[Case control study in northern Sweden. High risk of lung cancer among older smoking professional drivers].
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Adult↗
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Immune Markers and Risk of Pancreatic Cancer in the European EPIC Cohort.
The immune system is a major driver in pancreatic cancer development. Several prospective cohort studies have found associations for single immune system-derived proteins such as IL6 or CRP, but results are inconclusive, and Omics-based research is scarce. Hence, we aimed to investigate associations of a comprehensive protein panel with the risk of pancreatic cancer. Within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, 92 immune proteins were measured in baseline blood samples of 406 incident pancreatic cancer cases and 406 sex- and age-matched controls, using the Olink Immuno-Oncology panel. Multivariable adjusted conditional logistic regression was used to estimate odds ratios (OR, 95% CI) for protein levels in association with pancreatic cancer risk. Eight biomarkers were associated with pancreatic cancer risk (MMP12, LAMP3, CD28, IL-6, IL-12, FASLG, PD-L2, and PDCD1) but only MMP12 was significantly associated after multivariable adjustments for confounders and the seven proteins, with OR = 1.56 (95% CI: 1.20-2.03) for a doubling in protein concentration. After correction for multiple testing, none of the proteins were associated with risk. Restricting analyses to cases diagnosed within the first 4 years and 4-8 years after recruitment resulted in OR of 1.89 (95% CI: 1.28-2.80) and 1.37 (95% CI: 1.01-1.86) for MMP12, respectively. Higher levels of MMP12 were associated with pancreatic cancer risk specifically in those diagnosed shortly after recruitment, while other immune-related factors were not associated with risk. Further cohort studies are needed to confirm our initial findings.
Humans↗
The IL-1 system in inflammation and cancer.
Inflammation is a pathogenetic driver of several pathological conditions, including cancer. The tumor microenvironment, which includes cellular, molecular, and structural components, is an essential component of cancer, involved in tumor promoting or controlling processes. In particular, inflammatory players contribute to the establishment of a tumor-promoting microenvironment, which affects all stages of tumor development, from initiation to metastasis, as well as response to therapy. The IL-1 system includes two large sets of structurally related ligands and receptors, with agonist or regulatory activity, playing non-redundant roles in inflammation and immunity. Each of them has specific functions in tissue homeostasis, inflammation, innate and adaptive immune responses, and potentially contributes to processes related to carcinogenesis and metastasis, or immune-mediated control of cancer cells. Depending on the context and cellular target, IL-1 family members may play dual roles in cancer, driving both pro- or anti-tumor processes. IL-1α and IL-1β can directly promote cancer cell proliferation, survival, and plasticity, in addition to contribute to the establishment of a pro-inflammatory environment that promotes tissue remodeling, cellular stress responses, and genomic instability. On the other hand, IL-1 is a lymphoproliferative and activating molecule in innate and adaptive responses, thus contributing to anti-tumor immune mediated responses. In addition, members of the IL-1 system act as regulators of mechanisms involved in cancer, including emergency hematopoiesis, trained immunity, and metabolism. Here, we will provide an overview of the IL-1 system in cancer and discuss the functional complexity of IL-1 family cytokines, which orchestrate both protective and pro-tumorigenic responses, by directly acting on cancer cells and by driving environmental stimuli which indirectly act on cancer cells.
Humans↗
The landscape of structural variation in pediatric cancer.
Structural variants (SVs) account for over 60% of the driver variants in pediatric cancer, and in many cases act as the cancer initiating event. To study SVs from a pan-cancer perspective, we analyzed 1,616 pediatric cancer genomes in 16 major cancer types of hematological malignancies (n = 908), brain tumors (n = 183), and solid tumors (n = 525) and compared their profiles to those of 2,203 adult cancers. The SV burden varied ~100-fold across pediatric cancer types and demonstrated an 8- to 16-fold reduction compared to adult brain and solid tumors but was comparable in pediatric versus adult hematological malignancies. Recurrent SV hotspots occurred uniquely in pediatric acute lymphoblastic leukemias (ALLs) in proximity to RAG-mediated recombination signal sequences (RSS) and disrupted multiple immune-related loci as well as 69 genes, which often involved cryptic RSS sites. By contrast, such hotspots affected only immune-related loci but not driver genes in adult lymphoid cancers. Eight SV signatures extracted from the cohort had varying distributions across cancer types, with clustered translocations reflecting templated insertions in osteosarcoma, and medium-sized deletions (10 kb to 1 Mb) enriched in cancers with RAG-mediated deletions. Intra-patient evolutionary analysis in 13 patients with multiple spatiotemporally distinct samples revealed that RAG-mediated recombination in leukemia and complex rearrangements in solid tumors occurred both early in disease initiation and continuously during later diversification, contributing to clonal heterogeneity. Finally, we found that both driver genes and fragile sites were the two genomic regions most frequently disrupted by SVs. The unique and diverse SV landscapes that emerged from this comprehensive analysis expand the scope of RSS-mediated mutagenesis in pediatric ALL and will be a valuable resource for guiding future functional studies and the design of clinical genomic testing in pediatric cancer.
Journal Article↗
Mortality in a historical cohort of bus drivers.
In an attempt to address previously reported excesses of ischaemic heart disease (IHD), lung cancer and bladder cancer among professional drivers, the mortality (SMR) of 2134 Montreal city bus drivers employed for at least five years as of January 1962 and followed until 31 December 1985 was compared with that of the male population of greater Montreal. The vital status of 94% of the cohort was ascertained. The number of deaths observed was 804. The overall mortality was somewhat lower than expected (SMR = 97). A small, non-significant excess mortality was found for ischaemic heart disease (IHD) (O/E = 313/295, SMR = 106, 95% CI: 95-118) and circulatory system diseases (O/E = 441/405, SMR = 109, 95% CI: 99-119). However, no excesses were observed for lung cancer (O/E = 78/84.4, SMR = 92, 95% CI: 73-114) or bladder cancer (O/E = 4/7.4, SMR = 54, 95% CI: 15-138). These results are compatible with other studies which have found a small risk of IHD for bus drivers.
Adult↗
[State Changes and Stability Grading of Driver Genes in Non-small Cell Lung Cancer Based on Repeated NGS Testing].
BACKGROUND: Next-generation sequencing (NGS)-based driver gene testing has become a routine component of molecular subtyping and precision therapy for non-small cell lung cancer (NSCLC). Dynamic genomic monitoring facilitates early detection of resistance-related molecular alterations and informs timely therapeutic adjustments. However, standardized criteria for evaluating the stability of serial NGS testing are currently lacking, and the applicability of NGS using formalin-fixed paraffin-embedded (FFPE) specimens for dynamic monitoring remains poorly defined. This study aims to establish a stability grading system for driver gene status alterations based on repeated NGS testing, and to provide evidence-based support for clinical repeat biopsy strategies. METHODS: Data from 1232 patients with NSCLC who underwent two or more NGS tests on FFPE tissue specimens at Beijing Chest Hospital between June 2019 and April 2026 were collected retrospectively. Patients with an interval of ≥4 months between the initial and last tests were included to ensure the representativeness of temporal analysis, resulting in a main analysis cohort of 942 patients. The Kappa consistency test was used to evaluate the state stability of nine core driver genes [epidermal growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene homolog (KRAS), anaplastic lymphoma kinase (ALK), ROS proto-oncogene 1, receptor tyrosine kinase (ROS1), mesenchymal‑epithelial transition factor (MET), rearranged during transfection (RET), v-raf murine sarcoma viral oncogene homolog B1 (BRAF), erb‑b2 receptor tyrosine kinase 2 (ERBB2), and phosphatidylinositol‑4,5‑bisphosphate 3‑kinase catalytic subunit alpha (PIK3CA)] and to construct a five‑level grading system. Paired variant allele frequency (VAF) differences were compared using the Wilcoxon signed‑rank test. Independent influencing factors for mutation accumulation were identified by binary Logistic regression. RESULTS: The state stability of the nine genes was classified into five levels: EGFR showed high stability (Kappa=0.838), ROS1/ALK/KRAS good stability, BRAF/PIK3CA/RET moderate stability, and ERBB2 low stability, and MET showed high instability. MET exhibited the highest rate of state change (9.3%) with a raw observed agreement of 90.7%. Its Kappa value (0.172) was influenced by the low prevalence (3.7%) compression effect and should therefore be interpreted alongside the observed agreement (90.7%) and the prevalence-adjusted and bias-adjusted Kappa (PABAK). The VAF of PIK3CA increased significantly (P=0.005). T790M positivity increased from 5.8% to 10.8%, and 30 new C797S mutations were detected at the last test (13 with T790M, 17 without). The overall rate of new driver gene variants in the main cohort was 18.0%. Binary Logistic regression showed that a lower number of initial mutated genes was the only independent predictor of new variants [odds ratio (OR)=0.399, P<0.001], while sex and detection interval showed no independent association. CONCLUSIONS: A five level stability grading system for state changes of driver genes in NSCLC based on repeated NGS testing has been established. MET showed the most frequent state changes, which should be interpreted in conjunction with the prevalence effect. The VAF increase of PIK3CA is an observational finding, and its clinical significance requires further prospective validation. A lower initial mutation burden may reflect tumor clonal complexity and was associated with a higher likelihood of subsequent acquisition of new variants. FFPE based NGS is applicable for repeated testing at clinical treatment decision nodes.
Humans↗
[General and oncologic morbidity in Moscow municipal transport drivers].
A case study was undertaken to examine general and cancer mortality rates and cancer morbidity among municipal transport drivers in Moscow. The mortality and cancer morbidity in 1969 to 1988 were followed up among 2528 men and 212 women. In this period, male mortality rates due to malignant neoplasms, cardiovascular diseases and all causes taken together were statistically lower than the expected rates. Male cancer morbidity rates were also lower the expected ones. In the past decade 42 cases of gastric cancer were revealed in the cohort, which was statistically greater than the expected figures (29.8). In the first decade, prostatic cancer mortality was statistically significantly higher in bus drivers with length of service of over 20 years. Among women, there were only 12 deaths, with significantly decreased mortality rates. Esophageal cancer was detected in women who had worked as drivers for 20-29 years. The lower morbidity and mortality rates may be associated with the "healthy worker effect", i.e. with the fact that staff is strictly selected for this job.
Automobile Driving↗
Ubiquitination-Androgen Receptor Coupling in Prostate Cancer Therapeutics.
Prostate cancer is one of the most frequently diagnosed malignancies in men and a leading cause of cancer-related mortality worldwide. The androgen receptor (AR) remains the principal driver of prostate cancer progression and castration-resistant prostate cancer (CRPC), with its stability, localization, and transcriptional activity being tightly regulated by the ubiquitin-proteasome system (UPS). E3 ubiquitin ligases and deubiquitinases (DUBs) critically govern AR turnover and signalling output, thereby influencing tumour growth, therapeutic resistance, and disease progression. Emerging evidence further highlights a complex interplay between ubiquitination, DNA damage response (DDR) pathways, and ADP-ribosylation (ADPr) signalling, collectively shaping genomic stability and treatment responsiveness in prostate cancer. This review is organized into four major themes: (i) ubiquitin-mediated regulation of AR signalling, (ii) ubiquitination and DNA damage response in AR-driven prostate cancer, (iii) crosstalk between ubiquitination, ADPr, and AR-associated signalling pathways, and (iv) therapeutic strategies targeting the UPS and AR axis. This study also discusses recent advances in targeted protein degradation, modulation of E3 ligases, inhibition of deubiquitinases, and PARP-based therapeutic approaches. These emerging insights into the interconnected regulation of ubiquitination, AR signalling, DDR pathways, and ADP-ribosylation may facilitate the development of next-generation therapeutic approaches for advanced prostate cancer.
ADP-ribosylation (ADPr)↗
FMRP promotes gastric cancer progression via m6A-dependent stabilization of DVL2 and activation of the Wnt/PCP-JNK pathway.
BACKGROUND: N6-methyladenosine (m6A) modification has emerged as a critical regulator in gastric cancer progression. Fragile X messenger ribonucleoprotein 1 (FMRP), an RNA-binding protein with tumorigenic potential, remains poorly characterized in gastric cancer. METHODS: FMRP expression in gastric cancer was assessed through bioinformatic analyses and tissue microarray-based immunohistochemistry. Its biological functions were examined through loss-of-function experiments in vitro and in vivo. Mechanistic investigations, including RNA interaction, m6A site mutation, and RNA stability analyses, were performed to identify downstream targets and pathways regulated by FMRP. RESULTS: Bioinformatic analyses and tissue microarray-based immunohistochemistry showed that FMRP was significantly upregulated in gastric cancer tissues. FMRP depletion suppressed tumor growth and metastasis. Subsequently, Dishevelled segment polarity protein 2 (DVL2) was identified as a candidate downstream target of FMRP. DVL2 was also significantly upregulated in gastric cancer tissues, and its expression positively correlated with FMRP expression. Mechanistically, FMRP bound to DVL2 mRNA and enhanced its stability in an m6A-dependent manner. Among the candidate sites tested, mutation of 1271A attenuated FMRP-mediated regulation of DVL2 reporter activity, supporting the involvement of this site. Functionally, FMRP promoted activation of the noncanonical Wnt/planar cell polarity (PCP) signaling pathway and enhanced the proliferative, migratory, and invasive capacities of gastric cancer cells via DVL2. CONCLUSIONS: These results define FMRP as an oncogenic driver in gastric cancer that operates via the DVL2/Wnt/PCP axis. Targeting this pathway may provide a potential therapeutic strategy for gastric cancer.
Stomach Neoplasms↗
ZUP1 as a Novel Potential Oncogenic Driver and Prognostic Biomarker in Breast Cancer.
INTRODUCTION: Breast cancer is one of the main causes of cancer death in women globally. Identifying new predictive markers and therapeutic targets is important for improving patient outcomes. Zinc finger-containing U-rich RNA-binding protein 1 (ZUP1) is an RNA-binding protein containing a zinc finger structure that has not been systematically analyzed in breast cancer research. MATERIALS AND METHODS: The study used data from 1,231 samples from the Cancer Genome Atlas (TCGA) database. The ZUP1 expression in tumor tissues and normal tissues was compared. Its predictive value was assessed using survival analysis and regression models. Its biological role was explored through gene functional analysis. The immune cell analysis method was used to study the tumor immune environment, and the drug susceptibility database was used to predict drug responses. Predictive models were also built and validated. RESULTS: ZUP1 expression was significantly higher in breast cancer tissues than in normal tissues. High expression of ZUP1 is related to advanced tumor stage and is an independent indicator of poor survival prognosis in univariate and multivariate analyses. Functional enrichment revealed that ZUP1 is closely linked to cell cycle progression, DNA replication, and the Fanconi anemia (FA) pathway. Immune infiltration analysis demonstrated a significant negative link between ZUP1 levels and the abundance of resting mast cells and activated NK cells. Furthermore, high ZUP1 expression was associated with increased sensitivity to several targeted therapies, including Nutlin-3a and PD-0325901. A clinically applicable nomogram combining ZUP1 expression with key clinical factors (age, stage, T, N, M) was developed to predict 3- and 5-year OS with good calibration and discrimination. DISCUSSION: Our study identifies ZUP1 as a potential oncogenic factor and a robust independent prognostic biomarker in breast cancer. Its involvement in critical cellular processes and modulation of the tumor immune microenvironment highlights its potential as a novel therapeutic target. Functional experiments, including immunohistochemical staining and CCK8 proliferation assays, further supported the oncogenic role of ZUP1. The established nomogram provides a valuable tool for personalized risk assessment and clinical decision-making. CONCLUSION: Our findings suggest that ZUP1 is a novel multifaceted biomarker with significant implications for personalized treatment strategies in breast cancer.
ZUP1↗
Out of the driver's seat. The recurrence of cancer is a far different ride than the first diagnosis.
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Adaptation, Psychological↗
Increased risk for lung cancer and for cancer of the gastrointestinal tract among Geneva professional drivers.
A historical prospective cohort study of 6630 drivers from the Canton of Geneva was carried out to evaluate mortality and incidence of cancer in this occupation. The study population was all men (of all vocations) who held in 1949 a special licence for driving lorries, taxis, buses, or coaches and all new licence holders in the period 1949-61. Men born before 1900 and those with only an ordinary driving licence were excluded. According to the occupation registered on their licence, the 6630 drivers were distributed into three groups: (1) professional drivers (n = 1726), (2) non-professional drivers "more exposed" to exhaust gas and fumes (this group included occupations such as vehicle mechanic, policeman, road sweeper; n = 712), and (3) non-professional drivers "less exposed," composed of all other occupations (n = 4192). The cohort was followed up from 1949 to December 1986 and the trace of 197 men (3%) was lost. Compared with the general population of the Canton of Geneva, professional drivers experienced significant excess risks, taking into account 15 years of latency, for all causes of death (standardised mortality ratio (SMR) 115, 90% confidence interval (90% CI) 107-123) and for all malignant neoplasms (SMR 125, 90% CI 112-140; standardised incidence ratio (SIR) 128, 90% CI 115-142). Cause specific analysis showed significant excesses for lung cancer (SMR 150, 90% CI 123-181; SIR 161, 90% CI 129-198), oesophageal cancer (SMR 183, 90% CI 108-291), stomach cancer (SMR 179, 90% CI 117-263; SIR233, 90% CI 156-336), rectal cancer (SMR 258, 90% CIU 162-392; SIR 200, 90% CI 127-300), and cirrhosis of the liver (SMR 145, 90% CI 104-198). Risk of lung cancer increased significantly with time from first exposure. Among non-professional drivers no significant excess risk was found except for lung cancer mortality among the "less exposed" group (SMR 121, 90% CI 103-140), and for incidence of lung cancer among the "more exposed" group (SIR 161, 90% CI 111-227). The possible casual relation between exposure to engine exhaust emissions and the increased risk for lung cancer and for cancer of the gastrointestinal tract found among professional drivers is discussed.
Aged↗
Mortality among urban policemen in Rome.
A total of 3,868 urban policemen in Rome were investigated through a historical cohort study with emphasis on mortality from cardiovascular disease and cancer. Overall mortality from cardiovascular disease, respiratory conditions, digestive and genitourinary diseases, and accidents was lower than expected. An excess risk of ischemic heart disease was observed among subjects aged less than 50 years [14 deaths, standardized mortality ratio (SMR = 1.63), 95% CI = 0.89-2.73], corresponding to workers with a short duration of employment and a short latency since first employment. Overall cancer mortality was as expected and no excess was found for lung cancer (82 deaths, SMR = 1.05). Increased mortality was observed from colon cancer (16 deaths, SMR = 1.47), melanoma (four deaths, SMR = 2.34), bladder cancer (13 deaths, SMR = 1.27), renal cancer (seven deaths, SMR = 1.39), and non-Hodgkin's lymphoma (six deaths, SMR = 1.51), although none of the excesses were statistically significant. Two deaths from male breast cancer (SMR = 14.36) and three from cancer of endocrine glands were found (SMR = 3.44). Nested case-control studies were conducted to evaluate cancer mortality risk by job category. Bladder cancer was significantly increased among car drivers (OR = 4.17); for kidney cancer, an increased odds ratio (OR = 2.27) was found among motorcyclists; non-Hodgkin's lymphoma clustered among motorcyclists (OR = 5.14). In summary, excess risk for specific cancer sites (colon, male breast, and endocrine glands) might be linked to occupational exposures; professional drivers seem to be at higher risk of bladder cancer, kidney cancer, and non-Hodgkin's lymphoma.
Adolescent↗
Mortality from breast carcinoma among US women: the role and implications of socio-economics, heterogeneous insurance, screening mammography, and geography.
Despite rapid advances in medicine and beneficial lifestyle changes, the incidence and mortality rate of gynecologic carcinoma remains high worldwide. This paper presents the econometric model findings of the major drivers of breast cancer mortality among US women. The results have implications for public health policy formulation on disease incidence and the drivers of mortality risks. The research methodology is a fixed-effects GLS regression model of breast cancer mortality in US females age 25 and above, using 1990-1997 time-series data pooled across 50 US states and DC. The covariates are age, years schooled, family income, 'screening' mammography, insurance coverage types, race, and US census region. The regressions have strong explanatory powers. Finding education and income to be significantly and positively correlated with mortality supports the 'life in the fast lanes' hypothesis of Phelps. The policy of raising a woman's education at a given income appears more beneficial than raising her income at a given education level. The relatively higher mortality rate for Blacks suggests implementing culturally appropriate set of disease prevention and health promotion programs and policies. Mortality differs across insurance types with Medicaid the worst suggesting need for program reform. Mortality is greater for women ages 25-44 years, females 40-49 years who have had screening mammography, smokers, and residents of some US states. These findings suggest imposing more effective tobacco use control policies (e.g., imposing a special tobacco tax on adult smokers), creating a more tractable screening mammography surveillance system, and designing region-specific programs to cut breast cancer mortality risks.
Adult↗
Diesel exhaust and lung cancer in the trucking industry: exposure-response analyses and risk assessment.
BACKGROUND: Diesel exhaust is considered a probable human carcinogen by the International Agency for Research on Cancer (IARC). The epidemiologic evidence rests on studies of lung cancer among truck drivers, bus drivers, shipyard workers, and railroad workers. The general public is exposed to diesel exhaust in ambient air. Two regulatory agencies are now considering regulating levels of diesel exhaust: the California EPA (ambient levels) and the Mine Safety Health Administration (MSHA) (occupational levels). To date, there have been few quantitative exposure-response analyses of diesel and lung cancer based on human data. METHODS: We conducted exposure-response analyses among workers in the trucking industry, adjusted for smoking. Diesel exhaust exposure was estimated based on a 1990 industrial hygiene survey. Past exposures were estimated assuming that they were a function of 1) the number of heavy duty trucks on the road, 2) the particulate emissions (grams/mile) of diesel engines over time, and 3) leaks from trucks' exhaust systems for long-haul drivers. RESULTS: Regardless of assumptions about past exposure, all analyses resulted in significant positive trends in lung cancer risk with increasing cumulative exposure. A male truck driver exposed to 5 micrograms/m3 of elemental carbon (a typical exposure in 1990, approximately five times urban background levels) would have a lifetime excess risk of lung cancer of 1-2% above a background risk of 5%. CONCLUSIONS: We found a lifetime excess risk ten times higher than the 1 per 1,000 excess risk allowed by OSHA in setting regulations. There are about 2.8 million truck drivers in the U.S. Our results depend on estimates about unknown past exposures, and should be viewed as exploratory. They conform reasonably well to recent estimates for diesel-exposed railroad workers done by the California EPA, although those results themselves have been disputed.
Humans↗
Integrated transcriptomic and immunogenomic analysis unravels the immunological functions and prognostic landscape of WD repeat domain 76.
BackgroundWD Repeat Domain 76 (WDR76) plays a potential role in cellular regulation; however, its comprehensive landscape across human malignancies and its specific biological function in hepatocellular carcinoma (HCC) remain largely unexplored.MethodsWe conducted a systematic pan-cancer analysis utilizing multi-omics data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Cancer Cell Line Encyclopedia (CCLE) atabases to evaluate WDR76 expression, subcellular localization, and its correlation with clinicopathologic features, genomic instability, and immune infiltration. Diagnostic and prognostic values were assessed via Receiver operating characteristic (ROC) and Kaplan-Meier analyses. Furthermore, the functional role of WDR76 in HCC was validated in vitro using Hep-3B and Huh7 cell lines through siRNA-mediated knockdown, followed by CCK-8, wound-healing, and transwell assays.ResultsWDR76 was significantly upregulated in the majority of tumor types, including LIHC, LUAD, and COAD, while exhibiting nuclear localization. Elevated WDR76 expression correlated with advanced tumor staging, metastasis, and poor clinical outcomes across multiple cohorts, particularly in ACC, KIRP, and LIHC. ROC analysis highlighted its exceptional diagnostic precision in cancers such as GBM and LIHC. Immunologically, WDR76 expression was intricately linked to immune cell infiltration, immune checkpoint markers, and genomic instability parameters, suggesting a role in shaping the tumor microenvironment. Drug sensitivity profiling revealed that high WDR76 levels correlate with resistance to specific chemotherapeutic agents. Experimentally, silencing WDR76 in HCC cells significantly suppressed cell proliferation, migration, and invasion capabilities.ConclusionOur study establishes WDR76 as a robust pan-cancer prognostic biomarker and a potential immunotherapeutic target. Specifically, we provide experimental evidence that WDR76 functions as an oncogenic driver in liver cancer, promoting malignant phenotypes and offering a novel avenue for targeted therapeutic intervention.
Humans↗
Occupation and larynx and hypopharynx cancer: an international case-control study in France, Italy, Spain, and Switzerland.
OBJECTIVE: To estimate risks for laryngeal/hypopharyngeal cancer associated with occupational titles and industrial activities. METHODS: A multicentre population-based case-control study was conducted in the early 1980s in six southern European areas. Analyses included 1010 male cases and 2176 controls. Odds ratios (ORs) (adjusted for age, study area, tobacco consumption, and alcohol consumption) were estimated for 156 occupations and 70 industrial activities. RESULTS: An excess risk has been confirmed for categories of construction workers, potters (OR: 5.91, 95% confidence intervals 1.46-24.0), butchers (2.53, 1.22-5.22), barbers (2.33, 1.00-5.40), laborers not otherwise specified (1.52, 1.12-2.06), as well as for men who had been employed in railway transport (1.52, 0.97-2.39), shipbuilding (2.05, 0.89-4.94), and hotels (2.06, 0.89-4.75). An association was also found for shoe finishers (3.23, 0.75-13.9), loggers (2.07, 0.87-4.90), and some groups of metal workers. ORs for loggers, butchers, railway transport workers, laborers, and reinforced concreters increased with duration of employment. The suggestion of a risk for machine operators among woodworkers (3.10, 0.92-10.5) conflicts with previous findings. No significant excess of risk was found for categories previously reported to be associated with laryngeal and hypopharyngeal cancer, such as drivers, mechanics, welders, machinists, and painters. CONCLUSIONS: The present study provides additional evidence to the hypothesis of a risk of cancer of the larynx/ hypopharynx for workers engaged in jobs in the construction, metal, textile, ceramic, and food industries and in railway transport. Loggers were also found at risk; a previously unreported finding.
Adolescent↗
Chromosomal aberrations in peripheral lymphocytes of train engine drivers.
Studies of Swedish railway employees have indicated that railroad engine drivers have an increased cancer morbidity and incidence of chronic lymphatic leukemia. The drivers are exposed to relatively high magnetic fields (MF), ranging from a few to over a hundred microT. Although the possible genotoxic potential of MF is unclear, some earlier studies have indicated that occupational exposure to MF may increase chromosome aberrations in blood lymphocytes. Since an increased level of chromosomal aberrations has been suggested to predict elevated cancer risk, we performed a cytogenetic analysis on cultured (48 h) peripheral lymphocytes of Swedish train engine drivers. A pilot study of 18 engine drivers indicated a significant difference in the frequency of cells with chromosomal aberrations (gaps included or excluded) in comparison with seven concurrent referents (train dispatchers) and a control group of 16 office workers. The engine drivers had about four times higher frequency of cells with chromosome-type aberrations (excluding gaps) than the office workers (P < 0.01) and the dispatchers (P < 0.05). Seventy-eight percent of the engine drivers showed at least one cell per 100 with chromosome-type aberrations compared with 29% among the dispatchers and 31% among the office workers. In a follow-up study, another 30 engine drivers showed an increase (P < 0.05) in the frequency of cells with chromosome-type aberrations (gaps excluded) as compared with 30 referent policemen. Sixty percent of the engine drivers had one or more cells (per 100 cells) with chromosome-type aberrations compared with 30% among the policemen. In conclusion, the results of the two studies support the hypothesis that exposure to MF at mean intensities of 2-15 microT can induce chromosomal damage.
Adult↗