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1

Tang, Mei-Tzu Chen. "Induced abortion and risk of breast cancer /". Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/10929.

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2

Swartz, Esti. "Emotional intelligence and locus of control of adult breast cancer patients receiving treatment". Thesis, Nelson Mandela Metropolitan University, 2010. http://hdl.handle.net/10948/d1015686.

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Breast cancer is the most prevalent cancer of women in South Africa, with one in twenty-seven women diagnosed with breast cancer in their lifetime. By building on human strengths, ways can be found to cope effectively with adversity. This will contribute to psychological well-being and result in living constructive and meaningful lives. Emotional intelligence and locus of control are two constructs which, according to previous research, may be associated with psychological wellbeing. Limited research has been conducted on these constructs in populations facing adversity. Adaptation to breast cancer treatment is considered to be an extremely difficult process. The research aimed to explore and describe emotional intelligence and locus of control within an adult breast cancer population. A sample of 67 breast cancer patients receiving treatment was approached to complete a biographical questionnaire and two pencil-and-paper questionnaires. Descriptive and inferential statistics were be used to analyze the data. The results of the quantitative analysis indicated a significant negative correlation between emotional intelligence and locus of control which shows that patients with higher levels of emotional intelligence possess more internal locus of control orientations, while patients with lower emotional intelligence possess more external locus of control orientations. The population presented with above average emotional intelligence and an internal locus of control orientation. The study can be regarded as the first step in opening a field of research which could contribute to more effective coping and the overall psychological well-being of individuals facing adversity in South Africa. Furthermore, the findings of the study contributed to understanding the role of emotional intelligence and locus of control in these populations and encouraged further research and the development and implementation of programmes that promote skills development in these areas.
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3

Rohan, Thomas Edward. "Diet, hormones and breast cancer : a case-control study in women /". Title page, table of contents, summary and appendices only, 1986. http://web4.library.adelaide.edu.au/theses/09PH/09phr7373.pdf.

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4

Hong, Deli. "RUNX1 Control of Mammary Epithelial and Breast Cancer Cell Phenotypes". eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/949.

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Breast cancer remains the most common malignant disease in women worldwide. Despite the advantages of early detection and improved treatments, studies into the mechanisms that initiate and drive breast cancer progression are still required. Recent studies have identified RUNX1, which is an essential transcription factor for hematopoiesis, is one of the most frequently mutated genes in breast cancer patients. However, the role of RUNX1 in the mammary gland is understudied. In this dissertation, we examined the role of RUNX1 in both normal mammary epithelial and breast cancer cells. Our in vitro studies demonstrated that RUNX1 inhibits epithelial to mesenchymal transition (EMT), migration, and invasion, reflecting its tumor suppressor activity, which was confirmed in vivo. Moreover, RUNX1 also contributes significantly to inhibition of the phenotypes of breast cancer stem cells (CSC), which is responsible for metastasis and tumor relapse. We showed that Runx1 overexpression reduces the tumorsphere formation and cancer stem cell population. Overall, our studies provide mechanistic evidence for RUNX1 repression of EMT in mammary cells, anti-tumor activity in vivo and regulation of CSC-like properties in breast cancer. Our results highlight crucial roles for RUNX1 in preventing epithelial to mesenchymal transition and tumor progression in breast cancer. This RUNX1 mediated mechanism points to novel intervention strategies for early stage breast cancer.
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5

Yassaee, Vahid Reza. "Towards a general strategy for breast cancer : investigation of germline mutations of BRCA1 and BRCA2 genes in Iranian women with early-onset breast cancer". Thesis, University of Sheffield, 2002. http://etheses.whiterose.ac.uk/5987/.

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Breast cancer is the most common female malignancy and a major cause of death in middle-aged women. It results from genetic and environmental factors leading to the accumulation of mutations in essential genes, BRCA 1and BRCA2. To date, germline mutations in the BRCAI and BRCA2 genes in patients with early-onset breast and/or ovarian cancer have not been identified within the Iranian population. This study was set for two main purposes, in first for a cohort study of selected population (Iranian women) with early-onset breast cancer and secondly to evaluate and improve upon existing mutation detection techniques with respect to the BRCA genes. With the collaboration of two main centres for cancer research and treatment in Tehran-Iran, clinical information, family history and peripheral blood were obtained from 96 unrelated families for scanning of germline mutations in the BRCA 1 and BRCA2 genes. These sets of samples consists of 104 women under the age of forty-five, 88 patients affected with early-onset breast cancer or ovarian cancer and 16 unaffected individuals with strong family history of breast and/or ovary cancer. BRCA1 exons 11 and BRCA2 exons 10 and 11 by the Protein Truncation Test (PTT) and BRCAI exons 2, 3, 5, 13 and 20 and BRCA2 exons 9, 17,18 and 23 with the Single Strand Conformation Polymorphism (SSCP)assay were analysed on genomic DNA amplified by polymerase chain reaction. Ten sequence variants were identified: five are frame shift (putative mutations-four novel); three missense changes of unknown significant and two polymorphisms, one seen [BRCA2 (IVSI6-14T>C)] commonly in both Iranian and British population. Identification of these novel mutations suggests that any given population should develop a mutation database for its breast cancer screening. The pattern of mutations seen in the BRCA genes does not appear to differ from other populations studied. Early-onset breast cancer (less than 45 years) and a limited family history is sufficient to justify mutation screening with a detection rate of over 250/0 in this group, whereas sporadic early-onset breast cancer (detection rate less than 5%) is unlikely to be cost-effective. To address the penetrance and mutation spectrum of germline mutation of the contributed genes within Iranian population further studies should be performed. Meta-PCR technique was evaluated for its implication of BRCA genes scanning. Three distinct sets of BRCA gene fragments were selected to assemble with different approach for downstream analysis: the first set consisted ofBReA1 exons 2, 20 and BRCA2 exon 18 and their subsequent analysis by Protein Truncation Test; the second set comprised BRCAI exons 2, 20, 23 and 24 and their subsequent analysis by direct sequencing; and the last one contained six key coding regions from the BRCA genes, the 5' and 3'termini of exon 11 from both BRCAI and BRCA2 genes and exons 2 and 20 from BRCAI. Downstream analysis of Meta-PCR products by Protein Truncation Test was used rather than direct nucleotide sequencing because the total assembled above fragments size (~2.8kb) is sufficiently big to ignore analysing by the latter approach. PTT and direct sequencing were chosen because of their high sensitivity and specificity. These three trials were performed successfully suggesting that it may be possible to assemble the entire of coding regions of BRCAI and BRCA2 genes in a multi-step procedure.
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6

Caldon, Catherine Elizabeth Garvan Institute of Medical Research Faculty of Medicine UNSW. "Cell cycle control by ID1 and WT1 in breast cancer cells". Awarded by:University of New South Wales. Garvan Institute of Medical Research, 2007. http://handle.unsw.edu.au/1959.4/33125.

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Loss of proliferative control is a cornerstone of cancer development, induced by deregulation of mitogenic signalling, insensitivity to anti-proliferative signals and direct changes in cell cycle proteins. In breast cancer these alterations are frequently targeted through cyclins D1 and E, leading to defects in G1/S transition. I have investigated the role of two potential pro-proliferative oncogenes in breast cancer, id1 andwt1. Each protein promotes proliferation in distinct contexts, with unique consquences for breast cancer cells. Using a 3D culture model of non-transformed mammary epithelial cells, I identified that id1 undergoes downregulation via rapid proteosomal degradation and cytoplasmic relocalisation during mammary epithelial morphogenesis. Overexpression of Id1 led to an increase in acinar size via an increase in S phase, and wa dependent on the presence of an intact HLH domain in Id1. Co-expression with the proto-oncogene Bcl2 led to a more disorganised acinar structure, indicating that Id1 overexpression primed the cells for further oncogenic insult. Further, Id1 overexpression was unable to increase acinar size in cyclin D1-/- acini, indicating that Id1 is dependent on cyclin D1 for its proliferative effects. Overall these data identified Id1 as capable of altering the proliferation of normal mammary epithelial cells, a crucial step in early breast carcinogenesis. Wt1 was originally identified as a tumour suppressor, but our data lends support to Wt1 acting as an oncogene in breast cancer. Wt1 is expressed highly in a range of breast cancer cell lines, and is strongly regulated by progestins. Using siRNA, we identified that Wt1 is likely to be a molecular intermediary of progestin as the downregulation of Wt1 mimics a subset of progestin effects on cell proliferation and lipid synthesis. Conversely, the overexpression of the major Wt1 isoform, Wt1 (+/+), led to attenuation of progestin-induced differentiation and growth arrest via maintenance of cyclin D1 levels. The effects of Wt1 overexpression were specific to progestins, and did not affect the actions of anti-estrogens or androgens. Consequently the overexpression of Wt1 (+/+) may disrupt the endocrine response in mammary epithelial cells, and contribute to excess proliferation and failure to differentiate during breast oncogenesis.
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7

Lindahl, Thomas. "Prognostic markers in breast cancer associated with cell cycle control, proliferation and angiogenesis /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-860-2/.

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8

Levy, Anita Rochelle. "Progestin receptor heterogeneity in a breast cancer cell line". Thesis, Rhodes University, 1995. http://hdl.handle.net/10962/d1004100.

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Anti-oestrogens act via the oestrogen receptor whether they compete with the hormone for binding to the receptor and therefore interfere with DNA binding or inhibit transcriptional activity. These receptors exist as a large 85 complex and/or a small 45 form on sucrose density gradients. High performance ion-exchange chromatography has confirmed that the oestrogen and progestin complex is present in various isoforms. Progestin receptor heterogeneity could be influenced by the presence of oestrogens and anti-oestrogens in the culture media of hormone-dependent neoplastic cells. Cell culture methods offer the opportunity to test effects of specified components in repeated experiments on a homogeneous population of cells. MCF-7 and T47-D human breast cancer cell lines were conditioned to grow in a serum-free environment. There was no difference in cell proliferation rates, nor in their oestrogen or progestin receptor levels when compared to the same cells grown in conventional media. Receptors were present mainly in the large molecular 85 form. Both the MCF-7 and T47-D breast cancer cells showed an increase in proliferation rate with the addition of oestrogen or diethylstilbestrol. There was a corresponding loss of progestin receptor levels and an alteration in the high performance ion-exchange isoforms. Flow cytometry confirmed differences in the S-phase components of the cells following exposure to oestrogens. The proliferation rates of the cell lines as well as their progestin receptor levels decreased when treated with tamoxifen or the hydroxylated tamoxifen. There were marked changes on high performance ion-exchange chromatography profiles. DNA ploidy and S-phase showed signs of toxicity and there was an increase in cellular debris. The MCF-7 and T47-D human breast cancer cell line retained response to antioestrogen saturation.
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9

Veer, Pieter van 't. "Dietary habits and breast cancer a case-control study in the Netherlands /". [Maastricht : Maastricht : Rijksuniversiteit Limburg] ; University Library, Maastricht University [Host], 1990. http://arno.unimaas.nl/show.cgi?fid=5573.

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10

Bonilla, Carolina, Bernardo Bertoni, Pedro C. Hidalgo, Nora Artagaveytia, Elizabeth Ackermann, Isabel Barreto, Paula Cancela i in. "Breast cancer risk and genetic ancestry: a case-control study in Uruguay". BioMed Central Ltd, 2015. http://hdl.handle.net/10150/610306.

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BACKGROUND: Uruguay exhibits one of the highest rates of breast cancer in Latin America, similar to those of developed nations, the reasons for which are not completely understood. In this study we investigated the effect that ancestral background has on breast cancer susceptibility among Uruguayan women. METHODS: We carried out a case-control study of 328 (164 cases, 164 controls) women enrolled in public hospitals and private clinics across the country. We estimated ancestral proportions using a panel of nuclear and mitochondrial ancestry informative markers (AIMs) and tested their association with breast cancer risk. RESULTS: Nuclear individual ancestry in cases was (mean ± SD) 9.8 ± 7.6% African, 13.2 ± 10.2% Native American and 77.1 ± 13.1% European, and in controls 9.1 ± 7.5% African, 14.7 ± 11.2% Native American and 76.2 ± 14.2% European. There was no evidence of a difference in nuclear or mitochondrial ancestry between cases and controls. However, European mitochondrial haplogroup H was associated with breast cancer (OR = 2.0; 95% CI 1.1, 3.5). CONCLUSIONS: We have not found evidence that overall genetic ancestry differs between breast cancer patients and controls in Uruguay but we detected an association of the disease with a European mitochondrial lineage, which warrants further investigation.
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11

Costa, Marinna Maria de Andrade. "Knowledge, attitude and practice of women about control actions for cancer breast". Universidade Federal do CearÃ, 2016. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=19289.

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FundaÃÃo Cearense de Apoio ao Desenvolvimento Cientifico e TecnolÃgico
Breast cancer is the type of cancer that affects more women worldwide, accounting for 22% of new cases each year. The nurse takes vital role in breast cancer control actions. But the success of breast cancer control program is directly dependent on, among other factors, the participation of users, since they must attend gynecological consultations, conduct examinations, participate in educational activities and put into practice the knowledge acquired. Given the importance of strategies to reduce mortality from breast cancer and the role of women seen in primary care, the study aimed to assess the knowledge, attitude and practice of women about control actions for cancer breast. Treat It will be an evaluative study, cross-sectional survey using the Knowledge, Attitude and Practice (KAP). The study was developed in the city of Fortaleza-CE. hey were listed 43 units of Primary Health Care distributed among the six Regional Executive Secretariats. The users that are accompanied by the ESF and that are in the age of risk for incidence of breast cancer (> 20 years), according to the Ministry of Health, composed the sample, totaling 387 women. Data will be collected with from an interview using two instruments: the questionnaire adapted from Oliveira (2014) and the questionnaire that corresponds to the Economic Classification Criteria of Brazil Brazilian Association of Research Companies (ABEP).The data will be analyzed based on analytical statistics and presented in tables and charts with absolute and relative frequencies. The results showed us that 368 women (94.8%) had adequate knowledge, but 214 (55.1%) had inadequate and attitude 279 (71.9%) inadequate practice in relation to early detection methods of breast cancer. These factors were influenced by age and Executive Secretary Regional (SER) in which women lived. This knowledge about the characteristics of the population, identifying gaps in knowledge, difficulties in adhering to exams and the cultural behavior of women subsidizes the actions of health professionals, guiding them in the development of techniques and strategies for population mobilization for adoption and maintaining a healthy behavior that direct self-care and health promotion.
O cÃncer de mama à o tipo de cÃncer que mais acomete as mulheres em todo o mundo, respondendo por 22% dos casos novos a cada ano. O enfermeiro assume papel essencial nas aÃÃes de controle do cÃncer de mama. PorÃm o sucesso do programa de controle do cÃncer de mama à diretamente dependente, entre outros fatores, da participaÃÃo das usuÃrias, jà que as mesmas devem comparecer Ãs consultas ginecolÃgicas, realizar os exames, participar de atividades educativas e colocar em prÃtica os conhecimentos adquiridos. Tendo em vista a importÃncia de estratÃgias para reduÃÃo da mortalidade por cÃncer de mama e o papel das mulheres assistidas na atenÃÃo primÃria, o estudo teve como objetivo avaliar o conhecimento, atitude e prÃtica das mulheres acerca de aÃÃes de controle para o cÃncer de mama. Trata-se de um estudo avaliativo, de corte transversal, com a utilizaÃÃo do InquÃrito Conhecimento, Atitude e PrÃtica (CAP). O estudo foi desenvolvido no municÃpio de Fortaleza-CE. Foram elencadas 43 Unidades de AtenÃÃo PrimÃria à SaÃde distribuÃdas entre as seis Secretarias Executivas Regionais. As usuÃrias que sÃo acompanhadas pela ESF e que estÃo na faixa etÃria de risco para incidÃncia do cÃncer de mama (> 20 anos), segundo o MinistÃrio da SaÃde, compuseram a amostra, que totalizou 387 mulheres. Os dados foram coletados a partir de uma entrevista utilizando dois instrumentos: o questionÃrio adaptado de Oliveira (2014) e o questionÃrio que corresponde ao CritÃrio de ClassificaÃÃo EconÃmica Brasil da AssociaÃÃo Brasileira de Empresa de Pesquisa (ABEP). Os dados foram analisados com base na estatÃstica analÃtica e apresentados atravÃs de tabelas e grÃficos com frequÃncias absolutas e relativas. Os resultados nos mostraram que 368 mulheres (94,8%) tiveram conhecimento adequado, porÃm 214 (55,1%) apresentaram atitude inadequada e 279 (71,9%) prÃtica inadequada em relaÃÃo aos mÃtodos de detecÃÃo precoce do cÃncer de mama. Esses fatores foram influenciados pela idade e SecretÃria Regional Executiva (SER) em que as mulheres residiam. Esse conhecimento acerca das caracterÃsticas da populaÃÃo, com identificaÃÃo das lacunas no saber, dificuldades para a adesÃo aos exames e o comportamento cultural das mulheres subsidia as aÃÃes dos profissionais da saÃde, guiando-lhes no desenvolvimento de tÃcnicas e estratÃgias para mobilizaÃÃo da populaÃÃo para adoÃÃo e manutenÃÃo de um comportamento saudÃvel que direcionem ao autocuidado e promoÃÃo da saÃde.
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12

Moradi, Tahereh. "The role of physical activity in the prevention of breast and endometrial cancer /". Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4263-3/.

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13

Natalucci, Valentina. "Effect of exercise in Breast Cancer and its association with tumor characteristics, risk factors for recurrence and lifestyle". Doctoral thesis, Urbino, 2018. http://hdl.handle.net/11576/2663506.

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Graci, Gina M. "Optimism, Health Locus of Control, and Quality of Life of Women with Recurrent Breast Cancer". Thesis, University of North Texas, 1998. https://digital.library.unt.edu/ark:/67531/metadc278130/.

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Yu, David Sung-wen. "Role of the BRCA2 breast cancer susceptibility protein in control of RAD51 recombinase". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620033.

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16

Sproviero, Daisy. "Control of expression of glycosyltransferases involved in O-linked glycosylation in breast cancer". Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/control-of-expression-of-glycosyltransferases-involved-in-olinked-glycosylation-in-breast-cancer(744e424f-f8c5-44cc-8ebf-d454594484dd).html.

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Aberrant glycosylation is a common phenotypic change observed in malignancy. Changes in mucin-type O-glycosylation in breast cancer can result in the expression of truncated core 1-based sialylated glycans rather than core 2-based glycans found in the normal gland. This is partly due to changes in the expression of glycosyltransferases. C2GnT1 expression, the glycosyltransferase that initiates branching in normal mammary epithelial cells, can be decreased in tumour cells while, in contrast, the expression of the sialyltransferase ST3Gal-l, which causes chain termination, increases in breast cancer. When dendritic cells mature, prior to migration to lymph nodes, their O-glycosylation changes by decreasing C2GnT1 expression and increasing ST3Gal-l expression. This can be controlled by PGE2, the major product of COX-2. The project described in this thesis investigated the control by PGE2/COX-2 of ST3Gal-l and C2GnT1 expression in breast carcinomas. Importantly, COX-2 is normally only expressed during inflammation but is found to be upregulated by many carcinomas including those of the breast. In the breast cancer line T47D, mRNA expression of ST3Gal-l was induced by PGE2, resulting in increased sialyltransferase activity. Induction of COX-2 in the MDA-MB-231 breast cancer cell line also resulted in increased expression of ST3Gal-l and increased sialylation of the ST3Gal-l substrate. This effect on sialylation could be reversed by the selective COX-2 inhibitor celecoxib. The use of siRNA to knock-down COX-2 and the over-expression of COX-2 in MDA-MD-231 confirmed the involvement of COX-2 in the upregulation of ST3Gal-l. Moreover, analysis of the expression of ST3Gal-l and COX-2 in 78 primary breast cancers showed a significant correlation between the two enzymes. COX-2 expression in breast cancer has been associated with poor prognosis. Thus these results suggest the intriguing possibility that some of the malignant characteristics associated with COX-2 may be via the influence that COX-2 exerts on the glycosylation of tumour cells.
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Ablorh, Akweley. "Meta-Analysis of a Multi-Ethnic, Breast Cancer Case-Control Targeted Sequencing Study". Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:16121143.

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Breast cancer, the most commonly diagnosed cancer in American women, is a heritable disease with nearly one hundred known genetic risk factors. Using next generation sequencing, we explored the contribution of genetics at 12 GWAS-identified loci to breast cancer susceptibility in a multi-ethnic breast cancer case-control study. Methods: The study population consists of 4,611 breast cancer cases and controls (2,316 cases and 2,295 controls) from four mutually exclusive ethnicities: African, Latina, Japanese, or European American.We conducted rare variant association testing between sequenced genotypes and simulated phenotypes to compare the performance of several approaches for assessing rare variant associations across multiple ethnicities and the statistical performance of different ethnic sampling fractions, including single-ethnicity studies and studies that sample up to four ethnicities. Findings from simulation of causal rare variant penetrance models were then applied to a non-synonymous protein-coding rare variant association study of breast cancer. Next, we applied variance partitioning methods to determine what proportion of breast cancer heritability is explained by rare and common, coding and non-coding, and the complete set of sequenced genetic variants. Results: Variance component-based tests were better powered in several scenarios. Multi-ethnic studies were well powered, with inclusion of African Americans providing the largest gains in statistical power. Rare variation in several genes was nominally associated (alpha=0.05) with breast cancer risk. Common variants explained a significant amount of breast cancer heritability (5%; SE=2%). Total breast cancer heritability from all sequenced SNVs from all 12 loci was approximately 11% (S.E.=4%), a substantial portion of breast cancer heritability which ranges from 27% to 32% in European familial studies. Conclusion: Our findings suggest that association studies between rare variants and complex disease should consider including subjects from multiple ethnicities, with preference given to genetically diverse groups. We demonstrate practices with the potential to uncover and localize gene-based associations using gene-based rare variant association testing at 12 GWAS-identified breast cancer susceptibility loci. We also present strong evidence that just this subset of previously-identified loci explains a substantial portion of heritability which suggests that all GWAS-identified loci may explain more breast cancer heritability than the 17% previously reported.
Epidemiology
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18

Yousef, Fatimah Mohammadali. "Vitamin D Status and Breast Cancer in Saudi Arabian Women: Case Control Study". Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/202986.

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Vitamin D is an essential nutrient in the human diet. A unique property of vitamin D is that it can be produced by endogenous synthesis in the skin following sufficient Ultraviolet B (UVB) radiation. In fact, our understanding of this compound has changed, such that it is no longer consider a true vitamin, but rather a steroid hormone. De-identified data for this analysis were derived from women residing in Jeddah, Saudi Arabia who completed routine medical visits in the summer of 2009 at King Fahad Hospital (KFH). In Chapter 1,“THE ASSOCIATION BETWEEN VITAMIN D STATUS IN NORMAL WEIGHT VERSUS OBESE WOMEN RESIDING IN WESTERN SAUDI ARABIA” we evaluate the relationship between body size and serum 25(OH)D concentrations including the association between change in body size during adulthood and vitamin D status. This study examines whether the current weight and weight change since age 18 years are associated with vitamin D status. This study found that neither current weight nor adult weight gain were associated with vitamin D status in Saudi Arabian women. In chapter 2,“IS AVOIDING SUN EXPOSURE VIA SUN PROTECTION PRACTICES ASSOCIATED WITH LOW VITAMIN D STATUS IN SAUDI ARABIAN WOMEN?” we investigate whether women who avoid UV exposure have lower 25(OH)D concentrations than women who do not avoid exposure. UV exposure was defined by time in outdoor activities, use of protective clothing and sunscreen. This study demonstrated that avoiding UV exposure via indoor activity and the use of sunscreen or/and wearing protective clothing was not associated with vitamin D status. Chapter 3, “VITAMIN D STATUS AND BREAST CANCER IN SAUDI ARABIAN WOMEN: A CASE CONTROL STUDY” we examine if vitamin D status as assessed by serum concentrations of 25(OH)D would be lower in breast cancer cases as compared to controls. This study demonstrated that there is a significant relationship between higher serum concentrations of 25(OH)D and lower risk of breast cancer. Chapter 4, “IMPLICATIONS AND FUTURE DIRECTIONS” is presented a summary of key findings from the three studies in this dissertation to determine avenues of further research. The appendices consist of materials related to the dissertation work.
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Schneider, Karen L. "Applying advanced methods to population-based survey data for purposes of breast cancer control". View abstract/electronic edition; access limited to Brown University users, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3318359.

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Carter, Joanne Haidee. "Cyclin E as a potential tumour antigen target for cancer immunotherapy". Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310780.

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Webster, Elizabeth Natalie. "Health care Facilities as a Predictor of Breast Cancer Survival Rates". ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/6145.

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The disparity between survival rates for Black and White women with breast cancer is well documented and has been examined in terms socioeconomics, environment, tumor type, and genetics. However, there is little examination of the role of health care facilities in cancer disparities. Health care facilities are representative of societal norms and beliefs that include location, quality of care, finance, policies, and staffing; therefore, they are a proxy for social justice and social change. The purpose of this study was to examine correlations between health care facility type; social determinants of cancer such as poverty, culture, and social justice; and breast cancer survival rates. Using the social determinants of cancer theoretical framework, the breast cancer survival rate of 4,087 Black and White women in Georgia between the ages of 45 and 69 was studied. The relationship between breast cancer survival and predictors including race, income, health care facility type, grade, and tumor type (4 sub-variables) were examined using the Kaplan-Meier Method, log-rank test, and Cox proportional hazard model. The log-rank test suggested no statistically significant difference in the survival functions among patients in different health care facilities (Ï?2(2) = 0.0150, p = 0.9926). The Cox proportional hazard model suggested no statistically significant relationship between breast cancer survival and health care facility type, after controlling for other predictors (Ï?2(2) = 0.3647, p = 0.8333). This result indicates that healthcare facilities do not influence breast cancer survival rates, however, given the persistent health outcome disparities further research in the area is warranted.
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Stewart, Alistair James. "Control of breast cancer cell proliferation by oestrogen, oestrogen-regulated proteins and growth factors". Thesis, University of Newcastle Upon Tyne, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287416.

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Chen, Chi-Ling. "A nested case-control study of hormone replacement therapy in relation to breast cancer /". Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/10898.

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Graci, Gina. "Optimism, Health Locus of Control, and Quality of Life of Women with Initial versus Recurrent Breast Cancer". Thesis, University of North Texas, 2001. https://digital.library.unt.edu/ark:/67531/metadc2803/.

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Health Locus of Control (HLOC) and other predictors of Quality of Life (QL) were examined for women with an initial versus recurrent breast cancer diagnosis. Twenty-eight women with an initial breast cancer (IBC) diagnoses and twenty-eight women with recurrent breast cancer (RBC) diagnoses were recruited from doctors' offices and cancer support groups. Correlational analyses were used to assess the relationships between variables. No significant differences were found between women with IBC and RBC on Psychological QL. Doctor HLOC and Psychological QL were related for women with RBC (r = .481, p = .01) and marginally so for women with IBC (r = .329, p = .09). A positive correlation was also found between Doctor HLOC and Functional QL for both women with IBC (r = .464, p = .01) and women with RBC (r = .390, p = .04). After controlling for stage of cancer, women with RBC reported higher Functional QL than did women with IBC. Advanced (stages III or IV) versus early (stages I or II) cancer stage related to lower Functional QL, controlling for initial versus recurrent diagnosis (r = -.283, p = .01). A marginally significant relationship was also found for cancer stage, regardless of initial versus recurrent diagnosis, with higher Overall QL for women with early stages of breast cancer (r = -.157, p = .09). No significant differences in Optimism or Overall QL were found between women with IBC versus RBC. No differences were found between married and single women. This research begins to explore differences in Quality of Life for women with a new versus a recurrent breast cancer diagnosis.
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25

Salagame, Usha Ganesh. "Bisphosphonates, Menopausal Hormone Therapy and Risk Factors for Breast Cancer in Australia". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16527.

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In Australian women, breast cancer is the second most commonly diagnosed cancer after non-melanoma skin cancers. The use of Menopausal Hormone Therapy (MHT) is an important breast cancer risk factor in postmenopausal women. Prior to findings from large-scale studies on the benefits and harms of MHT, it was used widely, and often, for the management of chronic conditions attributed to menopause, along with its primary use for menopausal symptoms. However, following the availability of such evidence from the Women’s Health Initiative (WHI) trial and other studies in 2002-2003, recommendations for MHT use became more specific and a substantial drop in MHT prescribing was noted in many settings. Although MHT use in Australia dropped substantially after 2002, a significant proportion of women continue to use MHT. Quantifying the breast cancer risks associated with this potentially modifiable risk factor using contemporaneous data in Australian women constitutes an important part of this thesis. Furthermore, a number of other reproductive and lifestyle factors have been found to be associated with breast cancer risk, but these may have differing associations with breast cancer in pre- and postmenopausal women. As an important background to the assessment of MHTassociated risk, these other risk factor associations were quantified in Australian women. Menopause accelerates age-related bone loss which often leads to osteoporosis. Although MHT prevents fracture, because of its generally unfavourable risk profile, when used long-term, it is not recommended first-line for prevention or management of osteoporosis. Bisphosphonates (a class of anti-bone resorptive drugs) are the recommended first-line therapy for osteoporosis. Concurrent with the drop in MHT use after 2002, a substantial increase in bisphosphonate prescribing was noted in many settings. These data raised the possibility that bisphosphonates were replacing MHT, probably as an indirect effect of the WHI trial findings and subsequent revisions to recommendations which restricted its use primarily for short-term menopausal symptom relief. However, among postmenopausal women, evidence-based guidelines and health technology assessments suggest somewhat different target age groups for these two groups of medications. MHT is recommended for relief from vasomotor symptoms around the time of menopause, whereas bisphosphonate use is recommended to women who are at a significant risk of osteoporosis-related fractures, which usually occur a couple of decades after menopause. This thesis examines changes in MHT and bisphosphonate prescribing, in postmenopausal Australian women and a comparable group of women from Manitoba, Canada. The main aims of this thesis are to 1) quantify the relationship between reproductive and lifestyle factors, and breast cancer risk in pre- and postmenopausal Australian women, 2) quantify breast cancer risks associated with MHT use, and to test for this association for specific subtypes of breast cancer, in postmenopausal Australian women and 3) investigate changes in prescribing of MHT and bisphosphonates in women over the age of 50 from Australia and Manitoba, Canada, in relation to the age of the users and the recommendations for use in both settings, over the period 1996-2008. To address Aims 1 and 2, a review of the literature was performed to inform multivariable breast cancer risk factor analyses, which were carried out separately in premenopausal (523 cases/176 controls) and postmenopausal (1276 cases/865 controls) Australian women. Odds ratios for breast cancer associated with MHT use and other risk factors were obtained through multivariable regression analyses using data from an all cancer case-spouse control study-The NSW Cancer Lifestyle and EvAluation of Risk (CLEAR) study. Pathology data on hormone and epidermal growth factor receptor status for a subset of the breast cancer cases (n= 419) was obtained and used to estimate MHTassociated risks for specific breast cancer subtypes. For Aim 3, overall and age-specific MHT and bisphosphonate prescribing patterns in women aged ≥ 50 years, from Australia and Manitoba, Canada were described. In premenopausal women, increased age and family history of breast cancer were found to be associated with increased breast cancer risk, whereas breastfeeding was associated with a reduction in risk. Although limited by sample size, my findings for other factors were generally compatible with the literature. In postmenopausal women, reproductive factors such as nulliparity and increased age at first birth, and increased BMI were found to be associated with increased breast cancer risk. Current use of MHT was found to be associated with a doubling of breast cancer risk; risks were generally higher in users of oestrogen-progestagen combination therapy compared to oestrogen-only MHT, although heterogeneity by type of preparation was not evident. MHT use was associated specifically with an increased risk of developing oestrogen- and progesterone- receptor - positive breast cancers, consistent with the hypothesis that the hormone effects are receptor-mediated. The analyses using ecological data on dispensed medications confirmed that concurrent and substantial drops in MHT prescribing and increases in bisphosphonate prescribing occurred in Australia and Manitoba, Canada, but they occurred in different age-groups of postmenopausal women, in both settings. The drop in MHT prescribing which occurred in women in their fifties and sixties is in agreement with the post-2002 recommendations for more specific and targeted use. The increase in bisphosphonate prescribing in women in their seventies and eighties suggest that their use was generally consistent with recommendations, during the time period studied. A total of 13% of Australian women aged 50-69 currently use MHT with ~75% of them using MHT for ≥ 5 years. The MHT-associated risks estimated in this study provide important information to Australian women and provide additional support to the current guidance by regulatory authorities which recommend that MHT use should be limited to the shortest time possible, in women with moderate to severe menopausal symptoms, who are aware of the risks and benefits.
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26

Wu, Jiejun. "Genome-wide analysis of epigenetics and alternative promoters in cancer cells". Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1187019769.

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27

Li, Christopher I.-Fu. "Relationship between hormonal, reproductive, anthropometric, and lifestyle factors and risk of lobular and ductal breast cancer /". Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/10932.

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28

Overbeck-Zubrzycka, Dorota. "FOXP3 regulates metastatic spread of breast cancer via control of expression of CXCR4 chemokine receptor". Thesis, University of Newcastle Upon Tyne, 2012. http://hdl.handle.net/10443/1465.

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The FOXP3 transcription factor can regulate T cell migration by inhibiting expression of CXCR4, the receptor for the chemokine CXCL12. The increased expression of CXCR4 by breast cancer cells can drive metastatic migration towards sites that express CXCL12. Intracellular trafficking of FOXP3 to the nucleus is required in order for this factor to function. The presence of alternative splicing forms, mutations and post-translationally modified forms may disrupt FOXP3 nuclear localization. We hypothesised that FOXP3 tumour suppressor is inactive in breast cancer causing an increase in CXCR4 expression and the development of metastasis. The expression of FOXP3 and CXCR4 were measured at mRNA and protein (immunohistochemistry, immunofluorescence, FACS) levels. FOXP3 DNA sequences of normal and cancer cells were analysed. Stable FOXP3 overexpressing breast cancer transfectants were used to investigate the potential of FOXP3 to regulate chemotaxis. Normal breast epithelial cells (both patient-derived tissues and laboratory cultured cell lines) expressed FOXP3 in their nuclei but did not express CXCR4. Breast cancer cells overexpressed CXCR4 (p<0.05), whereas FOXP3 expression was decreased (p<0.05) and confined to the cytoplasm with negligible nuclear expression. Metastases expressed less FOXP3 and more CXCR4 than primary cancers (p<0.05). FOXP3 sequencing in breast cancer cell lines did not reveal mutations. However, there were at least three bands on the PCR electrophoreses gel. The predominant form in breast cancer cells contained an insertion of 120bp within the forkhead domain. Transfection of breast cancer cells with wild-type FOXP3 restored its nuclear expression, reduced CXCR4 expression and inhibited cell migration. This study demonstrated failure of nuclear localisation of FOXP3 in breast cancer cells and an inverse correlation between this failure and CXCR4 expression. Disruption of FOXP3 nuclear localisation may be due to abnormal co-expression of FOXP3 splice variants leading to increased CXCR4 expression and acquisition of the capacity to metastasize.
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29

Liozidou, Maria. "Genetic epidemiology of breast cancer in Cyprus : a case-control study of DNA repair genes". Thesis, Brunel University, 2009. http://bura.brunel.ac.uk/handle/2438/4111.

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The occurrence of early-onset breast cancer (EOBC) has been associated with germline mutations in the BRCA1 and BRCA2 genes. The first aim of this thesis was to evaluate the frequency and distribution of mutations in these genes, in a group of Cypriot women diagnosed with EOBC. Pathogenic mutations were identified in 6 of the 26 unrelated patients. This study supports a strong correlation between the early onset breast cancer phenotype and the presence of pathogenic BRCA1/2 mutations. It is of interest that pathogenic mutations were detected in patients without a family history of the disease. Based on these results, we recommend that BRCA1/2 screening should be offered to patients with a diagnosis of EOBC irrespective of their family history. The known breast cancer susceptibility genes explain only about 5% of breast cancer cases. Thus, it is likely that other breast cancer susceptibility genes exist. The second aim of the present thesis was to assess whether alterations in DNA repair genes modify breast cancer risk in the Cypriot population. Towards this objective, blood samples were collected and genomic DNA isolated from 1109 Cypriot female breast cancer patients diagnosed between 40-70 years old, and from 1177 age-matched healthy female controls. A total of 79 single nucleotide polymorphisms (SNPs) were genotyped in all samples. Significant associations with breast cancer risk were observed for eight of the SNPs studied. Five SNPs in the BRCA2, MRE11A, MUS81, PBOV1 and XRCC1 genes, were associated with an increased risk for breast cancer, while two SNPs in the NBS1 gene and one SNP in the MRE11A gene appeared to be associated with reduced risk for the disease. The data from this study support the hypothesis that genetic variants in DNA repair genes influence breast cancer risk and provides further evidence for the existence of a polygenic model for breast cancer.
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30

Bischoff, Annabell [Verfasser], i Monilola [Akademischer Betreuer] Olayioye. "miRNAs in control of oncogenic signaling in breast cancer cells / Annabell Bischoff. Betreuer: Monilola Olayioye". Stuttgart : Universitätsbibliothek der Universität Stuttgart, 2015. http://d-nb.info/1068810955/34.

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31

Ding, J. J. "Case control study on the effectiveness of using standard mammogram form to predict breast cancer risk". Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598545.

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The aim of my project was to associate breast density with cancer risk by comparing SMF to the conventional density measurement methods. This case control study comprised cancers with age-matched controls from the Cambridge and Norwich Breast Screening Programmes. Data collection involved assessing the films based on Wolfe’s patterns, SCC and 21-categorisation classification, and then digitising the films for computer analyses (Cumulus and SMF). Conditional logistic regression was used to produce odds ratios associated with mammographic density. Results from a pilot study of 220 cancers and 220 controls demonstrated that compared to the conventional methods the SMF measurement was the most effective means of predicting breast cancer risk. This was shown by a methods comparison graph illustrating that the SMF percent volume measurement scheme had the highest density-risk association. Compared to the other density assessment methods, SMF measure of percent volume most clearly discriminated between women at high risk for breast cancer from those at low risk (odds ratio up to 27.1). The study was then expanded to increase the population size to 505 cancers with 1830 controls. Results from the full study contradicted those from the pilot study by showing that SMF measurements were not as effective at predicting breast cancer risk as the gold standard Cumulus measurements. The odds ratios showed a risk of 1.79 (95% CI 1.26-2.55) using SMF percent volume method compared to 3.38 (95% CI 2.32-4.92) as obtained by Cumulus absolute area measurements. I looked into the inconsistencies in the results from the pilot and full studies. After I examined several factors including digitiser effect, reader subjectivity and SMF version effect, I concluded that the promising results in the pilot study were most likely due to chance as I could not explain them by epidemiological or clinical means.
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32

Griffin, Brian P. "The Role of SRSF3 in Control of Alternative Splicing of CPEB2 in Triple Negative Breast Cancer". VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3976.

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In the presented study, we identified that SRSF3 controls the alternative splicing of CPEB2 and consequently promotes a metastatic phenotype in triple negative breast cancer (TNBC). TNBC causes thousands of deaths annually, frequently due to a lack of effective treatments and a high rate of metastasis in patients. Alternative splicing has been found to be dysregulated in numerous cancers, while splicing factors such as SRSF3 are variably expressed. In this study we performed a siRNA panel to screen potential splicing factors, then used specific siRNA to study the effect of its knockdown on cellular function. These results showed that SRSF3 encourages the production of the pro-metastatic isoform of CPEB2, which contributes the aggressive phenotype of the tumor. We utilized numerous methods to measure the metastatic function of cultured TNBC cells to determine if SRSF3 strongly promoted the metastatic function. These data showed that siRNA reduction of SRSF3 was able to reduce the metastatic potential of cancer cells. These findings suggest that SRSF3 has great potential as a therapeutic measure to reduce and minimize the aggressiveness of TNBC tumors.
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33

D’Anello, Laura <1980&gt. "Epigenetic control of the basal-like gene expression profile via Interleukin-6 in breast cancer cells". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2011. http://amsdottorato.unibo.it/3368/1/d%27anello_laura_tesi.pdf.

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34

D’Anello, Laura <1980&gt. "Epigenetic control of the basal-like gene expression profile via Interleukin-6 in breast cancer cells". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2011. http://amsdottorato.unibo.it/3368/.

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35

ANDREIS, FEDERICO. "The role of HRT exposure in breast cancer etiology: a causal inference approach". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/19340.

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Cancer etiology is a topic of great interest in medical research. Assessing and quantifying causal links between an exposure (e.g. a treatment) and an outcome of interest (such as cancer prognosis or survival) is often not a trivial task. Methods have been proposed to deal with the problem ofbias in estimation of causal effects. A method is presented here, applied to the field of Hormone Replacement Therapy and Breast Cancer, which allows to obtain an (at least locally causal) estimate of a continuous exposure effect on an outcome of interest within the framework of Principal Stratification, under a case-control study design.
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36

Huff, Nicole S. "Social support, God locus of health control, and quality of life among African American breast cancer survivors". Thesis, Central Michigan University, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=3567665.

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As African American (AA) breast cancer survivors live longer with the disease, much attention should be directed to quality of life and factors influencing it. An understanding of survivors' belief that God controls their health and their social support needs is necessary as an effort to develop health care services and programs that are culturally sensitive. This study was the first to explore the association between an individual's belief that God controls their health, social support and quality of life among AA breast cancer survivors. The purpose of this study was to examine the relationship between social support, God Locus of Health Control (GLHC) and quality of life (QoL) among the survivors residing in Illinois. This study's alternative hypotheses predicted after controlling for age, location of residence, marital status, and time since diagnosis, social support and GLHC, combined and individually, would positively correlate to QoL for AA breast cancer survivors.

The study used a descriptive, correlational and quantitative design by testing the variables using hierarchical multiple regression and Pearson correlation. A convenience sample of 92 AA women was recruited from a community hospital, a Federally Qualified Health Centers, a beauty shop, two support groups, a member association that advocates for health care disparities, and local newspapers. Quantitative measures included Social Support Questionnaire (Northouse, 1988), GLHC scale (Wallston et al., 1999), Quality of Life Index - Cancer Version III (QLI - CV III) (Ferrans, 1990), and Demographic Characteristics form created by researcher.

Results concluded QoL was not affected by social support and GLHC, combined, and GLHC, individually. However, social support was a predictor of QoL. Statistically significant relationships were found between social support, QoL and its domains: a) health and functioning subscale, b) social and economic subscale, c) psychological/spiritual subscale and d) family subscale. Statistically significant relationships were not found between GLHC and QoL and its domains. The mean score for social support and GLHC scales were low compared to prior study results. The QLI - CV III mean score was moderately high compared to other study results.

Additional findings concluded women residing in the suburb had statistically significant higher mean QoL than those living in the rural or urban areas of Illinois. Also, married women in this sample had a higher mean QoL than unmarried women. Although AA breast cancer survivors' QoL was not increased by their belief that God controlled their health and the mean social support score was low, the study results provided valuable information for future research and the development of social support programs that are culturally sensitive.

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37

Bates, D. L. "Control of the RAD51 recombinase by the BRC repeat motifs in the breast cancer susceptibility protein BRCA2". Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596469.

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The interaction between the breast cancer susceptibility protein BRCA2 and the RAD51 DNA recombinase is essential for DNA repair via homologous recombination. Its disruption in human cells causes genomic instability and cancer predisposition. Studies to define the biochemical and biological features of the BRCA2:RAD51 interaction are described. Human BRCA2 features eight BRC repeat motifs encoded within exon 11 through which it can bind RAD51. The BRC repeat motifs are believed to mimic and disrupt RAD51 oligomerisation at its self-association interface. I defined the minimal structural determinants required for RAD51 binding by ‘humanising’ a primitive RAD51 from an Archaeon species lacking BRCA2. Surface Plasmon Resonance (SPR) technology supported by cell biology was employed to study the characteristics of RAD51 binding to each of the BRC repeat motifs, both independently and collectively within the context of the BRCA2 protein. A single point mutation within an individual BRC repeat motif impaired RAD51 binding. Further, RAD51 was unable to interact effectively with a BRC repeat motif in which the proposed interaction interface had been disrupted by mutagenesis. Kinetic data for the interaction of an individual BRC repeat motif with RAD51 were obtained. An SPR competition assay was developed, revealing that the binding affinity of each BRC repeat motif for RAD51 differs significantly, and that their organisation within the scaffold of BRCA2 contributes to efficient interaction. Thus, I propose that both the differential binding affinities of the individual BRC repeat motifs for RAD51, and their observed cooperativity, contribute to the control of RAD51 by BRCA2. The implications of this proposal for DNA repair via homologous recombination, and for the role of BRCA2 mutations in human carcinogenesis, are discussed.
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38

Jordan, Irmgard [Verfasser]. "Breast Cancer and nutrition in the Kilimanjaro Region of Northern Tanzania: a case-control study / Irmgard Jordan". Gießen : Universitätsbibliothek, 2012. http://d-nb.info/1063955203/34.

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39

Benevides, Jordana Prado. "Knowledge, attitude and practice of nurses in the control of breast cancer in the family health strategy". Universidade Federal do CearÃ, 2016. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=18936.

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This study aimed to assess the knowledge, attitude and practice of nurses working in the Family Health Strategy (FHS) in Fortaleza-CE on the early detection of breast cancer; it is a descriptive, cross-sectional, using the Survey Knowledge, Attitude and Practice (KAP) conducted from September to November 2015 with 122 nurses who make up teams of FHS Fortress health system. To collect the data we used a tool Oliveira (2015), which characterizes and assesses the knowledge, attitude and practice of nurses in Primary Care Units Health (UAP) in relation to the early detection of breast cancer. Data were organized in tables and graphs. The study was approved by the Research Ethics Committee of the Federal University of Cearà (COMEPE / UFC) with the protocol No. 1233383/15. Regarding the profile of nurses, it was found that most belong to an age group 30-49 years, 92.6% female, 62.3% between 10-20 years of graduate and 82.1% are experts , 75.4% has been operating for over 5 years in the ESF and 60.3% have some training on the subject. Regarding the knowledge of nurses, the majority (46.7%) were classified as regular (41.8%) as inadequate and only (11.5%) had adequate knowledge. As the attitude and practice, it was observed that (73.8%) had an adequate attitude and the majority (57.4%) resulted in a poor practice. Despite the associations between knowledge, attitude and practice did not achieve statistical significance, it is known the influence of knowledge in the perception of the value of adopting health prevention measures (attitude), processing and development of personal skills (practice) for achievement of health promotion. Based on these, the lack of knowledge, attitudes and inadequate practices for early detection of breast cancer reveal the need for ongoing training of professionals involved in the control of breast cancer.
Objetivou-se avaliar o conhecimento, a atitude e a prÃtica dos enfermeiros atuantes na EstratÃgia SaÃde da FamÃlia (ESF) de Fortaleza-CE acerca da detecÃÃo precoce do cÃncer de mama; trata-se de um estudo descritivo, de corte transversal, com a utilizaÃÃo do InquÃrito Conhecimento, Atitude e PrÃtica (CAP) realizado no perÃodo de setembro a novembro de 2015 com 122 enfermeiros que compÃem as equipes da ESF do sistema de saÃde de Fortaleza. Para a coleta dos dados foi utilizado um instrumento de Oliveira (2015), que caracteriza e avalia o conhecimento, atitude e prÃtica dos enfermeiros nas Unidades de AtenÃÃo PrimÃria à SaÃde (UAPS) no que se refere à detecÃÃo precoce do cÃncer de mama. Os dados foram organizados em tabelas e grÃficos. O estudo foi aprovado pelo Comità de Ãtica e Pesquisa da Universidade Federal do Cearà (COMEPE/UFC) com o protocolo de n 1.233.383/15. Quanto ao perfil dos enfermeiros, verificou-se que a maioria pertence a uma faixa etÃria de 30 a 49 anos, sendo 92,6% do sexo feminino, 62,3% entre 10 a 20 anos de graduado e 82,1% sÃo especialistas, 75,4% atua hà mais de 5 anos na ESF e 60,3% tem alguma capacitaÃÃo sobre a temÃtica. Em relaÃÃo ao conhecimento dos enfermeiros, a maioria (46,7%) foi classificada como regular, (41,8%) como inadequado e apenas (11,5%) apresentaram um conhecimento adequado. Quanto à atitude e à prÃtica, observou-se que (73,8%) apresentaram uma atitude adequada e a maioria (57,4%) resultou em uma prÃtica inadequada. Apesar das associaÃÃes entre conhecimento, atitude e prÃtica nÃo terem alcanÃado uma relevÃncia estatÃstica, sabe-se da influÃncia do conhecimento na percepÃÃo do valor em adotar medidas de prevenÃÃo à saÃde (atitude), na transformaÃÃo e desenvolvimento de habilidades pessoais (prÃtica) para a conquista da promoÃÃo da saÃde. Frente ao exposto, a falta de conhecimento, das atitudes e prÃticas inadequadas à detecÃÃo precoce do cÃncer de mama revelam a necessidade de capacitaÃÃo permanente dos profissionais envolvidos no controle do cÃncer de mama.
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40

Benton, Gabriel Jon. "Laminin-1 mediates epigenetic control of the epithelial cadherin for breast cancer cells in three-dimensional culture". Connect to Electronic Thesis (CONTENTdm), 2010. http://worldcat.org/oclc/525216707/viewonline.

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41

Montagner, Marco. "Role of TGFbeta and mutant-p53 in metastasis control". Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3425933.

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TGFbeta ligands act as tumor suppressors in early stage tumors but are paradoxically diverted into potent prometastatic factors in advanced cancers. The molecular nature of this switch remains enigmatic. Here we show the workings of a previously undescribed pathway by which TGFbeta fosters cell migration, invasion and metastasis. We found that TGFbeta, together with oncogenic Ras and mutant-p53, but notably neither of these factors alone, is required for the assembly of a mutant- p53/Smad biochemical complex that binds p63, antagonizing its antimetastatic properties. In vitro, mutant-p53 is required to empower TGFbeta-dependent invasion and migration and p63 is epistatic for these effects. Mechanically, Smad proteins bridge mutant-p53 to p63, allowing the former to inhibit the DNA binding of the latter, blocking the transcriptional activation of its downstream targets. In vivo, loss-of-mutant-p53, or gain-of p63, disables TGFbeta-driven metastatic spread. Conversely, inhibition of p63 transforms noninvasive cells into motile-invasive cells. By transcriptomic analyses, functional validation and clinical verification we found two novel candidate metastasis suppressor genes downstream of this pathway associated with metastasis risk in a large cohort of breast cancer patients. Together, these results support a model in which the combination of two common oncogenic lesions, mutant-p53 and Ras, selected in early neoplasms to promote growth and survival, also prefigure a cellular set-up with particular metastasis proclivity. This trait can be exploited later during progression to drive a metastatic switch, once cells gain access to high levels of TGFbeta, either autonomously produced or extracted from the microenvironment.
I ligandi della famiglia TGFbeta agiscono come oncosoppressori nei primi stadi della tumorigenesi, ma paradossalmente sono mutati in fattori prometastatici nei tumori avanzati. La natura molecolare di questo cambiamento rimane enigmatica. In questo lavoro presentiamo il funzionamento di una via di segnale mai caratterizzata attraverso cui TGFbeta stimola la migrazione cellulare, l’invasione tumorale e la metastasi. Abbiamo scoperto che TGFbeta, assieme a p53 mutante e ad un’attivazione aberrante di Ras, è richiesto per l’assemblamento di un complesso biochimico p53-mutante/Smad, che lega p63, antagonizzando la sua attività anti-metastatica. Questo fenomeno non si osserva con nessuno dei tre fattori singolarmente. In vitro, p53 mutante è richiesta per permettere una migrazione cellulare indotta da TGFbeta e p63 è epistatica a questo effetto. Meccanicisticamente, le proteine Smad fanno da ponte tra p53 mutante e p63, consentendo alla prima di bloccare il dominio di interazione al DNA della seconda, inibendo in questo modo l’attivazione trascrizionale dei geni bersaglio. In vivo, la perdita di p53 mutante, o l’acquisto di p63, disattivano la diffusione metastatica promossa da TGFbeta. Dall’altra parte, l’inibizione di p63 trasforma cellule non invasive in invasive. Per mezzo di analisi del trascrittoma, validazione funzionale e clinica abbiamo scoperto due nuovi geni soppressori delle metastasi che agiscono a valle di questa cascata di eventi e che sono associati a rischio di metastasi in una significativa coorte di pazienti con cancro alla mammella. Sommati, questi risultati supportano un modello in cui la combinazione di due lesioni oncogeniche frequenti, p53 mutante e Ras, selezionate negli stadi precoci dei tumori per promuovere la sopravvivenza e la crescita, favoriscano uno scenario con una particolare tendenza alla metastasi. Questo tratto può essere sfruttato successivamente durante la progressione tumorale per indurre un comportamento metastatico, una volta che le cellule entrano in contatto con alti livelli di TGFbeta prodotto autonomamente o dall’ambiente circostante.
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42

Sharpe, Colin R. "Population-based case-control study of the effects of nonsteroidal antiinflammatory drugs on the risk of breast cancer". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ64666.pdf.

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43

Шевченко, Володимир Володимирович, Владимир Владимирович Шевченко, Volodymyr Volodymyrovych Shevchenko, Володимир Порфирович Шевченко, Владимир Порфирьевич Шевченко, Volodymyr Porfyrovych Shevchenko, V. I. Konanihin i M. I. Solodchenko. "Results of using of octreatide on control of lymphorrhea after modified radical mastectomy (madden) in breast cancer patients". Thesis, Sumy State University, 2014. http://essuir.sumdu.edu.ua/handle/123456789/36581.

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Breast cancer remains the most common cancer diagnosed in women. Axillary lymph node dissection is necessary part of modified radical mastectomy (MRM). Lymphorrhea (LR) and seroma formation are disabling and serious complications of axillary lymphadenectomy. When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/36581
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44

Mokhtar, Noor Fatmawati. "Pharmacological studies of voltage-gated sodium channel expression in human breast cancer cells : control of metastatic cell behaviours". Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/7119.

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The overall aim of this PhD was to improve our understanding, including the clinical potential, of neonatal Nav1.5 (nNav1.5) expression in human metastatic breast cancer. Mainly, the strongly metastatic MDA-MB-231 cells were used throughout the studies. The specific aims were threefold, as follows: 1) To test the effects of several types of voltage-gated sodium channel (VGSC) blocker on nNav1.5 mRNA and protein expression and metastatic cell behaviours (MCBs); (2) to determine the effects of hypoxia on the drug treatments and MCBs; and (3) to elucidate a possible association of carbonic anhydrase-9 (CA9) and nNav1.5 expression/activity. There are three main Results chapters. Results-1 demonstrates the effects of the drugs on MCBs of MDA-MB-231 cells under normal oxygen level (normoxia). Two classes of blocker were used: a) Local anaesthetics (lidocaine and procaine) and (b) blockers of persistent current (INaP) (ranolazine and riluzole). In addition, a specific VGSC blocker, tetrodotoxin (TTX), was incorporated as a control. At concentrations not affecting the cells‘ viability or proliferative activity, 24 h treatment with all the drugs tested significantly reduced MCBs (lateral motility, transverse migration and Matrigel invasion). Concurrently, the treatments reduced nNav1.5 mRNA and protein levels. TTX had a similar effect. Overall, this chapter showed (i) that MCBs in MDA-MB-231 cells were enhanced by VGSC activity and (ii) that INaP played a significant role in the enhancement. Results-2 shows that viability and proliferative activity of MDA-MB-231 cells were not affected by hypoxia (mostly 2 % oxygen applied for 24 h). However, hypoxia increased the cells‘ invasiveness and this was accompanied by upregulation of HIF-1α (protein), nNav1.5 (mRNA) and CA9 (both mRNA and protein). Treatment for 24 h with INaP blockers; ranolazine and riluzole under hypoxia reduced lateral motility, transverse migration and Matrigel invasion. At concentrations not affecting cell viability and proliferation, the effects of ranolazine and riluzole in suppressing MCBs were generally greater under hypoxia compared to normoxia. It was concluded (i) that hypoxia enhanced VGSC-mediated MCBs and (ii) that the enhancements were likely to be increase in INaP amplitude induced by hypoxia. Results-3 examined a possible functional link between hypoxia (HIF-1α and CA9) and VGSCs. Acetazolamide was used as a general inhibitor of CAs and siRNA was used to silence specifically CA9. Under hypoxia, treatment with acetazolamide for 24 h had no effect on invasion, and treatment with TTX was without effect on CA9 expression. In contrast, silencing CA9 using siRNA (siCA9) reduced CA9 and nNav1.5 expression and Matrigel invasion was also significantly inhibited. It was concluded (i) that CA9 played a role in cellular invasion and (ii) that nNav1.5 was down-stream to CA9 in the control of MCBs. The Thesis is concluded with a General Discussion and Conclusion chapter integrating the findings and highlighting their clinical potential.
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45

Penney, Rosalind B. "Thioredoxin and Jab1 Control Estrogen- and Antiestrogen-Mediated Progression of the Cell Cycle Through p27 Interactions". FIU Digital Commons, 2011. http://digitalcommons.fiu.edu/etd/380.

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A major problem with breast cancer treatment is the prevalence of antiestrogen resistance, be it de novo or acquired after continued use. Many of the underlying mechanisms of antiestrogen resistance are not clear, although estrogen receptor-mediated actions have been identified as a pathway that is blocked by antiestrogens. Selective estrogen receptor modulators (SERMs), such as tamoxifen, are capable of producing reactive oxygen species (ROS) through metabolic activation, and these ROS, at high levels, can induce irreversible growth arrest that is similar to the growth arrest incurred by SERMs. This suggests that SERM-mediated growth arrest may also be through ROS accumulation. Breast cancer receiving long-term antiestrogen treatment appears to adapt to this increased, persistent level of ROS. This, in turn, leads to the disruption of reversible redox signaling that involves redox-sensitive phosphatases and protein kinases and transcription factors. This has downstream consequences for apoptosis, cell cycle progression, and cell metabolism. For this dissertation, we explored if altering the ROS formed by tamoxifen also alters sensitivity of the drug in resistant cells. We explored an association with a thioredoxin/Jab1/p27 pathway, and a possible role of dysregulation of thioredoxin-mediated redox regulation contributing to the development of antiestrogen resistance in breast cancer. We used standard laboratory techniques to perform proteomic assays that showed cell proliferation, protein concentrations, redox states, and protein-protein interactions. We found that increasing thioredoxin reductase levels, and thus increasing the amount of reduced thioredoxin, increased tamoxifen sensitivity in previously resistant cells, as well as altered estrogen and tamoxifen-induced ROS. We also found that decreasing levels of Jab1 protein also increased tamoxifen sensitivity, and that the downstream effects showed a decrease p27 phosphorylation in both cases. We conclude that the chronic use of tamoxifen can lead to an increase in ROS that alters cell signaling and causing cell growth in the presence of tamoxifen, and that this resistant cell growth can be reversed with an alteration to the thioredoxin/Jab1 pathway.
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46

Espejo, Herrera Nadia Carminia 1983. "Nitrate exposure and cancer risk : evidence from European case-control studies". Doctoral thesis, Universitat Pompeu Fabra, 2015. http://hdl.handle.net/10803/323894.

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Ingested nitrate is a precursor of N-nitroso compounds that are carcinogens in animals, with limited evidence in humans. The main objective of this thesis was to evaluate whether the exposure to nitrate through drinking water and diet is associated with carcinogenic effects in humans. This thesis has been conducted in the Centre for Research in Environmental Epidemiology (CREAL) from 2011 to 2015, under the supervision of Cristina M. Villanueva Belmonte PhD. The results of this thesis consists of a compilation of four scientific papers including: a) a descriptive study of nitrate levels in drinking water in Spain (paper I), and b) three large European case-control studies evaluating the risk of prevalent tumors (bladder, breast and colorectal) associated with nitrate exposure through drinking water and diet (papers II, III and IV). This document also includes a general introduction, a description of the methodology, an overall discussion of the results, conclusions and an appendix section.
El nitrato ingerido es un precursor de compuestos N-nitroso, que son carcinógenos en animales, con poca evidencia en humanos. El objetivo principal de esta tesis fue evaluar si la exposición a nitrato a través del agua de consumo y la dieta está asociada a efectos carcinogénicos en humanos. Esta tesis fue llevada a cabo en el Centro de Investigación en Epidemiología Ambiental (CREAL) entre 2011 y 2015, bajo la supervisión de Cristina M. Villanueva Belmonte PhD. La parte principal de esta tesis es una compilación de cuatro artículos científicos, que incluyen: a) un estudio descriptivo de los niveles de nitrato en agua de consumo en España (artículo I) y b) tres estudios caso-control que evaluaron el riesgo de tres tumores prevalentes (vejiga, mama y colorrectal), asociados con la exposición a nitrato a través del agua de consumo y la dieta (artículos II, III and IV). Este documento incluye también una introducción general, una descripción de los métodos, una discusión y conclusiones generales y una sección de anexos.
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47

Harris, Neil S. "Characterization of a polypeptide factor that inhibits the growth of a human breast cancer line in vitro". Master's thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/25852.

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This thesis concerns a melanoma-derived growth regulatory factor that inhibited proliferation of several malignant human cell lines, and, in particular, a line designated UCT-BR-1, which was derived from a human breast cancer metastasis. The work is presented in four chapters. Chapter 1 provides a review of the relevant literature at the time of writing; Chapters 2 and 3 describe the experimental work that was done; and in Chapter 4 I discuss the implications of my results for current and future work in growth factors. Experimental results are presented as Charts (which may be Figures or Tables) and the methods and experimental protocols that I used are described in the Chart legends and not in the main text of the thesis. The Appendix contains details of the tissue culture techniques and descriptions of the cell lines that were used. Sources of the various laboratory materials as well as the methods that were employed for the more routine procedures are also described in the appendix.
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48

Weber, Amy S. "Examining the relationship between female breast cancer survivor's diagnosis factors, perceived social support, internal control, and quality of life". University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1383644235.

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49

Heimdahl, Maria, i Eva Johansson. "Information inför mammografi som hälsokontroll". Thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-225273.

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Bakgrund: I Sverige inbjuds alla kvinnor i åldern 40 till 74 år regelbundet till mammografi som hälsokontroll. Undersökningen är frivillig och syftet är att minska dödligheten i bröstcancer. För att kvinnor ska kunna fatta ett välgrundat beslut om att medverka vid mammografi som hälsokontroll eller inte, bör informationen vara relevant och sanningsenlig. Evidensbaserad information som beskriver både för- och nackdelar med mammografi som hälsokontroll är därför av stor vikt. Syftet: Syftet med denna studie var att undersöka innehållet i den information som skickas till kvinnor i Sverige i samband med kallelsen till mammografi som hälsokontroll. Metod: Studien var av deskriptiv design med en kvantitativ och kvalitativ ansats. Kallelser som skickas till kvinnor inför sin mammografi som hälsokontroll, samlades in från alla mammografimottagningarna i Sverige som bedriver mammografi som hälsokontroll. Resultat: Studien visade tydligt att de allra flesta kallelser som skickas till kvinnor i Sverige inför mammografi som hälsokontroll saknade information som beskriver både för- och nackdelar med mammografiscreening. De flesta kvinnor i Sverige får allmän information och till viss del information som betonar fördelarna med mammografiscreening. Beträffande nackdelar med mammografi som hälsokontroll saknades den informationen i de allra flesta kallelser. Slutsats: De flesta kvinnorna i Sverige får inte relevant evidensbaserad information inför sin mammografi som hälsokontroll.
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50

Lenz, Sarah K. "A population-based, case-control study of breast cancer and alcohol consumption among postmenopausal women living in Montreal, Quebec, Canada /". Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31258.

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In the present population-based, case-control study of incident, postmenopausal breast cancer, we obtained an extensive history of alcohol consumption. Indices reflecting age-specific exposure, duration and cumulative exposure of alcohol were developed for specific types of alcoholic beverages as well as the combination of these beverages. Unconditional logistic regression, within the context of the Generalized Additive Models, was used to estimate adjusted odds ratios (OR) and 95% confidence intervals (CI). Case subjects included all new histologically-confirmed cases of malignant breast cancer among postmenopausal women, age 51--75 years, diagnosed or treated in 1996 and 1997 in all major hospitals in Montreal. Control subjects were selected randomly from other histologically-confirmed sites of cancer from the same hospitals as the cases. The response rate was 82% for cases and 75% for controls. Current drinkers of any kind of alcohol were at an increased risk of breast cancer (OR = 1.47; 95%CI: 1.01--2.15). In particular, the risk of breast cancer was increased by 1.6-fold among weekly and current exclusive drinkers of wine. Other factors suggestive of an increased risk of breast cancer include early-age at first consumption of alcohol (≤30 years old) and increased number of years (>15 years) of consuming wine among women who only drank wine. We did not find, however, monotonically increasing risks with levels of consumption. Although, the associations found were relatively weak, our findings provide further support for a positive association between the risk of breast cancer and alcohol consumption, particularly wine.
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