Дисертації з теми "Lung and breast/ovarian cancer"
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1
Woods, Tonya M. "Extracting meaningful statistics for the characterization and classification of biological, medical, and financial data." Diss., Georgia Institute of Technology, 2015. http://hdl.handle.net/1853/53857.
Анотація:
This thesis is focused on extracting meaningful statistics for the characterization and classification of biological, medical, and financial data and contains four chapters. The first chapter contains theoretical background on scaling and wavelets, which supports the work in chapters two and three.
In the second chapter, we outline a methodology for representing sequences of DNA nucleotides as numeric matrices in order to analytically investigate important structural characteristics of DNA. This methodology involves assigning unit vectors to nucleotides, placing the vectors into columns of a matrix, and accumulating across the rows of this matrix. Transcribing the DNA in this way allows us to compute the 2-D wavelet transformation and assess regularity characteristics of the sequence via the slope of the wavelet spectra. In addition to computing a global slope measure for a sequence, we can apply our methodology for overlapping sections of nucleotides to obtain an evolutionary slope.
In the third chapter, we describe various ways wavelet-based scaling may be used for cancer diagnostics. There were nearly half of a million new cases of ovarian, breast, and lung cancer in the United States last year. Breast and lung cancer have highest prevalence, while ovarian cancer has the lowest survival rate of the three. Early detection is critical for all of these diseases, but substantial obstacles to early detection exist in each case. In this work, we use wavelet-based scaling on metabolic data and radiography images in order to produce meaningful features to be used in classifying cases and controls. Computer-aided detection (CAD) algorithms for detecting lung and breast cancer often focus on select features in an image and make a priori assumptions about the nature of a nodule or a mass. In contrast, our approach to analyzing breast and lung images captures information contained in the background tissue of images as well as information about specific features and makes no such a priori assumptions.
In the fourth chapter, we investigate the value of social media data in building commercial default and activity credit models. We use random forest modeling, which has been shown in many instances to achieve better predictive accuracy than logistic regression in modeling credit data. This result is of interest, as some entities are beginning to build credit scores based on this type of publicly available online data alone. Our work has shown that the addition of social media data does not provide any improvement in model accuracy over the bureau only models. However, the social media data on its own does have some limited predictive power.
2
Ducrot, Lucas. "Réseaux bayésiens et analyse de survie pour l’estimation de courbes de pénétrance du cancer broncho-pulmonaire lié à des prédispositions génétiques." Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS055.
Анотація:
Cette thèse se concentre sur l'estimation de courbes de pénétrance de maladies génétiques à partir de données de pédigrée, avec un intérêt particulier pour la prédisposition génétique au cancer broncho-pulmonaire. Dans ce contexte, elle vise à proposer des résultats à la fois cliniques et épidémiologiques ainsi que des résultats méthodologiques.Les consultations en génétique sont proposées aux patients ayant des antécédents familiaux sévères de maladies génétiques. Les médecins généticiens doivent sélectionner, parmi ces patients, lesquels se voient proposer un test génétique, ainsi qu'évaluer les risques de maladie pour ces patients et leurs familles. La progression des connaissances en génétique est rapide et le nombre de variants pathogènes identifiés pour différentes maladies augmentent chaque année. Cela entraine un besoin d'outils de prédiction et d'évaluation de risque important, en particulier dans le cadre du cancer broncho-pulmonaire. En effet, les liens entre ce dernier et des variants pathogènes (SFTPA1/SFTPA2 et sur les gènes TP53 et EGFR) sont connus mais encore peu décrits.Les méthodes existantes pour évaluer le risque de survenue de maladies reposent sur les courbes de pénétrance, mais leur estimation présente des défis en raison du faible nombre de patients et du biais de sélection omniprésent dans les jeux de données collectés en génétique. Pour surmonter ces obstacles, la thèse explore l'utilisation de données familiales, en utilisant un ensemble d'outils statistiques dont les réseaux bayésiens, les modèles de mélange et l'analyse de survie, ainsi que des modèles existants, pour lesquels elle tente d'affaiblir certaines hypothèses.Le chapitre 1 propose une présentation du contexte médical de la thèse, introduisant les notions de maladies génétiques et de conseil en génétique. Le chapitre 2 est une introduction méthodologique présentant, et illustrant sur des exemples, les concepts d'analyse de survie, de réseaux bayésiens, d'algorithme somme-produit, de modèles de mélanges et d'algorithme EM. Il propose également un état de l'art de l'estimation de courbe de pénétrance pour des maladies génétiques et une mise en évidence du biais de sélection en génétiques. Il se conclue par un récapitulatif des questions de recherche abordées.Cette thèse s'est, ensuite, orientée autour de quatre projets. Les deux premiers projets, correspondant aux chapitres 3 et 4, proposent des résultats plutôt cliniques et épidémiologiques. La premier projet, décrit au chapitre 3, porte sur une comparaison de différentes méthodes de prédiction de variants pathogènes pour les cancers sein/ovaire (Score de Manchester et modèles familiaux, type BOADICEA). Le second projet, abordé au chapitre 4, propose une estimation des pénétrances de la pneumopathie interstitielle et du cancer broncho-pulmonaire pour les porteurs de variants pathogènes SFTPA1 et SFTPA2.Les deux derniers projets, correspondant aux chapitres 5 et 6, sont plus méthodologiques. Le chapitre 5 est consacré au développement d'une nouvelle méthode d'estimation de courbe de pénétrance de maladie génétique à partir de données de pédigrée lorsque la maladie présente des cas sporadiques. Elle se base sur une contrainte d'incidence de la maladie en population générale et une paramétrisation du ratio de risques instantanés entre les porteurs et les non-porteurs de variants pathogènes. Le chapitre 6 se consacre, lui, à la mise en évidence du biais introduit par la sélection en génétique et ses conséquences sur les résultats de la méthode développée au chapitre 5. Des méthodes de corrections connues, comme la Proband's phenotype Exclusion Likelihood (PEL) et la Genotype-Restricted Likelihood (GRL), combinées à notre méthode, sont appliquées à des données simuléesThis thesis focuses on estimating penetrance curves of genetic diseases from pedigree data, with a particular interest in the genetic predisposition to bronchopulmonary cancer. In this context, it aims to provide clinical and epidemiological results, as well as methodological findings.Genetic counselling is offered to patients with severe family histories of genetic diseases. Geneticists must select from these patients who should be offered genetic testing, and assess the disease risks for these patients and their families. Advances in genetics are rapid, and the number of identified pathogenic variants for different diseases increases each year. This necessitates significant predictive and risk assessment tools, especially in the context of bronchopulmonary cancer. Indeed , the links between the latter and pathogenic variants (such that SFTPA1/SFTPA2 and the genes TP53 and EGFR) are known but still poorly described.Existing methods for assessing the risk of disease occurrence rely on penetrance curves, but their estimation faces challenges due to the small number of patients and the omnipresent selection bias in genetics-collected datasets. To overcome these obstacles, the thesis explores the use of familial data, employing a set of statistical tools including Bayesian networks, mixture models, survival analysis, as well as existing models, for which it attempts to weaken certain assumptions.Chapter 1 provides an overview of the medical context of the thesis, introducing the concepts of genetic diseases and genetic counseling. Chapter 2 serves as a methodological introduction, presenting and illustrating concepts such as survival analysis, Bayesian networks, sum-product algorithm, mixture models and EM algorithm, using examples. It also offers a state-of-the-art review of penetrance curve estimation for genetic diseases and highlights the selection bias in genetics. The chapter concludes with a summary of the addressed research questions.Then, the thesis revolves around four projects. The first two projects, corresponding to chapters 3 and 4, offer predominantly clinical and epidemiological results. The first project, described in Chapter 3, compares different methods for predicting pathogenic variants for breast/ovarian cancers (Manchester Score and family models like BOADICEA). The second project, addressed in Chapter 4, provides estimates of penetrance for interstitial lung disease and bronchopulmonary cancer for carriers of pathogenic variants SFTPA1 and SFTPA2.The last two projects, corresponding to chapters 5 and 6, are more methodological. Chapter 5 is dedicated to developing a new method for estimating the penetrance curve of a genetic disease from pedigree data when the disease presents sporadic cases. It is based on an incidence constraint of the disease in the general population and a parameterization of the relative hazard between carriers and non-carriers of pathogenic variants. Chapter 6 focuses on highlighting the bias introduced by selection in genetics and its consequences on the results of the method developed in Chapter 5. Known correction methods, such as Proband's Phenotype Exclusion Likelihood (PEL) and Genotype-Restricted Likelihood (GRL), combined with our method, are applied to simulated data
3
Vehmanen, Paula. "Breast cancer-predisposing genes in Finnish breast and ovarian cancer families." Helsinki : University of Helsinki, 2001. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/vehmanen/.
4
Ford, Deborah. "Genetic epidemiology of breast and ovarian cancer." Thesis, Institute of Cancer Research (University Of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367527.
5
Schofield, Andrew C. "Molecular genetics of breast and ovarian cancer." Thesis, University of Aberdeen, 1998. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU100481.
Анотація:
Breast cancer is one of the most common malignancies in women, affecting one in twelve. Ovarian cancer, although not as frequent, is the leading cause of death from gynaecological cancer. Inherited predisposition to breast and ovarian cancer, which accounts for approximately 5 to 10% of these cancers, has been associated with mutations in the BRCA1 and BRCA2 genes. Mutations in both of these genes increase the lifetime risk of developing breast cancer by approximately 80%. BRCA1 confers a greater predisposition of ovarian cancer than BRCA2, however, BRCA2 has been associated with male breast cancer. Polymorphisms linked to BRCA1 and BRCA2 were studied to examine whether either of these genes were linked to breast and breast/ovarian cancer families. None of the five cancer families studied generated statistically significant lod scores although the segregation of a common haplotype with the disease in each family and positive lod scores did suggest that four of these families were linked to BRCA1 and the other to BRCA2. Subsequent mutation studies identified three germline mutations, thus confirming the initial linkage results in three families. A total of four deletions and six polymorphisms were identified in BRCA1 and BRCA2 from forty-eight breast and breast/ovarian cancer families, using SSCP analysis and PTT. The functional effect of these mutations is unclear although variable expression of the cancer phenotype suggests that other genes and environmental factors play an important role in the development of breast and ovarian cancer. Evidence of an abnormal protein was detected by the presence of clonal LOH of the normal allele, using BRCA1 antibodies in familial breast and ovarian tumours. In addition, BRCA1 immunostaining was negative in a greater proportion of benign tumours compared to malignant ovarian tumours. The loss of BRCA1 does not lead to malignancy, suggesting that BRCA1 may have another role in benign ovarian epithelial tumours.
6
Huusko, P. (Pia). "Predisposing genes in hereditary breast and ovarian cancer." Doctoral thesis, University of Oulu, 1999. http://urn.fi/urn:isbn:9514254422.
Анотація:
Abstract
In the present study, mutations in BRCA1 and BRCA2, the two major genes predisposing individuals to hereditary breast and ovarian cancer, were screened in Finnish and Turkish cancer families. Germline BRCA1 mutations were found in 7% (6/88) and BRCA2 mutations in 6% (5/88) of the Finnish families studied in Oulu. Two distinct BRCA1 (3745delT, 4216nt-2A→G) and three BRCA2 (999delTCAAA, 6503delTT, 9346nt-2A→G) mutations were identified, all of which are recurrently found in Finland. In the 15 Turkish cancer families studied, 5382insC and 5622C→T were detected in BRCA1, and 3414delTCAG in BRCA2. The novel 3414del4 mutation was found in a family with a case of male breast cancer.
In order to determine their ages and origin, 9 recurrent Finnish BRCA1 and BRCA2 mutations were studied further as regards haplotype conservation. Common origins approximately 18–80 generations (400–1600 years) ago were demonstrated for all studied mutations by partial haplotype sharing. The majority of the mutations showed geographical clustering, supporting the theory of regional founder effects. Four of the nine mutations are unique for Finland, whereas five have also been seen elsewhere. Mutations in the 5' end of BRCA1 tend to predispose individuals to ovarian cancer and those found in the 3' end to breast cancer. The age of ovarian cancer onset was significantly lower for BRCA1 (51 years) than for BRCA2 mutation carriers (61 years).
Germline TP53 mutations were sought in the Finnish breast cancer families found to be negative after BRCA1 and BRCA2 screening but who exhibited some phenotypic features of the Li-Fraumeni syndrome. The Asn235Ser was found in a family displaying Li-Fraumeni syndrome phenotype and the Tyr220Cys in a family with a milder Li-Fraumeni-like phenotype. The nature of both mutations as cancer-predisposing alterations was supported by means of loss of heterozygosity (LOH) and p53 immunohistochemistry studies.
Regional clustering of BRCA1 and BRCA2 founder mutations enables targeted genetic tests including especially those mutations characteristic of the birthplace of each patient. Additional genes are likely to explain a large proportion of the inherited susceptibility to breast cancer in particular. Germline TP53 mutations are expected to be found in the breast cancer families with other clinical features seen in the Li-Fraumeni syndrome.
7
Xintaropoulou, Chrysi. "Targeting aerobic glycolysis in breast and ovarian cancer." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29525.
Анотація:
Cancer cells, unlike normal tissue, frequently rely on glycolysis for the production of energy and the metabolic intermediates required for their growth regardless of cellular oxygenation levels. This metabolic reconfiguration, termed the Warburg effect, provides a potential strategy to preferentially target tumours from a therapeutic perspective. The present study sought to investigate the glycolytic phenotype of breast and ovarian cancer, and assess the possibility of exploiting several glycolytic targets therapeutically. Initially the growth dependency of breast and ovarian cancer cells on the availability of glucose was established. An array of 10 compounds reported to inhibit key enzymes of the glycolytic pathway were investigated and compared against an extended panel of breast and ovarian cancer cell line models. All inhibitors investigated, targeted against multiple points of the pathway, were shown to block the glycolytic pathway as demonstrated by glucose accumulation in the culture media combined with decreased lactate secretion, and attenuated breast and ovarian cancer cell proliferation in a concentration dependent manner. Furthermore their mechanism of action was investigated by flow cytometric analysis and their antiproliferative effect was associated with induction of apoptosis and G0/G1 cell cycle arrest. The glycolytic inhibitors were further assessed in combination strategies with established chemotherapeutic and targeted agents and several synergistic interactions, characterised by low combination index values, were revealed. Among them, 3PO (a novel PFKFB3 inhibitor) enhanced the effect of cisplatin in both platinum sensitive and platinum resistant ovarian cancer cells suggesting a strategy for treatment of platinum resistant disease. Furthermore robust synergy was identified between IOM-1190 (a novel GLUT1 inhibitor) and metformin, an antidiabetic inhibitor of oxidative phosphorylation, resulting in strong inhibition of breast cancer cell growth. This combination is proposed for the treatment of highly aggressive triple negative breast tumours. An additional objective of this research was to investigate the effect of the oxygen level on sensitivity to glycolysis inhibition. Breast cancer cells were found to be more sensitive to glycolysis inhibition in high oxygen conditions. This enhanced resistance at low oxygen levels was associated with upregulation of the targeted glycolytic enzymes as demonstrated at both the mRNA (by gene expression microarray profiling, Illumina BeadArrays) and protein level (by Western blotting). Manipulation of LDHA (Lactate Dehydrogenase A) by siRNA knockdown provided further evidence that downregulation of this target was sufficient to significantly suppress breast cancer cell proliferation. Finally, the expression of selected glycolytic targets was examined in a clinical tissue microarray set of a large cohort of ovarian tumours using quantitative immunofluorescence technology, AQUA. The role of the glycolytic phenotype in ovarian cancer was suggested and interesting associations between the glycolytic profile and clear cell and endometrioid ovarian cancers revealed. Increased PKM2 (Pyruvate kinase isozyme M2) and LDHA expression were demonstrated in clear cell tumours and also low expression of these enzymes was significantly correlated with improved survival of endometrioid ovarian cancer patients. Taken together the findings of this study support the glycolytic pathway as a legitimate target for further investigation in breast and ovarian cancer treatment.
8
Cheng, Wing-ming Edward. "Emotional well-being in Chinese lung cancer patients." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B3197157X.
9
Harbord, Sara Helen Alison. "X chromosome studies and breast and ovarian carcinoma." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/212.
Анотація:
Skewed somatic X inactivation (XCI), X-linked gene overexpression and abnormal X
content have been associated with breast and ovarian cancer. Partial or complete
reactivation of the inactive X in females may be a step in breast and ovarian cancer
progression, leading to overexpression of some tumour enhancing gene. Markers of an X
reactivation event were examined: X gene dosage, expression, and methylation in 8
ovarian cancer cell lines. Another marker of an X reactivation event, skewed XCI, was
assayed in peripheral blood DNA from 106 breast and/or ovarian cancer patients (52
BRCA1 mutation carriers, 24 BRCA2 mutation carriers, 30 non-mutation carriers), 147
age-matched population controls. Combined RNA/DNA FISH was used to quantify the
number of inactive Xs compared to total number of Xs. Five cell lines had increased X
content. Three cell lines localized XIST to the presumptive inactive X; however the
numbers of inactive Xs were variable. Expression levels of 8 X-linked genes were
assessed by real-time PCR. Expression was inconsistent between different genes and
among cell lines, ranging from a 2 to 300-fold increase compared to a control. Overall,
expression was greatly increased for genes subject to inactivation but not increased in
genes that escape inactivation for most ovarian cancer cell lines. Methylation at AR and FMR1 was quantified by a real-time PCR based assay and SNuPE respectively.
Methylation was lower than expected for 7 of 8 ovarian cancer cell lines at AR or FMR1,
while three cell lines had low or no methylation for both genes. Skewed XCI was
evaluated using a methylation-based PCR assay at AR. There was no significant increase in skewing above 90% for any cancer group assayed. In addition, two markers of X reactivation were assayed in two low passage cultures of normal ovarian surface epithelium from BRCA1 mutation positive breast cancer patients. One sample did not
localize XIST to the inactive X and three of five genes subject to inactivation were
overexpressed. In summary, there is evidence for loss of X silencing or gain of active X
content in ovarian cancer cell lines and normal ovarian surface epithelium from BRCA1
mutation carriers.
10
Bendrik, Christina. "Angiogenesis regulation in hormone dependent breast- and ovarian cancer." Doctoral thesis, Linköpings universitet, Institutionen för klinisk och experimentell medicin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-63745.
Анотація:
Angiogenesis is a key event in tumor progression and a rate-limiting step in the establishment of a clinical cancer disease. The net balance of pro- and anti-angiogenesis mediators in the tissue dictates the angiogenic phenotype of a tumor. Matrix metalloproteinases (MMPs) are major regulators of extracellular matrix turnover and have for long been associated with pro-tumorigenic activities due to their tissue degradation capacities. However, broad-spectra MMP inhibitors as anti-tumor therapy in clinical trials have failed, and it has now become evident that several MMPs may induce biological activities beneficial to the host, such as suppressed angiogenesis. In this thesis the protective role of specific MMPs in breast and ovarian tumor tissues was further demonstrated. The process of angiogenesis is essential for physiological functions in the female reproductive tract, where sex steroids regulate new blood vessel formation and regression in each cycle. Despite progress made during the past years, our knowledge in sex steroid regulation of angiogenesis in hormone-dependent tumor tissues remains limited. Tamoxifen is a cornerstone in the treatment of estrogen receptor (ER)-positive breast cancer. The therapeutic value of tamoxifen in the treatment of ER-positive ovarian cancer is to date less investigated. The results presented in this thesis suggest that tamoxifen may induce anti-tumorigenic responses in ER-positive ovarian cancer by means of both anti-proliferative and anti-angiogenic mechanisms. In experimental models of human ovarian cancer in vitro and in vivo, tamoxifen treatment increased extracellular levels of MMP-9 and enhanced generation of the angiogenesis inhibitor endostatin which resulted in significantly decreased angiogenesis and tumor growth. Low levels of MMP-9 and endostatin in ascites collected from ovarian cancer patients suggest a possibility to therapeutically enhance MMP-9 by administration of tamoxifen, and thereby counteract angiogenesis in ovarian tumors by increased generation of anti-angiogenesis fragments, such as endostatin. The significance of enhanced MMP activities in tumor tissues was further investigated by experimental models of intratumoral MMP gene transfer to human breast tumor xenografts, which were assessed by using microdialysis. Treatment of tumors with MMP-9 or MMP-3 resulted in dose-dependent inhibition of tumor growth. Low dose of either MMP induced tumor stasis whereas a higher dose induced significant tumor regression. MMP-9 and tamoxifen exerted synergistic therapeutic effects on breast tumor angiogenesis and growth whereas gene transfer of the MMP-inhibitor TIMP-1 counteracted the beneficial effects induced by tamoxifen. Further on, we confirm the pro-angiogenic potential of estradiol by demonstrating a significant correlation between local levels of estradiol and the pro-angiogenic cytokine IL-8 in normal human breast tissues and in ER/PgR-positive breast cancers of women. Estradiol-induced IL-8 secretion was additionally confirmed in normal human whole breast biopsies in culture and in experimental human breast cancer in vitro and in vivo. In conclusion, the results of this thesis may hopefully increase the overall understanding of several mechanisms involved in angiogenesis regulation and may additionally be useful in the development of novel approaches for targeted therapy in the treatment of hormone-sensitive breast- and ovarian cancer.
11
Gorringe, Kylie Louise. "Studies of genetic instability in breast and ovarian cancer." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621221.
12
James, C. R. "BRCA1, a predictive biomarker in breast and ovarian cancer." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479243.
13
Moraitis, Stavros. "The role of endothelins in ovarian and breast cancer." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/21430.
Анотація:
The aim of this project was to investigate the potential involvement of endothelins in breast and ovarian cancer by (i) measuring the expression and secretion of endothelin by epithelial and fibroblast cell lines derived from ovarian and breast cancers, (ii) determining the expression of specific receptors for endothelins in the same cell lines, (iii) monitoring the effects of exogenous additions of endothelins on the growth of the cell lines in culture, (iv) measuring the expression of endothelins and their receptors in a series of primary ovarian and breast cancers. The growth of breast carcinoma cell lines was unaffected by the exogenous addition of ETs while ET-1 and ET-2 but not ET-3 addition stimulated the growth of ovarian carcinoma cells. Exogenous addition of ET-1, ET-2 and ET-3 stimulated the growth of both ovarian and breast fibroblast cell lines. The antagonists BQ123 (ETA-R antagonist) and BQ788 (ETB-R antagonist) inhibited ET-stimulated growth in a manner consistent with the receptor subtypes present in each cell line. In the absence of exogenous ET, the antagonists produced small inhibitory effects of growth in the ovarian carcinoma cell lines. This may be caused by the antagonism of ETs secreted by the same cells and could be consistent with autocrine stimulation of growth by endothelins. Co-culture of epithelial and fibroblast cells produced increased growth of both cell types relative to that when individual cell types were cultured separately. This indication, that increased growth could be blocked by addition of ET antagonists, suggests possible paracrine regulation of growth by ETs. These results support the view that endothelins may affect the growth of ovarian and breast tumours and these influences may operate through autocrine/paracrine loops.
14
Devamitta, Perera Muditha V. "Statistical Analysis and Modeling of Ovarian and Breast Cancer." Scholar Commons, 2017. https://scholarcommons.usf.edu/etd/7395.
Анотація:
The objective of the present study is to investigate key aspects of ovarian and breast cancers, which are two main causes of mortality among women. Identification of the true behavior of survivorship and influential risk factors is essential in designing treatment protocols, increasing disease awareness and preventing possible causes of disease. There is a commonly held belief that African Americans have a higher risk of cancer mortality. We studied racial disparities of women diagnosed with ovarian cancer on overall and disease-free survival and found out that there is no significant difference in the survival experience among the three races: Whites, African Americans and Other races. Tumor sizes at diagnosis among the races were significantly different, as African American women tend to have larger ovarian tumor sizes at the diagnosis. Prognostic models play a major role in health data research. They can be used to estimate adjusted survival probabilities and absolute and relative risks, and to determine significantly contributing risk factors. A prognostic model will be a valuable tool only if it is developed carefully, evaluating the underlying model assumptions and inadequacies and determining if the most relevant model to address the study objectives is selected. In the present study we developed such statistical models for survival data of ovarian and breast cancers. We found that the histology of ovarian cancer had risk ratios that vary over time. We built two types of parametric models to estimate absolute risks and survival probabilities and to adjust the time dependency of the relative risk of Histology. One parametric model is based on classical probability distributions and the other is a more flexible parametric model that estimates the baseline cumulative hazard function using spline functions. In contrast to women diagnosed with ovarian cancer, women with breast cancer showed significantly different survivorship among races where Whites had a poorer overall survival rate compared to African Americans and Other races. In the breast cancer study, we identified that age and progesterone receptor status have time dependent hazard ratios and age and tumor size display non-linear effects on the hazard. We adjusted those non-proportional hazards and non-linear effects by using an extended Cox regression model in order to generate more meaningful interpretations of the data.
15
Cong, Chunling. "Statistical Analysis and Modeling of Breast Cancer and Lung Cancer." Scholar Commons, 2010. http://scholarcommons.usf.edu/etd/3563.
Анотація:
The objective of the present study is to investigate various problems associate with breast cancer and lung cancer patients. In this study, we compare the effectiveness of breast cancer treatments using decision tree analysis and come to the conclusion that although certain treatment shows overall effectiveness over the others, physicians or doctors should discretionally give different treatment to breast cancer patients based on their characteristics. Reoccurrence time of breast caner patients who receive different treatments are compared in an overall sense, histology type is also taken into consideration. To further understand the relation between relapse time and other variables, statistical models are applied to identify the attribute variables and predict the relapse time. Of equal importance, the transition between different breast cancer stages are analyzed through Markov Chain which not only gives the transition probability between stages for specific treatment but also provide guidance on breast cancer treatment based on stating information.
Sensitivity analysis is conducted on breast cancer doubling time which involves two commonly used assumptions: spherical tumor and exponential growth of tumor and the analysis reveals that variation from those assumptions could cause very different statistical behavior of breast cancer doubling time.
In lung cancer study, we investigate the mortality time of lung cancer patients from several different perspectives: gender, cigarettes per day and duration of smoking. Statistical model is also used to predict the mortality time of lung cancer patients.
16
Probert, Adam. "The genetic epidemiology of multiple primary breast and ovarian cancer." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0024/MQ50860.pdf.
17
Arver, Brita. "Hereditary breast/ovarian cancer : implementation of BRCA1 & BRCA2 testing /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4799-6/.
18
Probert, Adam. "The genetic epidemiology of multiple primary breast and ovarian cancer /." Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=20971.
Анотація:
Breast and ovarian cancers are among the most common tumours affecting Canadian women. A proportion of these tumours was thought to be due to family history and the breast cancer susceptibility gene and are more likely to occur before the age of 50. It is hypothesized that women who have both primary tumours of the breast and ovary are more likely to have a mutation in this gene. The main objective of this study is to examine the role of family history in those women with breast cancer that subsequently develop ovarian cancer. The role of chemotherapy and radiotherapy in the treatment of breast cancer, as a risk factor for future development of ovarian cancer, was also assessed.This was a case-control study. The cases studied were women with multiple primary breast and ovarian cancers and were identified from the Quebec Tumour Registry and a database at Sunnybrook Hospital in Toronto.
19
Brazil, Lucy Caroline Alexandra. "Gene Expression in High-risk Breast and Ovarian Cancer Patients." Thesis, Institute of Cancer Research (University Of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504783.
Анотація:
Germline mutations in human BRCA 1 and BRCA2 genes confer a lifetime risk of breast cancer of between 60 and 85% and a lifetime risk of ovarian cancer of between 15 and 40%. Identification of mutations in these genes either in healthy carriers or in those who have already developed cancer is important for clinical management, including prophylactic measures to reduce the risk of disease. BRCA 1 and BRCA2 were identified more than 10 years ago, but due to a number of features such as large gene size and heterogeneity of mutations, genetic testing of BRCA is both labour intensive and often inconclusive. The aim of this project is to find a characteristic phenotype that is indicative of BRCA heterozygosity in individuals without clinical signs of disease. This could be used as a functional preliminary screen for these high-risk patients. Previous studies have illustrated the differences in gene expression profiles between 'normal' and BReA derived tumours. Studies using chicken DT 40 cell lines have shown that a Brca2 heterozygote phenotype exil:?ts but, this is as yet to be conClusively demonstrated in humans. . In this study, gene expression profiles, from 'healthy' patients who are heterozygous for BRCA have been analysed using data from microarrays. RNA was prepared from immortalized Epstein-Barr virus transformed human lymphocyte (EBVTL) cell lines, taken from normal controls and carriers for BRCA 1 and BRCA2 mutations. Gene expression profiies were also assessed before and after exposure to DNA damaging agents.
20
Gornall, Robert J. "TP53 polymorphisms and haplotypes in breast, cervical and ovarian cancer." Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310562.
21
Cho, Jaeyong. "HRPAP20 in Ovarian Cancer and Its Regulation of AP-2 in Breast Cancer." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1229809878.
22
Cho, Jaeyong. "HRPAP20 in Ovarian Cancer and Its Regulation of AP-2 in Breast Cancer." Cincinnati, Ohio : University of Cincinnati, 2009. http://www.ohiolink.edu/etd/view.cgi?acc_num=ucin1229809878.
Анотація:
Thesis (M.S.)--University of Cincinnati, 2009.Advisors: Arthur Buckley PhD (Committee Chair), Giovanni Pauletti PhD (Committee Member), Karen Gregerson PhD (Committee Member). Title from electronic thesis title page (viewed April 25, 2009). Includes abstract. Includes bibliographical references.
23
McManus, Damian Terence. "Somatic genetic and chromosomal abnormalities in ovarian and breast carcinoma." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263336.
24
Chudasama, Dimple. "Discovery and development of liquid biomarkers for ovarian and lung cancer." Thesis, Brunel University, 2018. http://bura.brunel.ac.uk/handle/2438/16174.
Анотація:
Survival rates in cancers have improved vastly over the years. However, some survival rates remain extremely low, as is the case for ovarian and lung cancer. The lack of robust and reliable biomarkers is strongly reflected in the absence of pre-screening programs, and as such, most patients in these cancer types are diagnosed only in advanced stages, leaving few treatment options. Moreover, relapse and resistance to therapies adds to the complexities of treating these diseases, even in the era of targeted drug development. Research has shown the presence of cancer material, in the form of circulating cancer cells (CTCs) and genomic material in the blood of patients, opening the possibility of 'liquid biopsies'. Liquid biopsies allow sampling of the disease to provide phenotypic and genomic data on the cancer in real-time and on a routine basis. Moreover, they overcome obstacles currently faced by conventional tissue biopsies. In this work we evaluate the use of a novel CTC imaging flow-cytometry platform, and report the ability to characterise and quantify these cells in blood samples. Moreover, we report significantly higher levels of CTCs in cancer patients compared to controls, and found them to be associated with a poorer prognosis. In particular, in lung cancer we observe these findings even in the early stages, suggesting a potential diagnostic use for this assay. We detect a similar trend in when analysing the ctDNA and suggest the possibility of using this technique with a prognostic value in the advanced setting. We also report on the analysis of existing microarray data by use of unique gene regulatory networks to identify biomarkers of interest. RAD51AP1 was identified by this process. Clinical validation revealed an over-expression of this gene in both tissue and blood of ovarian and lung cancers. Moreover, the gene over-expression was associated with a poor overall survival. Functional analysis in vitro revealed silencing RAD51AP1 suppressed tumour growth, in addition, various tumorigenic proteins were down-regulated, whilst apoptotic and immune genes were up-regulated. These results suggest a role for RAD51AP1 as a potential therapeutic target. In this study, we also demonstrate the ability to further exploit tumour genomic material in the blood by means of RNAseq, cancer panels, and CNI scoring to identify novel markers, that play an important role in disease genesis and evolution. RNAseq analysis identified XIST as a gene up-regulated in the blood and tissue of lung cancers. The ovarian cancer panels revealed 2 unique gene signatures in the ovarian cancer patients. With the CNI analyses also highlighting chromosomal aberrations from plasma analysis of cancer patients. Collectively, the use of all these techniques and exploitation of available blood based biomarkers could see significant improvements to survival rates in these, currently devastating diseases.
25
Cheng, Wing-ming Edward, and 鄭永明. "Emotional well-being in Chinese lung cancer patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B3197157X.
26
Gupta, Gaorav. "Breast cancer metastasis to the lungs : from genes to mechanisms /." Access full-text from WCMC :, 2007. http://proquest.umi.com/pqdweb?did=1456287491&sid=10&Fmt=2&clientId=8424&RQT=309&VName=PQD.
27
Jacobs, Christine June. "Communication about genetic testing and hereditary cancer management with breast and ovarian cancer patients." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10046946/.
Анотація:
Background: Women with breast or ovarian cancer (patients) are increasingly offered genetic testing shortly after diagnosis to guide management and identify future cancer risks. As a result, new approaches to communication about hereditary cancer are needed to inform decision-making amongst patients and their relatives. Aims: This thesis aimed to investigate expert opinion and guideline recommendations about the communication needs of patients undergoing genetic testing, the information communicated by genetics health professionals and recalled by patients and their relatives and the experience of patients with newly diagnosed breast cancer who undergo genetic testing. Methods: A scoping review and five studies were conducted using UK data from patients and health professionals: an observational study, a Delphi survey, a content analysis, a document analysis and mixed methods matrix and a qualitative study. Results: Accuracy of information recall was low amongst patients and relatives following genetic counselling, especially about hereditary cancer management. Expert health professionals and service users agreed on the key messages required by patients to inform decision-making for themselves and their relatives. However, during genetic counselling, half of the key messages were communicated to patients and fewer key messages were communicated about hereditary cancer management than genetic testing. Recommended information to communicate to patients was identified from international genetics guidelines. Recommendations about hereditary cancer management were infrequently reflected in expert opinion, communicated by genetics health professionals or recalled by patients. Newly diagnosed patients experienced growing uncertainty and concern about inheritance and surgical decision-making, especially when their genetic test result was unexpected. Conclusions: Patients received insufficient information to understand their future cancer risks and make informed decisions about managing hereditary cancer. Steps are needed to improve information provision, especially when results are unexpected. These findings can help guide refinements to communication as genetic testing is integrated into mainstream oncology.
28
Launonen, V. (Virpi). "Genetic aberrations and their clinical significance in breast and ovarian cancer." Doctoral thesis, University of Oulu, 1999. http://urn.fi/urn:isbn:9514251946.
Анотація:
Abstract
In tumourigenesis, genetic alterations accumulate in the genes responsible for cell growth, proliferation and DNA repair: proto-oncogenes, tumour suppressor and DNA repair genes. Inactivation of tumour suppressor gene function is commonly recognised as a deletion of one of the two alleles; LOH, loss of heterozygosity. In the present study, LOH of several chromosomal regions was studied in both breast and ovarian cancer.
LOH for chromosome region 11q was examined in a large breast cancer consortium cohort (N = 988) and in a Finnish ovarian cancer cohort (N = 78), and the clinical significance of these alterations was evaluated. In breast cancer, LOH of the studied markers at 11q23.1, harbouring approximately 2 Mb of DNA, was seen to be associated with shortened cancer-specific survival. Two candidate genes, ATM (the ataxia telangiectasia disorder gene) and DDX10 (a putative RNA helicase gene) map to this chromosomal region.
In ovarian cancer, LOH at 11q23.1–q24 was assigned mainly to two chromosomal regions, A and B, which are proximal and distal to 11q23.2–q23.3, respectively. Only the distal B region was seen to be associated with an aggressive disease course. Therefore, it appears that inactivation of the ATM or DDX10 genes is not crucial for determining the outcome of ovarian cancer. The CHK1 gene at 11q24, encoding a protein kinase required for DNA damage checkpoint function, is a putative target gene at the B region. On the basis of the present results, the main TSG in the studied region involved in the progression of breast cancer maps to 11q23.1 and the corresponding gene for ovarian cancer more distally to 11q23.3-q24.
In addition, LOH at 3p, 6q, 8p, 11p, 16q and 17p was examined and their role in the genetic evolution of ovarian cancer was evaluated. Of the studied chromosomal regions, LOH at 17p appeared to be an early event and LOH at 16q24.3, 11q23.3/q24 and 11p appear to occur later in the progression of ovarian cancer.
29
Antoniou, A. C. "Developing a comprehensive risk model for familial breast and ovarian cancer." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596129.
Анотація:
The specific aim of this thesis was to combine data on mutation prevalence and risk from both high risk families and population based series, in order to develop a model for familial breast and ovarian cancer which incorporates both the effects of BRCA1, BRCA2 and other genes. The principal methodology used was segregation analysis and the genetic models were constructed using the computer program MENDEL. The first dataset consisted of 112 families containing two or more relatives with epithelial ovarian cancer. BRCA1 and BRCA2 germline mutations were detected in 50% of these families. When the effects of BRCA1, BRCA2 and a third ovarian cancer susceptibility gene were modelled simultaneously none of the models fitted gave significant evidence for a third gene. BRCA1 and BRCA2 were estimated to account for at least 38 % of the excess familial risk of ovarian cancer. Using data on the families of twelve BRCA1 mutation carriers in a study of 374 ovarian cancer cases unselected for family history, the estimated ovarian cancer risk by age 70 was 66% and the corresponding breast cancer risk was 45%. The breast cancer dataset consisted of 1484 women diagnosed with breast cancer under the age 55 from whom blood samples were analysed for mutations in BRCA1 and BRCA2. Using information on breast and ovarian cancer history in first degree relatives, and on the mutation status of the index cases we estimated the effects of BRCA1, BRCA2, a third gene BRCA3 and a polygenic effect. For this purpose the Hypergeometric Polygenic model was implemented in MENDEL.
30
Singh, K. J. D. L. "Ovarian reserve testing in premenopausal recipients of chemotherapy for breast cancer." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444394/.
Анотація:
The incidence of breast cancer has progressively increased, while survival rates have simultaneously improved. Young women with breast cancer are likely to suffer ovarian damage from chemotherapy, which can have a profound effect on their quality of life. At present, it is impossible to predict the functional lifespan of the chemotherapeutically damaged ovary as there is insufficient data. Ovarian reserve tests (ORT) have the potential to estimate the reproductive age of the ovaries, which would allow an accurate estimation of fertility status and the risk of premature ovarian failure. This project investigates the use of ORT in young women with breast cancer. To achieve this, biochemical and biophysical ORT were performed in a mixed longitudinal and cross-sectional study group comprising young women treated with chemotherapy for breast cancer and age-matched, regularly menstruating controls with proven fertility. Overall the results indicate potential for the use of inhibin B, anti-mullerian hormone, oestradiol and antral follicle count in the evaluation of these patients. An in vitro study was performed to supplement the clinical study, in which the effects of cytotoxic agents commonly used to treat breast cancer were examined by simultaneously applying equivalent doses of each to a breast cancer cell line and primary granulosa-luteal cell cultures respectively. The effects of these agents were measured in terms of cellular integrity (apoptosis) and functionality (hormones). Overall the results suggest variations in cytotoxicity (LD50) between breast and granulosa cells which have potential therapeutic implications.
31
Yuan, Baowen [Verfasser], and Barbara [Akademischer Betreuer] Burwinkel. "Identification of Plasma Metabolites Associated with Breast and Ovarian Cancer and Breast Cancer Prognosis / Baowen Yuan ; Betreuer: Barbara Burwinkel." Heidelberg : Universitätsbibliothek Heidelberg, 2020. http://d-nb.info/1214371698/34.
32
Laidlaw, Ian James. "Xenograft studies of normal human breast epithelium transplanted to athymic nude mice." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321307.
33
Wolstenholme, Jane. "Counting the costs of cancer care : breast, cervical and lung cancer in Trent." Thesis, University of Nottingham, 2001. http://eprints.nottingham.ac.uk/12097/.
Анотація:
The purpose of this thesis is to explore the theory, practice and application of costing with specific reference to cancer. In part it reviews the theory and guidelines related to costing methods including the recent focus on the analytical techniques used with cost data. In addition it examines how these theories and guidelines are applied in practice, by reviewing the literature on costs and cancer. The empirical research in this thesis applies costing methods to three specific cancer sites; breast, cervix and lung. This analysis provides information on the total burden of these specified cancers in terms of cost to a typical health authority (Trent). It also explores the hypothesis highlighted in previous studies that the cost of cancer increases with the stage of the disease. The final area of contribution for the thesis is in the application of recently suggested analytical techniques for cost data to the breast, cervical and lung cancer data sets; it investigates a number of proposed techniques for the analysis of skewed cost data and methods for data with incomplete patient follow up.
34
馮敬業 and King-yip Fung. "Screening of recurrent BRCA gene mutations in Chinese breast and ovarian cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31969720.
35
Tang, Kei-shuen, and 鄧紀旋. "Role of BRCA1 in stress-induced autophagy in breast and ovarian cancercells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45847204.
36
Fung, King-yip. "Screening of recurrent BRCA gene mutations in Chinese breast and ovarian cancer." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23829837.
37
Grude, Lillian. "Risk Factors for Breast, Uterine and Ovarian Cancer: A competing Risks Analysis." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for matematiske fag, 2011. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-13572.
Анотація:
A competing risks situation arises when a unit can fail due to several distinct failure types. In a competing risk situation, standard techniques from survival analysis may lead to incorrect and biased results. In this thesis, the theory of competing risks is used to identify possible risk factors for breast, uterine and ovarian cancer. This has been done by regression on the cause specific hazard functions, the subdistribution hazard functions and two approximate methods. Cox regression is used for a complete analysis of the medical data.By following 61457 women over approximately 50 years, it has been observed 3407 cases of breast cancer, 934 of uterine cancer and 843 of ovarian cancer. Summarized, it has been found that several births decrease the risk of breast, uterine and ovarian cancer. Obesity is associated with increasing risk of ovarian cancer for postmenopausal women, but not premenopausal. A long reproductive period (early menarche and/or late menopause) and high BMI increases the risk of breast and uterine cancer. Late first and last birth decreases the risk of uterine cancer, while it increases the risk of breast cancer. The data used in the analysis is selected from a screening program organized by the Norwegian Cancer Society for early diagnosis of breast cancer. postmenopausale women, but not premenopausale. A long reproductive period (early menarche and/or late menopause) and high BMI increases the risk of breast and uterine cancer. Late first and last birth decreases the risk of uterine cancer, while it increases the risk of breast cancer. The data used in the analysis is selected from a screening program organized by the Norwegian Cancer Society for early diagnosis of breast cancer.
38
Tomlinson, Victoria. "The putative oncogene EEF1A2 and its role in breast and ovarian cancer." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/25256.
Анотація:
I investigated the expression of eEF1A2 in breast and ovarian cancers at both the RNA and protein levels. I identified eEF1A2 overexpression in up to two-thirds of breast cancers and moderate to high levels of eEF1A2 expression were associated with estrogen receptor positive cancers (p=0.0087). In ovarian cancers eEF1A2 was found to be expressed in up to one-third of cancers and was highly expressed in clear cell carcinomas. The majority of ovarian cancers analysed showed amplification of the EEF1A2 locus regardless of whether they expressed eEF1A2, suggesting this is not the only mechanism mediating the overexpression of the elongation factor. Mutation analysis of the exonic sequence of EEF1A2 in low copy number ovarian cancers led to the identification of only one sequence variant that would not be predicted to alter the sequence of the protein but may have an effect on post transcriptional regulation of gene expression. Immunofluorescence analysis of the sub cellular localisation of eEF1A1 and eEF1A2 in breast (MCF-7) and ovarian (PEO1) cancer cell lines suggests that the two isoforms show a similar diffuse cytoplasmic localisation with some concentration in the perinuclear region of the cell. eEF1A1 and eEF1A2 partially co-localise with tubulin in the perinuclear region and with F-actin in cellular protrusions. Finally, analysis of eEF1A2 function in the breast cancer cell line MCF-7 using RNA interference of EEF1A2 showed that partial ablation of eEF1A2 does not alter the rate of proliferation, cell cycle distribution or the percentage of cells in apoptosis. Therefore, eEF1A2 is frequently overexpressed in breast and ovarian cancers and this overexpression does not appear to be consistently mediated by gene amplification, mutation or methylation.
39
Howard, Amanda Fuchsia Star. "Women's decision making regarding hereditary breast and ovarian cancer risk-reducing strategies." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/23498.
Анотація:
Women found to carry mutations in the BRCA1 or BRCA2 genes have up to an 88% lifetime risk of breast cancer and up to a 65% lifetime risk of ovarian cancer. Strategies to address these heightened risks include breast cancer screening, and risk-reducing (RR) surgeries (i.e., mastectomy and salpingo-oophorectomy). Some women might change their lifestyle or use complementary and alternative medicine to prevent hereditary breast and ovarian cancer (HBOC). The objectives of this research were to describe: a) the HBOC RR strategies used by women prior to receiving their genetic test results, the influence of individual and psychological factors on the uptake of these strategies, and their risk management information needs, b) how women construct the ‘right time’ to consider RR surgery decisions, and c) the process of making decisions regarding HBOC RR strategies. A survey of 143 women was conducted to address the first objective and in-depth interviews with 22 BRCA1/2 carriers were conducted to address the remaining two objectives.
Survey respondents engaged in breast cancer screening at the time of genetic testing and a sub-group modified their lifestyle to reduce their cancer risk. Qualitative analyses revealed women’s constructions of the ‘right time’ to consider RR surgery decisions to be when: (1) decisions fit into their lives, (2) they had enough time to think about decisions, (3) they were ready emotionally, (4) all the issues and conflicts were sorted out, (5) there were better options available, and (6) the health care system was ready for them. Grounded theory analyses suggested that the overarching process of making decisions about HBOC RR strategies was one of ‘preserving the self.’ This process was shaped by the characteristics of health services, the nature of HBOC RR decisions, gendered roles, and the women’s perceived proximity to cancer. The women engaged in five decision-making styles, which were characterized by combinations of seven decision-making approaches. Findings from these three studies capture the diverse trajectories of decision making about HBOC risk management and highlight the role of personal and social context in shaping these decisions.
40
Moyer, Cassandra L. "Understanding the role of BRIP1 missense variants in breast and ovarian cancer." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1562858015936498.
41
Collier, Ashley. "Integration of family health history in clinical guidelines for breast, ovarian, and colorectal cancer." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1337350837.
42
Prochazka, Michaela. "The risk of second primary lung carcinoma in breast cancer patients /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-649-2/.
43
Lewis, Deana L. "Angiogenic Characteristics of Tumor-Associated Dendritic Cells in Ovarian and Breast Cancer Models." Ohio University Art and Sciences Honors Theses / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ouashonors1462296303.
44
Baker, Sara Kay, and Sara Kay Baker. "Rural Arizona Nurse Practitioners' Knowledge of Hereditary Breast and Ovarian Cancer Risk Assessment." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/622972.
Анотація:
Problem statement: Mutations in the genetic material BRCA I/II are linked to increased incidence of cancer among the women who carry these alterations, raising lifetime risk of breast cancer to as high as 87%. Genetic testing exists to identify these alterations, empowering women to obtain advanced screening for breast and ovarian cancer, as well as incorporate prophylactic medications and surgeries for prevention of disease. Research has shown that appropriate risk assessment methods are not being utilized among primary care providers to identify those patients who would benefit from genetic counseling and testing. Purpose: To determine if a knowledge deficit about U.S. Preventative Services Task Force BRCA risk assessment recommendations exists among the rural Arizona nurse practitioner population, and to determine the level of confidence Arizona NPs have regarding the topic. Methods: A needs assessment completed via an 18-question online survey distributed through two provider organizations in Arizona. Inclusion criteria included NP must hold an active license in Arizona, NP must practice in primary healthcare, and practice site must serve patients who reside in a rural area of Arizona. Data collection remained open for three weeks. Analysis: Descriptive statistics using quantitative analysis evaluated provider demographics, responses to basic knowledge questions and clinical scenarios, and provider self-confidence analyses. Results: Participants were able to identify inheritance patterns of BRCA mutations, but incorrectly answered the majority of knowledge questions. Regarding self-reported confidence with awareness and use of the USPSTF guideline, nearly half of participants felt that they had at least average confidence. However, only one participant was able to answer every question correctly. Most agreed that the guidelines were relevant to their current practice. These results indicate a knowledge gap among NPs who care for patients living in rural Arizona. These results may inform future research aimed at educational interventions and practice improvement initiatives that will improve understanding and use of guidelines for screening, counseling, and testing patients at high-risk of carrying a harmful BRCA-mutation. Ultimately, these results will impact outcomes of patients living in rural Arizona.
45
Patel, Shreya. "MiRNAs Trageting Proto-Oncogene C-FMS mRNA in Breast and Ovarian Cancer Cells." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/321928.
46
Patel, Arpan Ajit. "ncRNA Targeting CSF-1 and CSF1R Expression in Breast and Ovarian Cancer Cells." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/579336.
Анотація:
Various sense ncRNA transcripts targeting nucleolin and vigilin, and shRNA transcripts targeting CSF-1 and c-fms mRNAs were introduced into Hey ovarian cancer and BT20 breast cancer cell lines to measure their influence on CSF1R and CSF1 protein expression. In BT20 cells transcripts c-fms-C-rich 104-S, c-fms-(CS-rCS), and c-fms-Py-S were found to downregulate CSF1R expression. In BT20 cells transcripts CSF-1-Exon-10-356-S and CSF-1 (CS-rCS) were found to have a downregulatory effect on CSF1 expression while transcript CSF-1-5'UTR-420-S was found to upregulate CSF1 expression. In Hey cells transcript CSF-1-3'UTR-AS-Pyrimidine was found to downregulate CSF1 expression while transcript CSF-1mRNA-Variant-4-5'UTR was found to have upregulate CSF1 expression. Also in Hey cells, both transcripts c-fms C-rich-104-S and c-fms-Py-S were found to upregulate CSF1R expression. These results indicate that ncRNAs are able to have a regulatory effect on CSF1 and CSF1R expression but also suggest that the mechanism of regulation is complex. Furthermore, the complex mechanism makes it difficult to predict if the transcript will have its intended effect. We concluded that differences in baseline RNA binding protein concentrations and other regulatory mechanisms, such as microRNAs, account for the conflicting results between the BT20 and Hey cell lines when comparing the same inserted transcript.
47
Denton, Graeme. "Immunological recognition of the tumour related mucin MUC1." Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284052.
48
Smith, Sarah Jane. "Cancer in Trent region : incidence, mortality and survival." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312199.
49
Arenas, Lahuerta Enrique Javier. "Identification of novel mechanisms in human breast cancer lung metastasis and chemoresistance." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/404730.
Анотація:
Breast Cancer (BC) is one of the major causes of cancer deaths in women. BC is a heterogeneous disease, and within the heterogeneity of the tumor, Tumor-Initiating Cells (TICs) have been reported as important drivers in tumor initiation and progression. On the basis of these observations, we hypothesized that TICs contribute to BC metastasis, as well to chemoresistance. Through genetic, transcriptomic, molecular and therapeutic analyses of tumor xenografts, BC cell lines, and/or human tumors, in this thesis we first demonstrate that RARRES3, a lung metastatic suppressor gene, prevents adhesion to the lung parenchyma and the initiation of metastatic lesions by enforcing the retention of differentiation features and that this retention is driven by its PLA1/2 catalytic activity. These results indicate that RARRES3 genetic activity blocks both tissue-specific metastasis to the lung and metastatic initiation properties. Next, we dissected functional interplay between stem cell (SC)-like master regulator genes (EVI1 and SOX9) and resistance to mTOR inhibitors, which leads to an aggressive metastatic cancer phenotype.
Collectively, the data shown in this thesis depict novel evidence regarding the role of tumor initiation properties in: I) BC progression and metastasis; II) how cancer progression is functionally linked to resistance to mTOR; and III) how resistance to therapy driven by tumor initiation properties may eventually produce an aggressive cancer phenotype.El cáncer de mama (BC, de sus siglas en inglés) es una de las mayores causas de muerte por cáncer en mujeres. El cáncer de mama es una enfermedad heterogénea, y en la heterogeneidad del tumor, las células iniciadoras tumorales (TICs, del inglés) han sido asociadas como importantes responsables en la iniciación y progresión tumoral. Basándonos en estas observaciones, nuestra hipótesis es si estas células contribuyen en la metástasis y quimioresistancia en el cáncer de mama. A través de análisis genéticos, transcriptómicos, moleculares y terapéuticos en xenoinjertos tumorales, líneas celulares y tumores humanos, en esta tesis hemos revelado en primer lugar que RARRES3, es un gen de supresión metastática en pulmón, que previene la adhesión al parénquima pulmonar y la iniciación de lesiones metastáticas, imponiendo las características de diferenciación, y cuya retención es causada por la actividad catalítica PLA1/2. Estos resultados indican que la actividad genética de RARRES3 bloquea específicamente la metástasis a pulmón y las propiedades de iniciación metastática. Además, hemos descrito una relación entre las los genes con características de autorenovación (EVI1 y SOX9) y resistencia a inhibidores de mTOR, que termina con una fenotipo más agresivo y metastático. Conjuntamente, los datos mostrados en esta tesis demuestras evidencias novedosas relacionadas con las propiedades de iniciación tumoral en distintos contextos: I) progresión y metástasis en el cáncer de mama; II) como la progresión tumoral está funcionalmente relacionada con la resistencia a inhibición de mTOR; y III) como la resistencia a terapia que está desencadenada por estas propiedades de iniciación tumoral pueden al final producir un fenotipo más agresivo y metastático
50
Iliopoulos, Dimitrios. "The role of the WWOX tumor suppressor in breast and lung cancer." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1155142398.