Potential Cancer Risk Factors Research Articles

Relationship between the white blood cell count and some lipid profile parameters in cancer patients with myocardial infarction

Hokkaido University (Tsumita T, 2022) researchers found that endothelial cells accumulate low-density lipoproteins (LDL) in tumor blood vessels. At the same time, the endothelium carries out neutrophil chemotaxis, which perform an immunosuppressive function contributing to cancer progression.Aim. To search for the relationship between the white blood cell (WBC) count and some lipid profile parameters in cancer patients with myocardial infarction (MI).Material and methods. We examined 319 patients who were treated at Dzhanelidze Research Institute of Emergency Medicine in 2018-2023, which were divided into three groups: MI in combination with an active cancer — 132 patients (Group I), MI+cancer in history — 58 patients (Group II), MI without cancer — 129 patients (Group III). Following laboratory data used in routine practice were assessed: WBC count, relative neutrophil count, total cholesterol, low-density lipoproteins.Results. Cancer patients with MI are characterized by higher WBC and neutrophil count than in other samples However, the total cholesterol level was significantly lower in this sample, and the LDL level was not significantly different. Patients with MI and previous cancer occupied an intermediate position between groups I and III in terms of studied parameters.Conclusion. In general, data on the role of cholesterol levels in cancer patients are contradictory. In particular, some studies have shown that elevated cholesterol levels are a potential risk factor for cancer. In our study, as in a number of others, no significant associations were identified between elevated cholesterol levels and the presence of cancer. Our study is a step towards understanding the connection between the cholesterol concentration and the immune response in cancer patients with MI.

Accurate and inaccurate beliefs about cancer risk factors among Spanish-preferring adults in the United States

ObjectiveTo characterize inaccurate and accurate beliefs about cancer risk factors held among Spanish-preferring adults in the United States. MethodsFrom a national probability panel, we surveyed 196 Hispanic adults who prefer completing questionnaires in Spanish. We also used data from a representative sample of 1200 adults in the US to compare belief acceptance. ResultsMany less accepted accurate beliefs about cancer risk factors related to topics like fruit/vegetable consumption, weight loss, and alcohol use. Several inaccurate beliefs were widely held, with some being more accepted in the Spanish-preferring sample than the general US adult sample. Higher levels of self-reported media literacy and information scanning associated with more acceptance of both accurate and inaccurate beliefs. Access to the internet at home associated with discernment between accurate and inaccurate beliefs about cancer risk factors. ConclusionAcceptance of accurate beliefs and rejection of inaccurate beliefs varied across potential cancer risk factors. Future Spanish-language public health messaging should address these belief inconsistencies when providing up-to-date cancer-related recommendations or correcting inaccurate information in the public communication environment. InnovationOur study provides comprehensive information about cancer beliefs among Spanish-preferring adults in the United States, which was not previously available, and find that media literacy is a concept likely to be important to consider when putting together intervention tools to combat misinformation.

Perfluoroalkyl and polyfluoroalkyl substances and Cancer risk: results from a dose-response Meta-analysis.

Perfluoroalkyl and polyfluoroalkyl substances (PFASs) are persistent organic pollutants in the environment. While some studies suggest that PFASs may contribute to cancer development, the link between PFAS exposure and cancer risk remains debated. This dose-response meta-analysis explores the relationship between PFASs and cancer. It employs odds ratio (OR) and standardized mean difference (SMD), along with their 95% confidence interval (CI), to assess the effects of PFASs on cancer risk. Relevant studies were sourced from Web of Science, PubMed, Embase, Medline, and CNKI databases. The dose-response relationship was assessed by the fixed-effects model and least-squares regression. Forty studies, involving a total of 748,188 participants, were included in this meta-analysis. Out of these, 13 studies were specifically analyzed for the dose-response relationship. Findings revealed that exposure to PFASs, especially PFDA, significantly raises the risk of genitourinary cancers, and PFDA exposure shows a dose-dependent increase in overall and breast cancer risk. Additionally, PFOS exposure is associated with an increased cancer risk, and elevated PFOA levels were significantly observed in breast cancer patients. The findings suggest that PFAS exposure is a potential cancer risk factor, with the carcinogenic potential of PFDA being dose-dependent. The online version contains supplementary material available at 10.1007/s40201-024-00899-w.

A multi-task fusion model based on a residual–Multi-layer perceptron network for mammographic breast cancer screening

Background and objectiveDeep learning approaches are being increasingly applied for medical computer-aided diagnosis (CAD). However, these methods generally target only specific image-processing tasks, such as lesion segmentation or benign state prediction. For the breast cancer screening task, single feature extraction models are generally used, which directly extract only those potential features from the input mammogram that are relevant to the target task. This can lead to the neglect of other important morphological features of the lesion as well as other auxiliary information from the internal breast tissue. To obtain more comprehensive and objective diagnostic results, in this study, we developed a multi-task fusion model that combines multiple specific tasks for CAD of mammograms. MethodsWe first trained a set of separate, task-specific models, including a density classification model, a mass segmentation model, and a lesion benignity–malignancy classification model, and then developed a multi-task fusion model that incorporates all of the mammographic features from these different tasks to yield comprehensive and refined prediction results for breast cancer diagnosis. ResultsThe experimental results showed that our proposed multi-task fusion model outperformed other related state-of-the-art models in both breast cancer screening tasks in the publicly available datasets CBIS-DDSM and INbreast, achieving a competitive screening performance with area-under-the-curve scores of 0.92 and 0.95, respectively. ConclusionsOur model not only allows an overall assessment of lesion types in mammography but also provides intermediate results related to radiological features and potential cancer risk factors, indicating its potential to offer comprehensive workflow support to radiologists.

Association between obstructive sleep apnoea and cancer: a cross-sectional, population-based study of the DISCOVERY cohort

ObjectivesNocturnal hypoxia in obstructive sleep apnoea (OSA) is a potential risk factor for cancer. We aimed to investigate the association between OSA measures and cancer prevalence in a large national...

Role of Xeroderma pigmentosum D (XPD) protein in genome maintenance in human cells under oxidative stress

Xeroderma pigmentosum D (XPD) protein plays a pivotal role in the nucleotide excision repair pathway. XPD unwinds the local area of the damaged DNA by virtue of constituting transcription factor II H (TFIIH) and is important not only for repair but also for basal transcription. Although cells deficient in XPD have shown to be defective in oxidative base-lesion repair, the effects of the oxidative assault on primary fibroblasts from patients suffering from Xeroderma Pigmentosum D have not been fully explored. Therefore, we sought to investigate the role of XPD in oxidative DNA damage-repair by treating primary fibroblasts derived from a patient suffering from Xeroderma Pigmentosum D, with hydrogen peroxide. Our results show dose-dependent increase in genotoxicity with minimal effect on cytotoxicity with H2O2 in XPD deficient cells compared to control cells. XPD deficient cells displayed increased susceptibility and reduced repair capacity when subjected to DNA damage induced by oxidative stress. XPD deficient fibroblasts exhibited increased telomeric loss after H2O2 treatment. In addition, we demonstrated that chronic oxidative stress induced accelerated premature senescence characteristics. Gene expression profiling revealed alterations in genes involved in transcription and nucleotide metabolisms, as well as in cellular and cell cycle processes in a more significant way than in other pathways. This study highlights the role of XPD in the repair of oxidative stress and telomere maintenance. Lack of functional XPD seems to increase the susceptibility of oxidative stress-induced genotoxicity while retaining cell viability posing as a potential cancer risk factor of Xeroderma Pigmentosum D patients.

Vitamin D deficiency: a potential risk factor for cancer in obesity?

Obesity is considered an abnormal or excessive accumulation of adipose tissue, due to a prolonged positive energy balance that arises when energy intake is greater than energy expenditure, leading to an increased risk for the individual health and for the development of metabolic chronic diseases including several different types of cancer. Vitamin D deficiency is a metabolic alteration, which is often associated with the obesity condition. Vitamin D is a liposoluble vitamin, which plays a pivotal role in calcium-phosphate metabolism but extraskeletal effects have also been described. Among these, it plays an important role also in adipocyte physiology and glucose metabolism, typically dysregulated in subjects affected by obesity. Moreover, it is now recognized that Vitamin D also influences the processes of cell proliferation, differentiation, adhesion potentially leading to carcinogenesis. Indeed, data indicate a potential link between vitamin D levels and cancer, and higher vitamin D concentrations have been associated with a lower risk of developing different kinds of tumors, including breast, colon, lymphoma, lung, and prostate cancers. Thus, this review will revise the literature regarding this issue investigating and highlighting the potential mechanism of action, which might lead to new therapeutical options.

Diagnostic and therapeutic approach to children with Nijmegen breakage syndrome in relation to development of lymphoid malignancies.

Nijmegen breakage syndrome (NBS) is a rare chromosomal instability disorder. The majority of patients carry founder mutation in the NBN gene (c.657_661del5). Characteristic features of the NBS include progressive microcephaly, dysmorphic facial features, immunodeficiency, and high predisposition to malignancy with cumulative cancer incidence by the age of 20 years, and amounted to over 70%. The aim of study is to present the latest methods of diagnosis, potential cancer risk factors and treatment of lymphoid malignancies in children with NBS. To review the evidence using PubMed and Google Scholar search which included articles published between 2009-2021, focusing on articles published between 2013-2021. The average delay in diagnosis of NBS ranges from 4-5 years. Neonatal screening of T-cell excision circles (TRECs) and kappa-deleting recombination excision circles (KRECs) seems favourable in NBS. There are no specific protocols for the treatment of lymphoid malignancies in children with NBS, and full- dose chemotherapy is the most frequently applied method. Reducing the doses of chemotherapy does not significantly reduce the toxicity. Main cause of death is cancer progression and treatment-related mortality mostly associated with infectious complications. Patients with diagnosed cancer who received haematopoietic stem cell transplantation (HSCT) had significantly higher 20-year OS than those who did not (42.7% vs. 30.3%). Further meta-analysis is essential to establish the best monitoring and treatment regimen in patients with NBS and lymphoid malignancies.

Climate change: A potential risk factor for cancer?

Cancer, mainly known for abnormal growth and altered cellular function is now the second prominent reason of death globally. There are so many factors responsible for this disease and one of the major factors is climate change. The deviations of weather patterns that is definitely as a result of human activities over long periods of times generally referred as climate change. The consequence’s, increasing temperature, melting of ice, rising of sea levels, increasing wind speed, changes in rainfall patterns etc. Due to all these concerns, the most important resource for a healthy life– Air, Water, and Food are gets disturbed and as a results causes several health related problems. Researches related to this field also demonstrated that climate change played critical role over cancer risk and cancer surveillance. It increases the amount of carcinogens and also its blocks patients’ access to cancer hospitality. Thus it can be potent risk factor.

Severe Salmonella spp. or Campylobacter spp. Infection and the Risk of Biliary Tract Cancer: A Population-Based Study.

Simple SummaryAlthough it is known that bacterial infection may increase risk of cancer, the relationship between certain infections and cancer remains ill-quantified. To identify potential risk factors, this study compared the incidence of biliary tract cancer (BTC) in patients with Salmonella spp. or Campylobacter spp. infection to the general population in a large Western cohort of 16,252 salmonellosis and 27,668 campylobacteriosis patients. Standardized relative incidence ratio for BTC was 1.53 (95% CI 0.70–2.91) in salmonellosis patients and 0.97 (95% CI 0.39–2.00) in campylobacteriosis patients. Patients with Salmonella spp. infection and BTC were significantly younger than BTC patients without Salmonella spp. infection. Potentially, the study was underpowered to detect differences in cancer incidence, or cancer etiology in Western patients differs from those in non-Western countries and instead of bacterial infection, other factors contribute to cancer risk. Better understanding of cancer etiology is needed to identify risk factors and facilitate screening and early detection of cancer patients.Salmonella spp. infection has shown to have oncogenic transformative effects and thereby increases the risk of certain cancers. For Campylobacter spp., similar effects have been demonstrated. Risk factor identification may allow for timely diagnosis and preventive treatment. To substantiate the oncogenic potential of Salmonella and Campylobacter spp., this study compared the incidence of extrahepatic biliary tract cancer (BTC) in patients with diagnosed Salmonella or Campylobacter spp. infection with BTC incidence in the Netherlands. National infectious diseases surveillance records of patients diagnosed with a laboratory-confirmed Salmonella or Campylobacter spp. infection during 1999–2016 were linked to the Netherlands Cancer Registry. Incidence of BTC in Salmonella and Campylobacter spp. patients was compared to the incidence of BTC in the general population using Standardized Incidence Ratios (SIRs). In total, 16,252 patients were diagnosed with Salmonella spp. and 27,668 with Campylobacter spp. infection. Nine patients developed BTC at a median of 46 months (13–67) after Salmonella spp. infection and seven at a median of 60 months (18–138) after Campylobacter spp. infection. SIR of BTC in salmonellosis patients was 1.53 (95% CI 0.70–2.91). In patients aged <60 years, the SIR was 1.74 (95% CI 0.36–5.04). For campylobacteriosis patients, the SIR was 0.97 (95% CI 0.39–2.00). Even though Salmonella or Campylobacter spp. infection was not significantly associated with increased BTC risk in this cohort, it remains extremely important to study potential risk factors for cancer to facilitate screening and ultimately improve prognosis of cancer patients.

Association between shift work and biological factors including FGF-23, klotho, and serum 25-(OH) vitamin D3 among Korean firefighters: a cross-sectional study.

Shift work is known to be detrimental to an individual's health as it disrupts the circadian rhythm and is a risk factor for cancer. It has been reported that elevated fibroblast growth factor (FGF)-23, increased serum soluble α-klotho, and decreased vitamin D3 are associated with cancer progression. We studied the relationship between shift work and the levels of FGF-23, α-klotho, and vitamin D3 amongst firefighters, as they work in long shifts outside the traditional daytime schedule. The study consisted of 450 participants who were firefighters. We measured FGF-23, α-klotho, and vitamin D3 levels in their blood and a set of questionnaires were given to the participants to evaluate their health habits. After determining and adjusting for potential confounding factors, we compared the levels of FGF-23, α-klotho, and serum vitamin D3 by job and shift types. FGF-23 and α-klotho levels were significantly higher in shift workers than traditional day workers, and in 3-day cycle shift workers than workers with another shift schedule. When the levels of these substances were compared based on different types of jobs, firefighters had a lower level of vitamin D3. We conclude that shift work is positively correlated with the levels of FGF-23 and α-klotho. Levels of FGF-23 and α-klotho were linked to shift work and job types. Although vitamin levels did not differ by shift types, vitamin D3 levels were lower in firefighters. These findings suggest that high levels of FGF-23 and α-klotho are potential risk factors for cancer among firefighters.

A quantified risk-scoring system including the visceral fat area for peritoneal metastasis of gastric cancer.

Background: Peritoneal metastases of gastric cancer are usually detected using imaging, However, the results of imaging modalities are not always reliable; therefore, the prediction of prognosis based on these findings is therefore inaccurate. As visceral obesity has been identified as a potential risk factor for cancer, the present study aimed to evaluate the predictive value of visceral fat area (VFA), a representative marker of visceral obesity, for peritoneal metastasis in patients with gastric cancer and to construct a reliable preoperative prediction system for peritoneal metastasis.Patients and methods: We enrolled 859 patients with gastric cancer. The VFA and other objective clinical tumor characteristics were evaluated using receiver operating characteristic (ROC) curves. Independent predictors of peritoneal metastasis were determined using logistic regression analysis; a prediction system was also evaluated using ROC curves.Results: The ROC curves indicated a VFA cutoff value of 91.00 cm2 as predictive of peritoneal metastasis. On logistic regression, visceral obesity (VFA ≥91.00 cm2) was identified as an independent predictor of peritoneal metastasis, with an area under the ROC curve of 0.659; the platelet-to-lymphocyte ratio (PLR), invasion depth, and vascular invasion were also identified as independent predictors. On integrating these predictors into a single prediction system, peritoneal metastases were more reliably predicted (area under the ROC curve=0.779).Conclusions: Visceral obesity, as defined by the VFA, effectively predicted peritoneal metastases in our cohort. Our scoring system may be a reliable instrument for identifying patients with peritoneal metastasis.

Cryptochrome 2 (CRY2) Suppresses Proliferation and Migration and Regulates Clock Gene Network in Osteosarcoma Cells.

BackgroundCircadian disruption is a potential cancer risk factor in humans. However, the role of the clock gene, cryptochrome 2 (CRY2), in osteosarcoma (OS) is still not clear.Material/MethodsTo evaluate the potential role of CRY2 in HOS osteosarcoma cells, CRY2-silenced cell lines were established. Furthermore, we investigated the effect of CRY2 knockdown on HOS cells by CCK-8, colony formation, migration assay, and flow cytometry, in vitro.ResultsCRY2 knockdown promoted HOS OS cell proliferation and migration. We used a cell cycle assay to show that CRY2 knockdown increased the S phase cell population and reduced the G1 phase cell population. Western blot analyses showed that CRY2 knockdown decreased P53 expression and increased expression of c-myc and cyclin D1. Simultaneously, CRY2 knockdown increased the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, but did not change the phosphorylation of c-Jun N terminal kinase (JNK) and P38. CRY2 knockdown also increased the expression of matrix metalloproteinase (MMP)-2 and β-catenin, and increased OS cell proliferation and migration by inducing cell cycle progression and promoting mitogen-activated protein kinase (MAPK) and Wnt/β-catenin signaling pathways. Although it has previously been unclear whether the expression of CRY2 affects the expression of other clock genes in the clock gene network, our results show that knockdown of CRY2 significantly increased the mRNA expression of CRY1, Period (PER) 1, PER2, BMAL1, and CLOCK.ConclusionsOur results suggest that CRY2 may be an anti-oncogene in OS, whose functions involve both downstream genes and other circadian genes.

Pilot assessment of cyanotoxins as potential risk factors for cancer in Bulgaria

Cyanoprokaryotes (=cyanobacteria, blue-green algae) are the most ancient oxygen-producing phototrophic microorganisms, spread all over the Globe, which form the important basis of different food chains in aquatic and terrestrial habitats. However, due to strong anthropogenic pressure during the last decades they are also responsible for causing nuisance algal blooms in different water bodies with deleterious effects on the mankind and ecosystems mainly due to production of toxic substances (cyanotoxins). Amongst them are the microcystins, nodularins, lyngbyatoxins and aplysiatoxins, known as tumor-promotors with increase of exposure routes through which humans and animals can be placed at risk (Meriluoto et al. 2017). However, the investigations on the relations between the occurrence and development of such diseases with the cyanotoxins and their producers are extremely scarce at a global scale (Yu and Chen 1994, Ueno et al. 1996, Fleming et al. 2002, Svircev et al. 2009, Drobac et al. 2011, Labine et al. 2015). During the last 15 years cyanoblooms and microcystins, nodularins and saxitoxins were detected in 16 different Bulgarian freshwater bodies, including some drinking-water reservoirs (Stoyneva-Gärtner et al. 2017). Amongst the detected toxins some new forms were recognized by their characteristic spectra (Pavlova 2007, Pavlova et al. 2007), and, more recently, a new potential producer of lyngbyatoxin was found in the Black Sea (Stoyneva et al. 2015). The poster shows a pilot assessment of the spread of cancer distribution and mortality vs. spread of cyanoblooms and cyanotoxins in Bulgaria. The pilot assessment is made on the basis of comparison of the general regions of spread of cyanotoxins in Bulgarian water bodies and toxin-producing cyanospecies during the period 2000-2017 (Stoyneva-Gärtner et al. 2017) with the spread of cancer in Bulgaria (e.g. Valerianova et al. 2015). The comparison shows general conformities between the spread of the “most dangerous” water bodies and main regions of cancer diseases in the country. The results obtained served as a basis for a new project proposal which aims at a deepening of the studies for improvement of prevention of cancer in the country.

Prevalence of Modifiable Cancer Risk Factors Among U.S. Adults Aged 18–44 Years

IntroductionCarcinogen exposure and unhealthy habits acquired in young adulthood can set the stage for the development of cancer at older ages. This study measured the current prevalence of several cancer risk factors among young adults to assess opportunities to intervene to change the prevalence of these risk factors and potentially reduce cancer incidence.MethodsUsing 2015 National Health Interview Survey data (analyzed in 2016), the prevalence of potential cancer risk factors was estimated among U.S. adults aged 18–44 years, based on responses to questions about diet, physical activity, tobacco product use, alcohol, indoor tanning, sleep, human papillomavirus vaccine receipt, and obesity, stratified by sex, age, and race/ethnicity.ResultsThe prevalence of some risk factors varied by age and race/ethnicity. Obesity (one in four people) and insufficient sleep (one in three people) were common among men and women. Physical inactivity (one in five men, one in four women); binge drinking (one in four men, one in eight women); cigarette smoking (one in five men, one in seven women); and frequent consumption of red meat (one in four men, one in six women) also were common. More than half of the population of adults aged 18–44 years consumed sugar-sweetened beverages daily and processed meat at least once a week. Most young adults had never had the human papillomavirus vaccine.ConclusionsFindings can be used to target evidence-based environmental and policy interventions to reduce the prevalence of cancer risk factors among young adults and prevent the development of future cancers.

Abstract B06: Trajectories of inflammatory biomarkers: A randomized longitudinal 12-months intervention promoting anti-inflammatory food consumption among breast cancer survivors

Abstract U.S. breast cancer survivors (BCSs) are expected to increase to 4 million in the next 5-10 years. Cancer recurrence risk is highest in obese survivors. Inflammatory (Pro-I) biomarkers including C-reactive protein (CRP), Interleukins -3, -6, and -8 (IL-3, IL-6, IL-8), and Tumor Necrosis Factor (TNF)-α have been associated with cancer severity and recurrence. Nutritional interventions aimed at reducing inflammation may contribute to reduced recurrence risk and increase survival rates. However, studies have been limited to animal models. The goals of this one-year culinary-based intervention were to: 1) decrease Pro-I biomarkers and increase anti-inflammatory (AI) cytokines like IL10, by promoting AI food incorporation into BCS dietary routines; and 2) examine effects on potential cancer risk factors including body mass index (BMI) and circulating adipose stromal cells (ASCs). A total of 153 BCSs was recruited. Overweight and obese women aged 18 or older, diagnosed with Stage 0-III breast cancer and at least 2 months post-systemic therapy at time of enrollment were randomized into Intervention (IG; n=76) and Control (CG; n=77) groups. CG received monthly nutritional brochures from the American Institute for Cancer Research. IG attended 6 monthly workshops (brief lectures on AI topics and chef-prepared food demonstrations), and received monthly tailored newsletters and telephone calls incorporating Motivational Interviewing techniques. At baseline, 6- and 12-month assessments, fasting serum was collected and assayed for Pro-I/AI marker and ASC levels; BMI was calculated from measured height and weight. We examined trajectories of inflammatory biomarkers and whether these are affected by intervention group assignment and potential confounders. For each biomarker, we identified groups of trajectories from baseline to 12 months by modeling log-transformed longitudinal data using a discrete mixture model with censored normal distribution. Model fit diagnostics based on Bayesian information criterion, classification measures, and clinical judgement were used to determine the number of groups. Then, we investigated the association between trajectory group classification and covariates using chi-square test for categorical variables and ANOVA for continuous variables. Participants' mean age at baseline was 56.6 (SD=9.4); mean BMI 32.4 kg/m2 (SD=4.9). There were no significant differences between groups on demographic variables. Intervention resulted in small changes in expected direction for CRP and IL-6 markers overall at 6 and 12 months, and for IL-8 only at 6 months. Between two and five trajectory patterns (linear or quadratic) were identified across all biomarkers. These patterns suggest that distinct BCS subpopulations that benefit differentially from nutritional interventions exist; therefore, suggesting tailoring strategies for future interventions. Future studies in larger samples are needed to provide more robust parameter estimation and facilitate generalizability of results. Citation Format: Amelie G. Ramirez, Edgar Munoz, Dorothy Long-Parma, Alan EC Holden, Michael J. Wargovich. Trajectories of inflammatory biomarkers: A randomized longitudinal 12-months intervention promoting anti-inflammatory food consumption among breast cancer survivors. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr B06.

Thyroid Hormone, Cancer, and Apoptosis.

Thyroid hormones play important roles in regulating normal metabolism, development, and growth. They also stimulate cancer cell proliferation. Their metabolic and developmental effects and growth effects in normal tissues are mediated primarily by nuclear hormone receptors. A cell surface receptor for the hormone on integrin [alpha]vβ3 is the initiation site for effects on tumor cells. Clinical hypothyroidism may retard cancer growth, and hyperthyroidism was recently linked to the prevalence of certain cancers. Local levels of thyroid hormones are controlled through activation and deactivation of iodothyronine deiodinases in different organs. The relative activities of different deiodinases that exist in tissues or organs also affect the progression and development of specific types of cancers. In this review, the effects of thyroid hormone on signaling pathways in breast, brain, liver, thyroid, and colon cancers are discussed. The importance of nuclear thyroid hormone receptor isoforms and of the hormone receptor on the extracellular domain of integrin [alpha]vβ3 as potential cancer risk factors and therapeutic targets are addressed. We analyze the intracellular signaling pathways activated by thyroid hormones in cancer progression in hyperthyroidism or at physiological concentrations in the euthyroid state. Determining how to utilize the deaminated thyroid hormone analog (tetrac), and its nanoparticulate derivative to reduce risks of cancer progression, enhance therapeutic outcomes, and prevent cancer recurrence is also deliberated. © 2016 American Physiological Society. Compr Physiol 6:1221-1237, 2016.

Abstract A66: An anti-inflammatory dietary intervention to reduce breast cancer recurrence risk: Preliminary data from a pilot study

Abstract Background: U.S. breast cancer survivors (BCSs) are expected to increase from 3 to 4 million in the next 5-10 years. Cancer recurrence risk is highest in obese survivors. Pro-inflammatory biomarkers including C-reactive protein (CRP), Interleukins -3, -6, and -8 (IL-3, IL-6, IL-8), and Tumor Necrosis Factor (TNF)α have been associated with cancer severity and recurrence. Nutritional interventions aimed at reducing inflammation (INF) may contribute to reduced recurrence risk and potentially increase survival rates. However, studies to date have been conducted predominantly in animal models. The primary goal of this one-year culinary-based pilot intervention is to improve BCS biomarker profiles -- decrease pro-inflammatory biomarkers and increase anti-inflammatory (AI) cytokines like IL-10 -- by promoting incorporation of AI foods into dietary routines. The secondary goal is to examine effects on potential cancer risk factors including body mass index (BMI), stress and depression levels. Methods: A total of 153 BCSs was recruited. Overweight and obese women aged 18 or older, diagnosed with Stage 0-III breast cancer who were at least 2 months post-systemic therapy at time of enrollment were randomized into Intervention (IG; n=76) and Control (CG; n=77) groups. The CG received monthly nutritional brochures from the American Institute for Cancer Research. IG participants attended 6 monthly workshops consisting of brief lectures on AI topics and chef-prepared food demonstrations, and received monthly tailored newsletters and follow-up telephone calls incorporating Motivational Interviewing techniques. At baseline and 6- and 12-month follow-up assessments, fasting blood samples were collected from all participants and assayed for inflammatory marker levels. BMI and waist circumference were measured, and self-reported data on dietary habits, demographics, physical activity (PA), perceived stress (PSS) and depression levels were collected. Violin plots of baseline, 6- and 12-month BMI were generated in R version 3.1.3 (R Core Team, 2013) for participants who had completed all three assessments (n=46). Path Analysis and Structural Equation Modeling were conducted using both R and Stata version 13 (Stata Corp, College Station, TX, 2014) to test hypothesized relationships among latent and observed variables. Results: Participants were characterized at baseline by mean age of 56.6 ± 9.4 years and mean BMI of 32.4 ± 4.9 kg/m2. Women self-identified as U.S. Latino or Anglo (41.2% and 43.1%, respectively), had college-level education or bachelor's degree (65.4%), were employed full-time (51.6%) and privately insured (80.9%). There were no significant differences between groups. All Interleukins were significant predictors of INF (standardized coefficient βs&amp;gt;0.83, p&amp;lt;0.001). Although not significant, INF had positive relationships with BMI (βs=0.06) and PSS (βs=0.10), and negative relationships with PA (βs=-0.01) and AI diet (βs=-0.03). AI diet was negatively correlated with depression (r=-0.47). The IG plots (n=20) showed a progressive decrease in median BMI from baseline to 12 months (32.3, 31.6, 30.6, respectively; Interquartile ranges [IQR] 7.3, 6.2, 7.7). In contrast, the CG (n=26) demonstrated minimal change (median BMI=30.0, 30.7, 30.5, respectively; IQR=4.3, 5.2, 5.3). Conclusion: Ongoing analyses will determine relationship significance over the entire study period. Future studies are needed in larger populations with increased INF-related morbidity and mortality risks, to provide more robust estimation of parameters and fit statistics and facilitate generalizability of results. Citation Format: Amelie G. Ramirez, Edgar Muñoz, Dorothy Long-Parma, Kristin D. Mendoza, Alan E.C. Holden, Michael J. Wargovich. An anti-inflammatory dietary intervention to reduce breast cancer recurrence risk: Preliminary data from a pilot study. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr A66.

Association between the FTOrs8050136 polymorphism and cancer risk: a meta-analysis.

A meta-analysis on cancer risk relevant to FTOrs8050136 polymorphism. To investigate the comprehensive effect of FTOrs8050136 polymorphism on cancer risk based on a pooled result. Carcinogenesis is closely related to obesity. Both obesity and cancer share common pathogenic factors such as hereditary susceptibility and environmental predisposition. Recently, several studies had reported that the FTOrs8050136 polymorphism, a genetic variation highly associated with obesity, can be a potential cancer risk factor, while these results were inconsistent. With the help of PubMed, EMBASE, Chinese National Knowledge Infrastructure considerable research was done for potential studies without language restriction. Pooled odds ratio combined with 95 % confidence interval was employed to evaluate the potential correlations, and subgroup analyses were performed based on the cancer types and ethnic populations. There were eight articles comprising 21,810 cases and 85,070 controls met the eligibility criteria. Overall, there was no significant association between the FTOrs8050136 polymorphism and cancer risk (P = 0.163). Subgroup analysis illustrated that no association existed between the FTOrs8050136 polymorphism and cancer risk in Caucasians (P = 0.809), Asians (P = 0.412) and the mixed population (P = 0.093). With regard to cancer types, the result suggested that the FTOrs8050136 polymorphism had no connection with pancreatic cancer (P = 0.089), endometrial cancer (P = 0.353), prostate cancer (P = 0.578), colorectal cancer (P = 0.054) and melanoma (P = 0.357), while the inverse result was obtained in the subgroup of papillary thyroid cancer (P = 0.010). The FTOrs8050136 polymorphism may be not associated with carcinogenesis apart from papillary thyroid cancer, and further studies are needed to investigate the potential correlation.

Association of the IL6 polymorphism rs1800796 with cancer risk: a meta-analysis.

The human IL6 [interleukin 6 (interferon, beta 2)] gene encodes IL-6, a cytokine which not only plays regulatory roles in inflammation, but may be also involved in the progression of cancer. Rs1800796 is a single nucleotide polymorphism (SNP) in the promoter region of IL6, and is associated with IL-6 production. A number of studies have been carried out to determine whether this SNP is associated with cancer risk. However, the results are inconsistent due to small sample sizes of individual studies and limited statistical power. Therefore, to evaluate the overall effect on all investigated cancer types, we conducted a meta-analysis by combining all available studies. Nineteen eligible case-control studies including 23,030 subjects (9,985 cases and 13,045 controls) were included for this meta-analysis. Our study demonstrates that rs1800796 is significantly associated with cancer risk in three genetic models (allele G vs allele C, pooled OR = 1.182, P = 0.009; CG + GG vs CC, pooled OR = 1.333, P = 0.006; CG vs CC, pooled OR = 1.323, P = 0.007).Our meta-analysis suggests that polymorphism rs1800796 within the IL6 gene may be a potential risk factor for cancer.