Risk Factor For Cancer Research Articles

Circulating Estrogen Metabolites and Risk of Breast Cancer among Postmenopausal Women in the Nurses' Health Study.

Estradiol and estrone are well-established risk factors for postmenopausal breast cancer (BC). Experimental evidence suggests that specific estrogen metabolites, produced via irreversible hydroxylation of estrone and estradiol at the 2- or 16-position may independently influence carcinogenesis. We performed a nested case-control study of BC (328 BC cases; 639 controls) among postmenopausal women within the Nurses' Health Study (NHS)to examine the role of estrogens and estrogen metabolites (jointly referred to as EM). Plasma concentrations of each EM (unconjugated+conjugated forms) were measured by liquid chromatography-tandem mass spectrometry. Multivariable conditional logistic regression, adjusting for BC risk factors, estimated relative risks (RR) and 95% confidence intervals (CI) of BC across quintiles of individual EM, EM pathways, and pathway ratios. Associations by estrogen/progesterone receptor (ER/PR) status were analyzed by unconditional logistic regression. Estradiol and estrone were strongly associated with increased BC risk [estradiol: RRQ5v.Q1 (95% CI)=2.64 (1.64-4.26), estrone: 2.78 (1.74-4.45); both p-trends<0.001]. The 2-hydroxylation pathway was strongly associated with risk [RRQ5v.Q1=3.09 (1.81-5.27), p-trend<0.001], and remained so after adjusting for unconjugated estradiol [RRQ5v.Q1=2.23 (1.25-3.96), p-trend=0.01]. While the 16-hydroxylation pathway was modestly associated with risk [RRQ5v.Q1=1.62 (1.03-2.54), p-trend=0.01], the association was attenuated after unconjugated estradiol adjustment [RRQ5v.Q1=1.24 (0.77-1.99), p-trend=0.19]. Similar positive associations with the 2-pathway and 16-pathway were observed for ER+/PR+ and ER-/PR- tumors. In this cohort of postmenopausal women, 2-hydroxylation of estrone and estradiol was associated with increased BC risk, independent of unconjugated estradiol. These results highlight the need to revisit the role of estrogen metabolism in BC etiology and prevention.

Endometriosis as a risk factor for ovarian cancer: an update on screening, risk reduction, treatment and prognosis

Key content: Endometriosis affects up to 10% of women. While many regard endometriosis as a benign (non‐cancerous) disease, there are well‐established links to epithelial ovarian cancer (EOC). Proposed mechanisms for malignant transformation include chronic inflammation, hyperestrogenism and oxidative stress. Mutations in the tumour suppressor gene ARID1A have also been implicated in the development of endometriosis‐associated ovarian cancer (EAOC). Endometriosis is reported to almost double a woman's background risk of ovarian cancer. Risk reduction strategies are effective in reducing the incidence of EAOC. These include tubal ligation, excision of endometriosis and combined hormonal contraception. Novel therapies targeting tumour suppressor gene mutations present in EAOC are undergoing phase I &amp; II clinical trials. Learning objectives: To increase knowledge of the association between endometriosis and EOC. To understand the updated evidence for screening, risk and risk reduction strategies. To be informed of potential novel therapies currently in the clinical trial stage of development. Ethical issues: Increased public awareness and improved clinician knowledge may lead to more and earlier‐stage disease detection. Women are more informed, necessitating clinicians to deliver evidence‐based counselling to meet their informational needs.

Helicobacter pylori induce circ_0046854 to regulate microRNA-511-3p/CSF1 axis and enhance the resistance of gastric cancer to cisplatin.

Helicobacter pylori (HP) is considered a major risk factor for gastric cancer (GC) and during this process, cytotoxin‑associated gene A (CagA) plays in essence. The study mainly focused on the molecular mechanism of circular RNA 0046854 (circ_0046854) in HP-induced GC. Clinically, 56 cases of GC and normal tissues were collected, and the GC tissues were divided into HP-negative GC tissues (HP-) and 33 HP-positive GC tissues (HP+). Tissue expression of circ_0046854, microRNA (miR)-511-3p and colony-stimulating factor 1 (CSF1) was tested. BGC-823/Cisplatin (DDP) resistant strain was induced and cell growth and DDP resistance were detected after HP infection. In vivo experiments were performed using a mouse xenograft model. The relationship between circ_0046854, miR-511-3p and CSF1 was confirmed. GC tissues especially HP+ cancer tissues expressed high circ_0046854 and CSF1 and low miR-511-3p. HP-induced circ_0046854 expression in GC cells through CagA. Inhibition of circ_0046854 or miR-511-3p elevation inhibited the growth and DDP resistance in GC cells. Circ_0046854 acted as a sponge for miR-511-3p, which targeted CSF1. Restoring CSF1 could abolish the inhibitory effect of miR-511-3p overexpression on CagA+ HP-induced GC progression in vitro. Circ_0046854 silencing repressed tumor growth and aggrandized the inhibiting effects of DDP on tumorigenesis in vivo. Circ_0046854/miR-511-3p/CSF1 axis may be involved in the development of HP-induced GC, thus providing new ideas for studying the mechanism of HP-related gastric diseases.

Integrated evaluation of workplace exposures and biomarkers of bladder cancer among textile dyeing workers

BackgroundThe textile industry is the second risk factor for bladder cancer, after smoking. Previous studies focused on the impact of exposure to high concentrations of bladder carcinogenic chemicals in the textile dyeing industry on the elevation of bladder cancer biomarkers. This study aimed to evaluate bladder carcinogenic air pollutants in a textile dyeing factory and investigate its role and the role of serum 25-hydroxyvitamin D (25-OH vit. D) on cancer bladder biomarkers in exposed workers.MethodsA cross-sectional study was conducted. Particulate and vapor forms of polycyclic aromatic hydrocarbons (PAHs) and volatile organic compounds (VOCs) were monitored in the printing, dyeing, and preparing sections of a textile factory. Bladder tumor antigen (BTA), nuclear matrix protein 22 (NMP-22), and 25-OH vit. D were estimated in all the exposed workers (147 exposed workers) and in workers not occupationally exposed to chemicals (130 unexposed workers).ResultsAromatic bladder carcinogenic compounds were either in low concentrations or not detected in the air samples of working areas. BTA and NMP-22 of exposed workers were not significantly different from the unexposed. However, 25-OH vit. D was significantly lower in the exposed than unexposed workers. There was a significant inverse correlation between 25-OH vit. D and duration of exposure in exposed workers.ConclusionThe mean levels of PAHs and VOCs were within the safe standard levels in the working areas. The non-significant difference in BTA and NMP-22 between the exposed and unexposed groups suggests the presence of occupational exposures to safe levels of bladder carcinogenic aromatics, while the significantly lower 25-OH vit. D levels among the exposed than the unexposed groups could suggest the potential association of 25-OH vit. D with occupational exposures to low levels of PAHs and VOCs, and this association was found to be inversely correlated with the duration of exposures. Accordingly, more specific predictor tests must be applied for early diagnosis of bladder cancer among the exposed workers.

Systematic review and meta-analysis of the association between gallstones and cholecystectomy with liver cancer

Introduction: Cholelithiasis and related treatments are associated with several gastrointestinal cancers. Thus, the present systematic review and meta-analysis aimed to investigate the relationship between cholelithiasis and cholecystectomy with the risk of liver cancer. Materials and Methods: The present study is a systematic review and meta-analysis conducted using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). We performed a search on the databases of Web of Science, Cochrane, ProQuest, PubMed, and Google Scholar until January 21, 2024. Moreover, the statistical analysis was performed using the STATA 14, and the significance level was set at P&lt;0.05. Results: The present meta-analysis included 15 studies with a total sample size of 1426704 participants. According to our results, a significant association between cholelithiasis and liver cancer (OR: 1.76, 95% CI: 1.52, 2.03), as well as cholecystectomy and liver cancer (OR: 1.55, 95% CI: 1.29, 1.87) were detected. Moreover, the relationship between cholelithiasis and liver cancer was significant in cohort studies (OR: 1.76, 95% CI: 1.51, 2.04) and insignificant in case-control studies (OR: 1.69, 95% CI: 0.86). However, there was a significant relationship between cholecystectomy and liver cancer in both the cohort (OR: 1.62, 95% CI: 1.29, 2.04) and case-control studies (OR: 1.26, 95% CI: 1.12, 1.41). Conclusion: In conclusion, cholelithiasis and cholecystectomy increased the risk of liver cancer by 76% and 55%, respectively. Thus, they can be considered as risk factors for liver cancer. Registration: This study has been compiled based on the PRISMA checklist, and its protocol was registered on the PROSPERO (ID: CRD42024508640) and Research Registry (UIN: reviewregistry1787) website.

Causal association between hyperthyroidism and risk of gastroesophageal reflux or esophageal cancer: a bidirectional Mendelian randomization investigation.

Emerging observational studies indicated an association between hyperthyroidism and gastrointestinal disorders. However, it remains unclear whether this association is causal, particularly in the case of gastroesophageal reflux (GERD) and esophageal cancer. To assess the potential causal relationship between hyperthyroidism and GERD or esophageal cancer, we conducted a bidirectional 2-sample Mendelian randomization study. Independent genetic instruments for hyperthyroidism from the UK Biobank (N case=3,545 and N control=459,388) and public genome-wide association study (GWAS) dataset (N case=3,731 and N control=480,867) were used to investigate the association with esophageal cancer in the UK Biobank study (N case=740 and N control=372,016) and GERD in the public GWAS database (N case=20,381 and N control=464,217). Four different approaches (inverse variance weighted (IVW), weighted mode, MR-Egger, and weighted median regression) were used to ensure that our results more reliable. Additional sensitivity analyses were also performed to validate our results. When hyperthyroidism was considered as the exposure factor, it appeared to act as a protective factor for GERD (ORIVW = 0.88, 95% CI, 0.79-0.99, P = 0.039), while as a risk factor for esophageal cancer (ORIVW = 1.03, 95% CI, 1.01-1.06, P = 0.003). However, there is no evidence supporting a reverse causal relationship between genetic susceptibility to hyperthyroidism and GERD or esophageal cancer. Our findings provided genetic evidence supporting bidirectional causal relationships between hyperthyroidism and GERD or esophageal cancer. These results substantiate certain discoveries from previous observational studies on a causal level and provide insight into relevant genetic susceptibility factors.

The association between postdiagnosis smoking cessation and survival in advanced non-small cell lung cancer patients in Southern Taiwan: A retrospective cohort study

ABSTRACT Objectives: Smoking is a major lung cancer risk factor. Studies show that smoking after lung cancer diagnosis is associated with an increased risk of developing other cancers and shorter survival. The purpose of this study was to examine the association between postdiagnosis smoking cessation and survival in patients with advanced non-small cell lung cancer (NSCLC). Materials and Methods: A retrospective cohort study was conducted. Data were collected between January 2014 and December 2019 in three hospitals in Southern Taiwan. Patient data were collected from the hospitals’ databases, and the correlation between smoking status and patient survival was analyzed using Kaplan–Meier curves and Cox proportional hazards regression modeling. Results: A total of 681 patients with advanced NSCLC were included in this study. The numbers (percentage) of ex-smokers and current smokers were 334 (49%) and 347 (51%), respectively. More than half of the patients in this study continued to smoke postdiagnosis advanced NSCLC. Furthermore, ex-smokers had lower mortality risk, even though this was not statistically significant (P = 0.212). The results of this study suggest that older than 65 years, men, Eastern Cooperative Oncology Group performance score of 3 and higher, history of chronic disease, receive chemotherapy, and targeted therapy are correlated with and have predictive effects on advanced NSCLC survival. Conclusion: There is no significant difference between postdiagnosis smoking cessation and survival in patients with advanced NSCLC. The reason for this finding may be due to lower survival rates after diagnosis with advanced NSCLC, and the benefits of smoking cessation cannot be seen immediately.

Urinary bladder carcinogenic potential of 4,4'-methylenebis(2-chloroaniline) in humanized-liver mice.

Occupational exposure to 4,4'-methylenebis(2-chloroaniline) (MOCA) has been linked to an increased risk of bladder cancer among employees in Japanese plants, indicating its significance as a risk factor for urinary bladder cancer. To investigate the role of MOCA metabolism in bladder carcinogenesis, we administered MOCA to non-humanized (F1-TKm30 mice) and humanized-liver mice for 4 and 28 weeks. We compared MOCA-induced changes in metabolic enzyme expression, metabolite formation, and effects on the urinary bladder epithelium in the two models. At week 4, MOCA exposure induced simple hyperplasia, cell proliferation, and DNA damage in the urothelium of the humanized-liver mice, while in the non-humanized mice these effects were not observed. Notably, the concentration of 4-amino-4'-hydroxylamino-3,3'-dichlorodiphenylmethane (N-OH-MOCA) in the urine of humanized-liver mice was more than 10 times higher than that in non-humanized mice at the 4-week mark. Additionally, we observed distinct differences in the expression of cytochrome P450 isoforms between the two models. Although no bladder tumors were detected after 28 weeks of treatment in either group, these findings suggest that N-OH-MOCA significantly contributes to the carcinogenic potential of MOCA in humans.

The BRD4 Inhibitor I-BET-762 Reduces HO-1 Expression in Macrophages and the Pancreas of Mice.

In pancreatic cancer, the tumor microenvironment (TME) accounts for up to 90% of the tumor mass. Pancreatitis, characterized by the increased infiltration of macrophages into the pancreas, is a known risk factor for pancreatic cancer. The NRF2 (nuclear factor erythroid 2-related factor 2) transcription factor regulates responses to oxidative stress and can promote cancer and chemoresistance. NRF2 also attenuates inflammation through the regulation of macrophage-specific genes. Heme oxygenase 1 (HO-1) is expressed by anti-inflammatory macrophages to degrade heme, and its expression is dependent on NRF2 translocation to the nucleus. In macrophages stimulated with conditioned media from pancreatic cancer cells, HO-1 protein levels increased, which correlated with higher NRF2 expression in the nuclear fraction. Significant differences in macrophage infiltration and HO-1 expression were detected in LSL-KrasG12D/+; Pdx-1-Cre (KC) mice, Nrf2 whole-body knockout (KO) mice and wildtype mice with pancreatitis. Since epigenetic modulation is a mechanism used by tumors to regulate the TME, using small molecules as epigenetic modulators to activate immune recognition is therapeutically desirable. When the bromodomain inhibitor I-BET-762 was used to treat macrophages or mice with pancreatitis, high levels of HO-1 were reduced. This study shows that bromodomain inhibitors can be used to prevent physiological responses to inflammation that promote tumorigenesis.

Helicobacter pylori induces GBA1 demethylation to inhibit ferroptosis in gastric cancer.

This research investigates potential therapeutic targets for gastric cancer, focusing on ferroptosis-related genes. Gastric cancer is known for its lower survival rates, necessitating new treatment strategies. This study employed Mendelian randomization to identify ferroptosis-related genes and methylation sites in gastric cancer, examining correlations between Helicobacter pylori infection, GBA1 gene expression, and promoter methylation with single-cell datasets and the TCGA-STAD database. We used Helicobacter pylori-infected gastric cancer cell models and used next-generation sequencing to monitor methylation changes pre- and post-infection. GBA1 expression levels were assessed via qRT-PCR and Western blot both before and after infection. The effect of Helicobacter pylori on GC cell proliferation was analyzed using CCK-8 and EdU assays after knocking down the GBA1 gene. The association between Helicobacter pylori infection and ferroptosis, including its reversibility after GBA1 knockdown, was evaluated using FerrOrange, GSH, MDA, and C11-BODIPY assays. Mass spectrometry measured the impact of Helicobacter pylori and GBA1 knockdown on lipid metabolism. An in vivo subcutaneous tumor-bearing model was also established to confirm these findings. Mendelian randomization analysis revealed that high GBA1 expression and reduced methylation levels of its promoter are risk factors for gastric cancer. Single-cell sequencing and TCGA-STAD datasets indicated a positive correlation between Helicobacter pylori infection and GBA1 expression, with a concurrent negative correlation between GBA1 promoter methylation and GBA1 expression. In gastric cancer cell lines, Helicobacter pylori infection was observed to enhance GBA1 expression and decrease methylation levels at its promoter. Additionally, Helicobacter pylori promoted GC cell proliferation, an effect mitigated by knocking down GBA1. Infection also reduced lipid peroxidation, increased glutathione levels, and impeded ferroptosis in GC cells; however, these effects were reversed following GBA1 knockdown. Changes in sphingolipid metabolism induced by I were detected in GC cell lines. In vivo experiments using a subcutaneous tumor-bearing model demonstrated that Helicobacter pylori infection fosters tumorigenesis in GC cells. Our study demonstrates that Helicobacter pylori infection triggers demethylation and upregulation of GBA1, subsequently inhibiting ferroptosis in gastric cancer cells. These findings suggest that targeting the GBA1 pathway may offer a novel therapeutic approach for managing gastric cancer.

Human papillomavirus infection of the fallopian tube as a potential risk factor for epithelial ovarian cancer

Human papillomaviruses (HPVs) and herpesviruses are detected in patients with epithelial ovarian cancer (EOC). We sought to analyze the prevalence of HPV’s 16 and 18, cytomegalovirus (CMV), and Epstein-Barr virus (EBV) DNA in peripheral blood, ovarian, and fallopian tube (FT) tissue samples collected from 97 EOC patients, including 71 cases of high-grade serous ovarian carcinoma (HGSOC), and from 60 women with other tumors or non-neoplastic gynecological diseases. DNA isolates were analyzed by PCR methods, including droplet digital PCR. The results demonstrate that (1) HPV16 DNA has been detected in one-third of the FT and tumor samples from EOCs; (2) the prevalence and quantity of HPV16 DNA were significantly higher in FT samples from HGSOCs, non-HGSOCs, and ovarian metastases than in those from non-neoplastic diseases; (3) CMV and EBV have been detected in approximately one-seventh of EOC samples. The results suggest that HPV16 might be a potential risk factor for EOC development.

Risk Factors and Prevention of Stomach Cancer, Excluding Helicobacter pylori

Gastric cancer is a significant health problem owing to its high incidence and mortality rate. The risk factors for gastric cancer include both uncontrollable (e.g., age, sex, and genetic predisposition) and controllable factors (e.g., &lt;i&gt;Helicobacter pylori&lt;/i&gt; infection, smoking, alcohol consumption, obesity, and high-salt diets). Although treatment of &lt;i&gt;H. pylori&lt;/i&gt; infections has been implemented as a primary preventive measure, the risk of gastric cancer may persist, highlighting the need for additional preventive measures. This review discusses various risks and protective factors associated with gastric cancer, studies conducted on these factors, and chemoprevention. Smoking is a risk factor for this disease; thus, is not recommended and current smokers are encouraged to quit because cessation can reduce the risk of gastric cancer. Excessive alcohol intake has been reported to increase the risk of gastric cancer as has the consumption of high-salt foods that can damage the gastric mucosa. Additionally, increasing the intake of fruits and vegetables, known for their protective effects against gastric cancer, can aid in its prevention. Studies on chemopreventive agents, including nonsteroidal anti-inflammatory drugs (e.g., aspirin), statins, and metformin, have been reported; however, evidence of their effectiveness remains insufficient to recommend these agents as preventive treatments. Additional well-planned studies on preventive medications and dietary approaches are necessary.

Abstract A061: DKK3 in pancreatic cancer – Elucidating the roles of a double-edged sword

Abstract Pancreatic ductal adenocarcinoma (PDAC) remains a highly challenging disease with a poor prognosis due to lack of diagnostic biomarkers and high tumor heterogeneity. Therefore, it is crucial to meticulously examine the intricate molecular mechanisms in PDAC. We previously identified DKK3 (Dickkopf-3) as a novel factor promoting organ regeneration during pancreatitis and established a previously unknown link between DKK3 and the Wnt and Hedgehog signaling. Given that pancreatitis is a significant risk factor for pancreatic cancer, we were motivated to investigate the potential role of DKK3 in PDAC development. We utilized PDAC mouse models driven by LSL-KrasG12D/+; Ptf1aCre/+ with wildtype, homozygous/heterozygous DKK3 deletion in both epithelial and stromal compartment while employing in vitro and ex vivo systems to examine the stage and compartment-specific roles of the same. Through a comprehensive and time-resolved analysis of tumor characteristics, we discovered that the loss of DKK3 led to rapid oncogenic transformation, marked by a significant increase in metaplasia and desmoplasia starting at an early stage (10 weeks). Ex vivo acinar-to-ductal metaplasia assay and rescue experiments with wildtype and DKK3-null acinar cells revealed that secreted DKK3 operates as a tumor suppressive roadblock in PDAC-initiating steps. This advanced preneoplastic stage translated into accelerated progression toward invasive tumors at 36 weeks, a shortened overall survival, and a higher liver metastasis incidence in the DKK3-null animals at the endpoint. Interestingly, transcriptomic analyses further validated our observation and revealed the involvement PI3-AKT signaling pathway as an underlying mechanism. Further characterization of isolated tumor cells confirmed our observations, revealing prominent mesenchymal features and enhanced migratory capacities upon loss of DKK3. Interestingly, DKK3-null PDACs exhibited a pronounced stroma remodeling with a myofibroblastic cancer-associated fibroblast-enriched environment, as well as an immunosuppressive stroma with abundant regulatory T cells and cytotoxic T cell depletion, as substantiated by coculture experiments. Intriguingly, while displaying similar phenotypic features to DKK3-null tumors, Dkk3+/- heterozygotes exhibited the most aggressive outcome. To further dissect this finding, we conducted a set of in silico approaches and immunostainings revealing persistent stromal DKK3 expression in DKK3- proficient PDACs. This suggested a possible dual role of DKK3 that could operate either as a friend or a foe depending on its spatiotemporal expression in PDAC. In line, in vitro systems demonstrated a distinct oncogenic effect of DKK3 on endpoint tumor cells, particularly promoting malignant cell migration. In summary, we propose that epithelial DKK3 exerts cell-autonomous tumor suppressive functions during the onset of PDAC, while stromal DKK3 acts as an oncogenic cue driving cancer progression. These findings highlight DKK3 as a promising biomarker and a novel therapeutic target for PDAC tumors. Citation Format: Dharini Srinivasan, Frank Arnold, Elodie Roger, Anna Härle, Michael K Melzer, Chantal Allgöwer, Patrick C Hermann, Lukas Perkhofer, Johann Gout, Alexander Kleger. DKK3 in pancreatic cancer – Elucidating the roles of a double-edged sword [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Advances in Pancreatic Cancer Research; 2024 Sep 15-18; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2024;84(17 Suppl_2):Abstract nr A061.

Assessing the Use of Educational Interventions Promoting Preventive Measures for Sun Exposure in Rural Guatemala

Background: Sun exposure is a well-known risk factor for skin cancer. Preventative education regarding sun damage protection has been shown to be effective. However, the efficacy of similar interventions in underserved Guatemala is unclear. This study assesses the affect of educational interventions on understanding of sun protective measures among this population. Methods: Participants were adults in Guatemala that attended a free community clinic in February 2024 and were provided a 7-minute educational video in Spanish discussing skin cancers types,warning signs, and sun protection. Patients were administered a 12-question pre-survey using yes or no responses to evaluate baseline understanding. An 8-question post-survey was administered to assess changes in willingness to use sun protection, comfort in identifying warning signs, and understanding of risk factor . Descriptive statistics and Chi-square analysis were performed. Results: 29 participants completed the study. 58.6% were aged 18-30y, 24 (82.8%) were women and 5 (17.2%) were men. After watching the video, participants were more willing to use sun protection methods daily (58.6% pre-intervention vs 96.6% post-intervention; p=0.001), more comfortable with identifying warning signs of skin cancer (3.4% pre-intervention vs 96.6% post-intervention; p&lt;0.001), and had a better understanding of sun exposure as a risk factor for skin cancer irrespective of Fitzpatrick skin type (37.9% pre-intervention vs 96.6% post-intervention; p&lt;0.001). Conclusion: Patients who underwent educational intervention were significantly more likely to implement sun protective measures into their daily routine, were more comfortable identifying skin cancer warning signs, and had a better understanding that all skin types can get skin cancer.

Alcohol-related cancer risk awareness and support for cancer warning labelling among adults in Estonia

ObjectivesThe aim of this study was to describe alcohol-related cancer risk awareness and examine sociodemographic and alcohol-related variance in attitudes towards implementation of cancer warning labelling on alcohol containers in Estonia. Study designNationally representative data from a 2022 cross-sectional survey (n = 2059) among the 15–74-year-old population in Estonia were used. MethodsDescriptive statistics on the prevalence of alcohol-related cancer risk awareness and support for the implementation of cancer risk warning labelling on alcohol containers are presented. Poisson regression analysis was used to investigate whether support for warning labelling varied by sociodemographic variables, individual alcohol consumption and cancer risk awareness indicators. ResultsStudy found that 73.2% of respondents associated alcohol consumption with increased cancer risk for one or more cancer sites, but implementation of alcohol cancer risk labelling was only supported by 54%. Women, younger age groups, non-Estonians and those with lower education level expressed higher support for warning labelling, whereas lower support was found among those with high-risk alcohol consumption. As expected, awareness of alcohol-related cancer risk and perceiving individual alcohol consumption as a cancer hazard were associated with support for warning labelling. ConclusionsThese findings emphasise the need for better communication of alcohol-related cancer risks as public awareness on the link between alcohol consumption and site-specific cancer risk was low. Increased awareness of alcohol as a cancer risk factor would potentially build public support for introducing cancer-risk warning labelling on containers of alcoholic drinks.

Correlation of risk factors for prostate cancer with doubtful prostate antigen values

Correlation of risk factors for prostate cancer with doubtful prostate antigen values

Effect of smoking on the recurrence and progression of non-muscle-invasive bladder cancer.

It is well established that smoking is the most significant risk factor for bladder cancer, yet the impact of smoking on the recurrence and progression of non-muscle-invasive bladder cancer (NMIBC) remains a contentious issue. To review all relevant literature published to date, providing a comprehensive assessment of the effects of smoking on the recurrence and progression of NMIBC, thereby offering a basis for smoking cessation management in NMIBC patients. A search was conducted for all relevant literature published up to April 2024 in PubMed, Web of Science, and Embase databases. The existing literature results and deficiencies were analyzed, and the gaps in understanding between different studies were highlighted, with recommendations for future research. A total of 24 studies were included in this work. Among them, 14 studies suggested that smoking promotes the recurrence and progression of NMIBC, while another 10 studies concluded that smoking has no effect on the recurrence and progression of NMIBC patients. Our research indicates that smoking increases the risk of recurrence and progression in NMIBC patients, and quitting smoking can improve health-related quality of life. High-quality, large-sample prospective cohort studies (or randomized controlled studies) are still needed in the future.

Oral Metastasis to the Oral Cavity - An Emerging Prostate Cancer Risk Factor: A Review

Oral Metastasis to the Oral Cavity - An Emerging Prostate Cancer Risk Factor: A Review

Global Research Trends in the Links between Periodontal Disease and Cancer: A Bibliometric Analysis.

Both periodontal disease and cancer are prevalent conditions with significant impacts on individuals and society. Extensive research has suggested a potential link between these two diseases. This study conducted a bibliometric analysis using the Thomson Reuters Web of Science Core Collection database, focusing on publications from 2014 to 2023. The analysis included data extraction and examination of authors, affiliations, publication dates, journals, countries, citation counts, keywords, and the H-index. A total of 253 relevant articles were identified, showing an increasing trend in both publications and citations over the years. The analysis highlighted the most productive authors, institutions, and countries/regions, with Michaud DS and Abnet CC leading in the number of publications. Highly cited articles emphasized the role of specific oral microbiota, particularly F. nucleatum and P. gingivalis, in various cancers, suggesting their potential as diagnostic markers and therapeutic targets. Four key thematic clusters emerged from the keyword analysis: the broader health implications of periodontal disease, the microbiome's role in carcinogenesis, inflammation, and specific bacteria in cancer, and epidemiological methods in studying the disease-cancer association. This bibliometric analysis underscores the growing interest in the connection between periodontal disease and cancer. Future research should adopt interdisciplinary approaches, focus on large-scale microbiome studies and longitudinal research to understand the systemic effects of periodontal disease, identify cancer-associated bacterial profiles, and investigate the molecular mechanisms of bacterial carcinogenesis. Additionally, public health interventions aimed at improving oral hygiene and reducing cancer risk factors are recommended.

Acute pancreatitis as a risk factor of chronic pancreatitis and pancreatic cancer. An overview.

This is an overview of relation between acute and chronic pancreatitis and between acute pancreatitis and pancreatic cancer. Acute pancreatitis and recurrent acute pancreatitis are an etiological factor of chronic pancreatitis. Population-based studies have calculated the risk of acute recurrent pancreatitis after the first attack of acute pancreatitis to be 20% and development of chronic pancreatitis after first attack of acute pancreatitis is 10%. An important risk factor is tobacco smoking. Acute and chronic pancreatitis are risk factors for pancreatic cancer. The risk of acute pancreatitis is related to the number of recurrences of acute pancreatitis, but not the etiology of acute pancreatitis. Acute pancreatitis, as well as chronic pancreatitis, are risk factors for pancreatic cancer. After an attack of acute pancreatitis or recurrent acute pancreatitis a patient should be regarded as a high risk.