evidence that exposure to NDMA through ranitidine increases the risk of cancer.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C.C Van 't Klooster ◽  
P.M Ridker ◽  
N.R Cook ◽  
J.G.J.V Aerts ◽  
J Westerink ◽  
...  

Abstract Background As treatment for cardiovascular disease (CVD) has improved substantially over the last decades, more patients survive acute CVD manifestations and are at risk for developing cancer as well as recurrent CVD. Due to similar risk factors, including smoking and obesity, patients with established CVD are at higher risk for cancer. Objectives The aim of this study was to develop and externally validate prediction models for the estimation of 10-year and lifetime risk for total, colorectal, and lung cancer in patients with established CVD. Methods Data from patients with established CVD from the UCC-SMART prospective cohort study (N=7,280) were used for model development, and data from the CANTOS trial (N=9,322) were used for model validation. Predictors were selected based on previously published cancer risk prediction models or cancer risk factors, easy clinical availability, and availability in the derivation dataset (UCC-SMART cohort). A Fine and Gray competing risk-adjusted lifetime model was developed for total, colorectal, and lung cancer. Results Selected predictors were age, sex, smoking status, weight, height, alcohol use, antiplatelet use, diabetes mellitus, and C-reactive protein. External calibration for 4-year risks of the total cancer, colorectal cancer, and lung cancer models was good (Figure 1), and C-statistics were 0.63–0.74 in the CANTOS trial population. Median predicted lifetime risks in CANTOS were 26% (range 1%-52%) for total cancer, 4% (range 0%-13%) for colorectal cancer, and 5% (range 0%-37%) for lung cancer. Conclusions Lifetime and 10-year risk of cancer can be estimated with easy to measure variables in patients with established CVD, showing a wide distribution of predicted lifetime risks for total cancer and lung cancer. Using these lifetime models in clinical practice could increase understanding of cancer risk and aid in emphasizing healthy lifestyle changes. Figure 1. Calibration plots of cancer models Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): University Medical Center; Additional funding: CANTOS trial was funded by Novartis Pharmaceuticals.


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