ABSTRACT Background Oesophageal cancer has a high mortality; it is the 6th most common cause of death due to cancer worldwide. Of the common subtypes of oesophageal cancer, it is the adenocarcinomas that have been rising rapidly in incidence throughout the western world. The incidence of adenocarcinomas now exceeds the previously common squamous cell carcinoma. These recent changes in the incidence patterns of oesophageal cancer suggests that the environmental risk factors associated with these subtypes differ, and that changes in the prevalence of these exposures over time are the most likely explanation for the observed shifts in the incidence. However, due to its low incidence until a few decades ago, the adenocarcinoma subtype has been less studied compared to squamous cell carcinoma, and the environmental factors associated with this cancer have not been so clearly defined. Smoking and alcohol have been the strongest environmental risk factors reported for oesophageal squamous cell carcinoma (OSCC) whereas for oesophageal adenocarcinoma (OAC), the effect of smoking appears to be weaker, and the evidence for an effect of alcohol is scant and inconsistent. However, epidemiologic studies consistently identify people with frequent symptoms of gastro-oesophageal reflux (GOR) as having the highest risk of OAC, but the effect of GOR on OSCC has been negligible. Furthermore, it has been argued that adenocarcinoma occurring at the gastro-oesophageal junction (GOJAC) may have different aetiology again. Together, these reports suggest the three subtypes of oesophageal cancers (OAC, GOJAC and OSCC) may arise through different mechanisms with different strengths in the impact of risk factors. This thesis investigated the independent associations of smoking, alcohol and gastro-oesophageal reflux on cancers of the oesophagus by considering the possibility of variation in the risks due to differences in the dose effect patterns of various measures such as smoking, alcohol and GOR. Method Data from a population-based case-control study of oesophageal and ovarian cancers in Australia were used. Study participants comprised histologically confirmed cases of OSCC (n=308), OAC (n=367) and GOJAC (n=426) who were frequency matched to 1580 controls from the general population. Exposure history for both cases and controls were derived from health and lifestyle questionnaires. Unconditional multivariate logistic regression was used to calculate the odds ratios and 95% confidence intervals for the risk factors analysed. In addition, generalised additive model with a logit link was also used to explore and present the non-linearity in the dose effect pattern for continuous exposures adjusting for other confounding factors. The effects of two exposures combined on these cancers were assessed by obtaining synergy index. Results Smokers were at significantly higher risk of all three subtypes of oesophageal cancer with the risk greatest for OSCC. The effect of smoking was greater for adenocarcinoma occurring at the gastro-oesophageal junction compared to that of the oesophagus. Of the various measures of smoking, duration was significantly associated with all three subtypes of cancer whereas intensity was associated with only OSCC and GOJAC and the dose effect was non-linear. Time since quitting was associated with a steady decline in risk of all three cancers emphasising the health benefits of quitting among smokers. Alcohol was not associated with OAC or GOJAC but was significantly associated with OSCC among those drinking in excess of 170g/week. The association between alcohol and OSCC was modified by smoking; the association with alcohol was significantly greater among current smokers with effect. Low to moderate wine consumption was associated with significant risk reduction for all three cancers compared to non-drinkers. Increased frequency of GOR symptoms was associated with increased risks of OAC and GOJAC, although the risk of OSCC was constrained to frequent GOR symptoms only. The effect of GOR symptoms were exacerbated by smoking whereas it was weakened by regular NSAID use. Lastly, the sensitivity analysis that assessed the effect of non-participation among controls in the estimated effect of smoking and BMI (the two risk factors most likely to be affected by non-participation) showed a slight overestimation of effect of smoking assuming higher exposure rate among non-participants but not BMI while the effect remained strong and statistically significant. Conclusion Smoking, alcohol and GOR symptoms were the environmental factors strongly associated with all subtypes of oesophageal cancers. However, the dose effect patterns of these exposures varied by cancer subtypes. Smoking and alcohol were the larger contributing factors for OSCC whereas smoking and GOR symptoms had greater impact on OAC and GOJAC. Low to moderate wine consumption and regular NSAID use reduced the risk of all three subtypes significantly. While selection bias may have led to mildly inflated risks for smoking, the effects persisted even when modelled under extreme scenarios of biased participation amongst controls, and there was no evidence that selection bias materially affected the other associations.

ABSTRACT Background Oesophageal cancer has a high mortality; it is the 6th most common cause of death due to cancer worldwide. Of the common subtypes of oesophageal cancer, it is the adenocarcinomas that have been rising rapidly in incidence throughout the western world. The incidence of adenocarcinomas now exceeds the previously common squamous cell carcinoma. These recent changes in the incidence patterns of oesophageal cancer suggests that the environmental risk factors associated with these subtypes differ, and that changes in the prevalence of these exposures over time are the most likely explanation for the observed shifts in the incidence. However, due to its low incidence until a few decades ago, the adenocarcinoma subtype has been less studied compared to squamous cell carcinoma, and the environmental factors associated with this cancer have not been so clearly defined. Smoking and alcohol have been the strongest environmental risk factors reported for oesophageal squamous cell carcinoma (OSCC) whereas for oesophageal adenocarcinoma (OAC), the effect of smoking appears to be weaker, and the evidence for an effect of alcohol is scant and inconsistent. However, epidemiologic studies consistently identify people with frequent symptoms of gastro-oesophageal reflux (GOR) as having the highest risk of OAC, but the effect of GOR on OSCC has been negligible. Furthermore, it has been argued that adenocarcinoma occurring at the gastro-oesophageal junction (GOJAC) may have different aetiology again. Together, these reports suggest the three subtypes of oesophageal cancers (OAC, GOJAC and OSCC) may arise through different mechanisms with different strengths in the impact of risk factors. This thesis investigated the independent associations of smoking, alcohol and gastro-oesophageal reflux on cancers of the oesophagus by considering the possibility of variation in the risks due to differences in the dose effect patterns of various measures such as smoking, alcohol and GOR. Method Data from a population-based case-control study of oesophageal and ovarian cancers in Australia were used. Study participants comprised histologically confirmed cases of OSCC (n=308), OAC (n=367) and GOJAC (n=426) who were frequency matched to 1580 controls from the general population. Exposure history for both cases and controls were derived from health and lifestyle questionnaires. Unconditional multivariate logistic regression was used to calculate the odds ratios and 95% confidence intervals for the risk factors analysed. In addition, generalised additive model with a logit link was also used to explore and present the non-linearity in the dose effect pattern for continuous exposures adjusting for other confounding factors. The effects of two exposures combined on these cancers were assessed by obtaining synergy index. Results Smokers were at significantly higher risk of all three subtypes of oesophageal cancer with the risk greatest for OSCC. The effect of smoking was greater for adenocarcinoma occurring at the gastro-oesophageal junction compared to that of the oesophagus. Of the various measures of smoking, duration was significantly associated with all three subtypes of cancer whereas intensity was associated with only OSCC and GOJAC and the dose effect was non-linear. Time since quitting was associated with a steady decline in risk of all three cancers emphasising the health benefits of quitting among smokers. Alcohol was not associated with OAC or GOJAC but was significantly associated with OSCC among those drinking in excess of 170g/week. The association between alcohol and OSCC was modified by smoking; the association with alcohol was significantly greater among current smokers with effect. Low to moderate wine consumption was associated with significant risk reduction for all three cancers compared to non-drinkers. Increased frequency of GOR symptoms was associated with increased risks of OAC and GOJAC, although the risk of OSCC was constrained to frequent GOR symptoms only. The effect of GOR symptoms were exacerbated by smoking whereas it was weakened by regular NSAID use. Lastly, the sensitivity analysis that assessed the effect of non-participation among controls in the estimated effect of smoking and BMI (the two risk factors most likely to be affected by non-participation) showed a slight overestimation of effect of smoking assuming higher exposure rate among non-participants but not BMI while the effect remained strong and statistically significant. Conclusion Smoking, alcohol and GOR symptoms were the environmental factors strongly associated with all subtypes of oesophageal cancers. However, the dose effect patterns of these exposures varied by cancer subtypes. Smoking and alcohol were the larger contributing factors for OSCC whereas smoking and GOR symptoms had greater impact on OAC and GOJAC. Low to moderate wine consumption and regular NSAID use reduced the risk of all three subtypes significantly. While selection bias may have led to mildly inflated risks for smoking, the effects persisted even when modelled under extreme scenarios of biased participation amongst controls, and there was no evidence that selection bias materially affected the other associations.

ABSTRACT Background Oesophageal cancer has a high mortality; it is the 6th most common cause of death due to cancer worldwide. Of the common subtypes of oesophageal cancer, it is the adenocarcinomas that have been rising rapidly in incidence throughout the western world. The incidence of adenocarcinomas now exceeds the previously common squamous cell carcinoma. These recent changes in the incidence patterns of oesophageal cancer suggests that the environmental risk factors associated with these subtypes differ, and that changes in the prevalence of these exposures over time are the most likely explanation for the observed shifts in the incidence. However, due to its low incidence until a few decades ago, the adenocarcinoma subtype has been less studied compared to squamous cell carcinoma, and the environmental factors associated with this cancer have not been so clearly defined. Smoking and alcohol have been the strongest environmental risk factors reported for oesophageal squamous cell carcinoma (OSCC) whereas for oesophageal adenocarcinoma (OAC), the effect of smoking appears to be weaker, and the evidence for an effect of alcohol is scant and inconsistent. However, epidemiologic studies consistently identify people with frequent symptoms of gastro-oesophageal reflux (GOR) as having the highest risk of OAC, but the effect of GOR on OSCC has been negligible. Furthermore, it has been argued that adenocarcinoma occurring at the gastro-oesophageal junction (GOJAC) may have different aetiology again. Together, these reports suggest the three subtypes of oesophageal cancers (OAC, GOJAC and OSCC) may arise through different mechanisms with different strengths in the impact of risk factors. This thesis investigated the independent associations of smoking, alcohol and gastro-oesophageal reflux on cancers of the oesophagus by considering the possibility of variation in the risks due to differences in the dose effect patterns of various measures such as smoking, alcohol and GOR. Method Data from a population-based case-control study of oesophageal and ovarian cancers in Australia were used. Study participants comprised histologically confirmed cases of OSCC (n=308), OAC (n=367) and GOJAC (n=426) who were frequency matched to 1580 controls from the general population. Exposure history for both cases and controls were derived from health and lifestyle questionnaires. Unconditional multivariate logistic regression was used to calculate the odds ratios and 95% confidence intervals for the risk factors analysed. In addition, generalised additive model with a logit link was also used to explore and present the non-linearity in the dose effect pattern for continuous exposures adjusting for other confounding factors. The effects of two exposures combined on these cancers were assessed by obtaining synergy index. Results Smokers were at significantly higher risk of all three subtypes of oesophageal cancer with the risk greatest for OSCC. The effect of smoking was greater for adenocarcinoma occurring at the gastro-oesophageal junction compared to that of the oesophagus. Of the various measures of smoking, duration was significantly associated with all three subtypes of cancer whereas intensity was associated with only OSCC and GOJAC and the dose effect was non-linear. Time since quitting was associated with a steady decline in risk of all three cancers emphasising the health benefits of quitting among smokers. Alcohol was not associated with OAC or GOJAC but was significantly associated with OSCC among those drinking in excess of 170g/week. The association between alcohol and OSCC was modified by smoking; the association with alcohol was significantly greater among current smokers with effect. Low to moderate wine consumption was associated with significant risk reduction for all three cancers compared to non-drinkers. Increased frequency of GOR symptoms was associated with increased risks of OAC and GOJAC, although the risk of OSCC was constrained to frequent GOR symptoms only. The effect of GOR symptoms were exacerbated by smoking whereas it was weakened by regular NSAID use. Lastly, the sensitivity analysis that assessed the effect of non-participation among controls in the estimated effect of smoking and BMI (the two risk factors most likely to be affected by non-participation) showed a slight overestimation of effect of smoking assuming higher exposure rate among non-participants but not BMI while the effect remained strong and statistically significant. Conclusion Smoking, alcohol and GOR symptoms were the environmental factors strongly associated with all subtypes of oesophageal cancers. However, the dose effect patterns of these exposures varied by cancer subtypes. Smoking and alcohol were the larger contributing factors for OSCC whereas smoking and GOR symptoms had greater impact on OAC and GOJAC. Low to moderate wine consumption and regular NSAID use reduced the risk of all three subtypes significantly. While selection bias may have led to mildly inflated risks for smoking, the effects persisted even when modelled under extreme scenarios of biased participation amongst controls, and there was no evidence that selection bias materially affected the other associations.

6 pp. / Research has shown a correlation between a healthy diet and reduced risk of breast cancer. Additional research is also demonstrating a link between regular physical activity and the reduction of breast cancer risk. A healthy diet is beneficial for the prevention of numerous diseases, including breast cancer. Regular physical activity is preventative for many diseases and health concerns, including breast cancer. This article outlines basic information about breast cancer, risk factors related to diet and physical activity, and breast cancer prevention through healthy diet and physical activity.

Introduction: Breast density is an important independent risk factor for breast cancer and is negatively associated with diagnostic sensitivity of mammography. Measurement of breast density can be used to identify women at increased risk of developing breast cancer and those who would benefit from additional imaging. However, measurement techniques are generally subjective and do not reflect the true three-dimensional nature of the breast and its component tissues.Method: A semi-automated method for determining the volume of glandular tissue from digitised mammograms has been developed in Manchester. It requires a calibration device (stepwedge) to be imaged alongside the breast during mammography, with magnification markers on the compression paddle to accurately determine breast thickness. Improvements to the design of the stepwedge and markers have enabled the method to be applied to the screening population for the first time. 1,289 women had their volumetric breast density measured using this method and additionally completed a questionnaire on breast cancer risk factors.Results: The method has demonstrated excellent intra- and inter-observer agreement. The median percentage breast density in the study cohort was 8.4% (interquartile range 4.9 – 14.2%). There was no significant difference between left and right breasts; the difference between MLO and CC views was significant (CC view was denser), but values were closely correlated (r = 0.92, p < 0.001). The median glandular volume was 60.1cm3 and exhibited no significant variation between left/right breasts or CC/MLO views. A number of breast cancer risk factors were found to be significantly correlated with glandular volume and percentage breast density, including age, weight, BMI, parity, current HRT use and current smoking. The strength of correlation was equal to or greater than that of visually assessed mammographic density. Glandular volume and percentage breast density measurements demonstrated strong relationships with visually assessed mammographic density, which has been shown to be highly correlated with risk.Conclusions: These findings are promising and suggest that volumetric breast density measured using this method should be associated with breast cancer risk. However, further work is required to establish this relationship directly. The method will be used in a large study, known as PROCAS (Predicting Risk Of Cancer At Screening) which aims to develop individualised breast cancer risk prediction models; these have the potential to form the basis of tailored screening intervals. Preliminary work has been undertaken to adapt the method for full field digital mammography, which suggests that it is possible to use the integrated digital detector as the calibration device.

One of the most common types of cancer among women is breast cancer. It represents one of the diseases leading to a high number of mortalities among women. On the other hand, prostate cancer is the second most frequent malignancy in men worldwide. The early detection of prostate cancer is fundamental to reduce mortality and increase the survival rate. A comparison between six types of machine learning models as Logistic Regression, Decision Tree, Random Forest, Gradient Boosting, k Nearest Neighbors, and Naïve Bayes has been performed. This research aims to identify the most efficient machine learning algorithms for identifying the most significant risk factors of prostate and breast cancers. For this reason, National Health Interview Survey (NHIS) and Prostate, Lung, Colorectal, and Ovarian (PLCO) datasets are used. A comprehensive comparison of risk factors leading to these two crucial cancers can significantly impact early detection and progressive improvement in survival. / Includes bibliography. / Thesis (P.S.M.)--Florida Atlantic University, 2021. / FAU Electronic Theses and Dissertations Collection

This follows an earlier study of the same data set, which, through its findings, presented new questions that are investigated in this study. Both studies used a prospective controlled design, wherein women receiving genetic counseling for breast cancer risk were randomized into two groups. Subjects receiving an audiotaped recording of their genetic consultation (tape group) were compared to subjects who also had a genetic consultation but did not receive an audiotaped recording of it (no-tape group). Participants were drawn from attendees at the genetic clinics of two London hospitals and included 115 women with a family history of breast cancer. Cancer worry and psychological distress were assessed before genetic consultation (baseline), and at one- and six-month follow-ups by post. Objective risk was estimated by the geneticist during the consultation, and subjective risk was assessed at one month follow-up. The goals of the current study were to investigate relationships between cancer worry, psychological distress, and recall of genetic risk for breast cancer in a sample of women receiving genetic counseling for breast cancer risk, and to investigate the role sociodemographic variables on cancer worry, psychological distress, or risk recall for these women. Results for this sample of women with a family history of breast cancer found that there were consistent relationships between cancer worry, psychological distress, objective risk, and subjective risk before and after genetic consultation. This suggests that women=s psychological responses are appropriate to their level of cancer risk. There were no differences found between the tape and no-tape groups for objective or subjective risk, or for nearness of recall accuracy or degree of under-/over-estimation. Provision of an audiotaped recording of the genetic consultation did not appear to enhance recall of risk information. The role of sociodemographic variables on the psychological and risk variables assessed in this study was very minor. Age was mildly correlated with cancer worry, and employment was predictive of cancer worry only at baseline.

This paper discusses the lessons learned by our collaborative, transdisciplinary team while developing a pilot/demonstration educational health campaign geared toward underserved communities in the Columbus, Ohio metropolitan area. The objective of the current study was to determine the feasibility of a campaign to raise awareness of the association between family history and cancer risk and to inform individuals of the availability of Jameslink, an online familial cancer risk assessment tool. The research team included members of The Ohio State University Primary Care Research Institute, which includes a unique combination of expertise in Genetics, Behavioral Science, Social and Health Psychology, Communication, Medicine, and Methodology. The experience of the team in developing university and community partnerships, identifying stakeholders and formulating campaign messages is described. Groups who aided in this process as well as the perspectives they brought to the project are discussed. The lessons learned may be helpful to those developing similar community health projects.

American Cancer Society estimates that in 2021 nearly 300,000 women in the United States will be diagnosed with invasive breast cancer, and about 43,600 women will die from breast cancer. While many have access to health care and cancer screening, women from rural or underdeveloped communities often have limited access. Therefore, there is a need for an inexpensive and easy-to-use breast cancer identification device, which can be employed in small clinics to provide support to primary care physicians. This work aims to develop a method to characterize breast tumors and tissue using non-invasive imaging modalities. The proposed bimodal imaging system has tactile and multispectral imaging capabilities. Tactile imaging modality characterizes tumors by esti-mating their depth, size, and stiffness, along with the Tactile Index. Multispectral imaging modality identifies breast asymmetry, texture, and inflammation changes, together with the Spectral Index. These indices are combined with the BCRAT Index, the risk score devel¬oped by the National Institute of Health, to form the Multimodal Index for personalized breast cancer risk assessment. In this study, we will describe the development of the bimodal imaging system. We will present the algorithms for tactile and multispectral modalities. Tactile and Multispec¬tral Profile Diagrams are developed to capture broad imaging signals in a compact and application-specific way. A Tactile Profile Diagram is a pictorial representation of the rel¬ative depth, size, and stiffness of the imaged tumor. A Multispectral Profile Diagram is a representative pattern image for breast tissue superficial optical properties. To classify the profile diagrams, we employ the Convolutional Neural Network deep learning method. We will describe the results of the experiments conducted using tissue-mimicking phan¬toms and human in-vivo experiments. The results demonstrate the ability of the method to classify and quantify tumor and tissue characteristics. Finally, we describe the method to calculate Multimodal Index for the malignancy risk assessment via tactile and multispectral imaging modalities and the risk probability based on the health records. / Electrical and Computer Engineering

Yes / Objective The hypothesis that sleeve gastrectomy (SG) is not associated with an increase in mucosal colorectal cancer (CRC) biomarkers, unlike Roux-en-Y gastric bypass (RYGB), was tested. Design and Methods Rectal mucosa, blood, and urine were obtained from morbidly obese patients (n = 23) before and after (median 28 months) SG, as well as from nonobese controls (n = 20). Rectal epithelial cell mitosis and apoptosis, crypt size/fission, and pro-inflammatory gene expression were measured, as well as systemic inflammatory biomarkers, including C-reactive protein (CRP). Results The mean pre-operative body mass index in SG patients was 65.7 kg/m2 (24.7 kg/m2 in controls). Mean excess weight loss post-SG was 38.2%. There was a significant increase in mitosis frequency, crypt size, and crypt fission (all P < 0.01) in SG patients versus controls, as well as evidence of a chronic inflammatory state (raised CRP and mononuclear cell p65 NFκB binding), but there was no significant change in these biomarkers after SG, except CRP reduction. Macrophage migration inhibitory factor mRNA levels were increased by 39% post-SG (P = 0.038). Conclusions Mucosal biomarkers of CRC risk do not increase at 6 months following SG, unlike RYGB. Biomarkers of rectal crypt proliferation and systemic inflammation are increased in morbidly obese patients compared with controls.