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1
Dadvar, Ehsan. "Characterization of cancer/testis antigen MAGE-A11 for immunotherapy of prostate cancer." Master's thesis, Université Laval, 2014. http://hdl.handle.net/20.500.11794/26789.
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Les antigènes testiculaires du cancer sont des cibles idéales pour l’immunothérapie du cancer car ce sont des protéines immunogéniques dont l’expression est restreinte aux cellules germinales et au cancer. Le but de cette étude est d’évaluer le potentiel de MAGE-A11, un antigène testiculaire du cancer, comme cible pour développer un vaccin contre le cancer de la prostate. Pour ce faire, l’anticorps monoclonal 5C4 qui a la capacité de reconnaître la présence de MAGE-A11 dans les tissus fixés et inclus en paraffine a été produit. De plus, l’expression de MAGE-A11 a été analysée sur plusieurs lignées de cellules cancéreuses. Il a été démontré que MAGE-A11 est exprimé dans plusieurs types de cancers notamment dans le cancer du côlon et du cerveau. Finalement, nous avons identifié trois épitopes du CMH classe II HLA-DR1 dans la protéine MAGE-A11 confirmant ainsi l’immunogénicité de cet antigène et son potentiel comme cible pour l’immunothérapie du cancer.<br>Cancer/testis antigens are ideal targets for cancer immunotherapy because of their limited expression in normal tissues, aberrant expression in malignancies and their immunogenic properties. The aim of this study was to evaluate the potential of cancer/testis antigen, MAGE-A11, as an immunotherapeutic target for development of a prostate cancer vaccine. To accomplish this, we produced the monoclonal antibody 5C4 that is capable of recognizing MAGE-A11 in formalin-fixed paraffin-embedded tissues. We also investigated the expression of MAGE-A11 in a wide variety of cancer cell lines to determine the scope of its expression in cancer. It was shown that MAGE-A11 is widely expressed in malignancies. The highest MAGE-A11 expression was observed in colon cancer and astrocytoma brain tumors. Finally, we identified three naturally processed MHC class II HLA-DR1 epitopes in MAGE-A11 protein, thus confirming its immunogenicity and its potential as a target for cancer immunotherapy.
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Bergeron, Marie-Ève. "Effet de la cryptorchidie sur le transcriptome testiculaire humain." Master's thesis, Université Laval, 2012. http://hdl.handle.net/20.500.11794/23010.
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Les niveaux d’expression de nombreux gènes peuvent être affectés par l’environnement et mener au développement de la cryptorchidie. Cette malformation congénitale est la plus commune dont une des conséquences majeures est l’infertilité masculine due au testicule non-descendu, auquel un risque plus élevé de cancer testiculaire est associé. L’expression des ARN totaux isolés à partir de biopsies testiculaires ont été analysés par micropuces, puis par une analyse bio-informatique et une validation par RT-qPCR de plusieurs gènes sélectionnés. Ces analyses m’ont permis d’identifier plus de deux milles candidats montrant une expression différente entre des sujets cryptorchides et normaux. Certains de ces gènes sélectionnés peuvent être associés à la descente testiculaire, d’autres au cancer testiculaire ou encore aux divers types cellulaires retrouvés dans cet organe. Les différences dans le transcriptome dues à la cryptorchidie vont nous aider à comprendre la cause génétique de cette maladie.<br>Expression level of numerous genes may be affected by environmental condition and lead to development of cryptorchidism. The most common congenital malformation in male is cryptorchidism. One major consequence of this anomaly is infertility due to undescended testis, to which an increased risk of testicular cancer is associated. Expression of total RNAs isolated from testicular biopsies were analysed with microarray. This was followed by subsequent bioinformatic analysis and RT-qPCR validation of many highlighted genes. Those analyses allowed me to identified more than two thousand genes that showed a differential expression between normal and cryptorchid subjects. Among these highlighted and validated genes, some can be either associated to testicular descent, to testicular cancer, or to specific cell types in testes. Differences in transcriptome due to cryptorchidism should give us clues to identify the genetic causes of this malformation.
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Hoa, Annie. "Epidémiologie du cancer du testicule." Montpellier 1, 1991. http://www.theses.fr/1991MON11224.
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Mings, Christopher. "Athletic Trainers' Knowledge and Perceptions of Testicular Cancer and Testicular Cancer Prevention Practices." Honors in the Major Thesis, University of Central Florida, 2014. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/1623.
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Context: Collegiate male athletes have a higher risk of testicular cancer due to their age group, an increased risk of testicular contusions, and a lack of secondary prevention education. As the athletic training profession increases emphasis on evidence-based practice, it is important for athletic trainers to understand testicular cancer and testicular-self examination as it is outlined within their scope of practice. A general understanding of testicular cancer and the prevention techniques will be important for athletic trainers to promote awareness and health behavior practices. Objective: To examine the athletic trainers' actual knowledge, concern, perceived responsibility, training, feeling of embarrassment, and professional/personal practices. Design: Cross sectional survey. Participants: 249 randomly selected athletic trainers employed in collegiate settings. 65.6% of the respondents reported being between the ages of 21 and 35 years old. Intervention: Actual knowledge, concerned, perceived responsibility, trained, embarrassed, and personal and professional practice behavior scores served as dependent variables. Main Outcome Measures: A Pearson correlation coefficient was calculated between participants' actual knowledge, perceived responsibility, and concerned scores. Two one-way MANOVAs were conducted to determine if there was a difference in actual knowledge, perceived responsibility, and concerned scores that was dependent upon participants' age and gender. Results: Athletic trainers in collegiate settings had a fairly high actual knowledge of testicular cancer (X=7.62[plus or minus]1.42 out of 10). Athletic trainers reported that they should be concerned about testicular cancer in male athletes (X=7.26[plus or minus].167 out of 10). Athletic trainers had a low feeling of responsibility suggested by their reported score (X=3.93[plus or minus]0.18 out of 10). A weak correlation (r(169)=.199, P[less than].009) was found between the actual knowledge and perceived responsibility scores, and between the actual knowledge and concerned scores (r(169)=.285, P[less than]<.001). A medium to strong correlation (r(169)=.486, P[less than].001) was found between the concerned and perceived responsibility scores. Athletic trainers reported a decreased feeling of training about testicular cancer and testicular selfexamination (X=2.28[plus or minus]2.10 out of 10). Also, athletic trainers reported (X=2.71[plus or minus]2.42 out of 10) that they were not embarrassed to discuss testicular cancer. Athletic trainers reported performing either a testicular self-exam or breast-self examination on themselves (X=76%). Conclusions: College athletic trainers have a low feeling of embarrassment, adequate knowledge, and a high feeling of concern regarding testicular cancer, but report a low feeling of perceived responsibility and training.<br>B.S.<br>Bachelors<br>Health Professions<br>Health and Public Affairs<br>Athletic Training
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Falcou, Magali. "Métastases testiculaires du cancer de la prostate : à propos d'un cas et revue de la littérature." Montpellier 1, 1988. http://www.theses.fr/1988MON11037.
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Lutke, Holzik Martijn Frederik. "Genetic predisposition to testicular cancer." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2007. http://irs.ub.rug.nl/ppn/304254797.
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Tuinman, Marrit Annika. "Surviving testicular cancer relationship aspects /." [S.l. : Groningen : s.n. ; University Library of Groningen] [Host], 2008. http://irs.ub.rug.nl/ppn/.
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Calvary, Ronan. "Les tumeurs bilatérales consécutives du testicule : à propos de 7 observations, réflexions sur le carcinome in situ." Bordeaux 2, 1996. http://www.theses.fr/1996BOR2M093.
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Le, Cornet Charlotte. "Évolution du cancer du testicule en Europe : expositions environnementales et professionnelles." Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10277/document.
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Les tumeurs germinales du testicule (TGT) représentent le cancer le plus fréquent chez les hommes Européens âgés de 15 et 39 ans. L'incidence a doublé dans la plupart des pays Européens depuis 30 ans. Cette augmentation rapide, les variations géographiques d'incidence et les études chez les populations migrantes suggèrent un rôle des facteurs environnementaux dans le développement des TGT. Cette thèse propose de contribuer à l'amélioration des connaissances concernant l'évolution du TGT en clarifiant l'impact des expositions environnementales et professionnelles, notamment pendant la période prénatale. Les objectifs principaux sont de: 1. Prédire l'incidence du TGT jusqu'en 2025 en estimant la part d'augmentation due aux changements démographiques afin d'obtenir une estimation de l'augmentation due aux risques. 2. Faire un bilan de l'état des connaissances sur l'association entre les expositions environnementales et professionnelles et le développement du TGT dans une revue systématique de littérature 3. Investiguer l'association entre l'exposition parentale professionnelle aux pesticides en période prénatale et le TGT parmi la descendance Les résultats montrent que l'incidence du TGT continue d'augmenter, mettant en avant un fort impact environnemental dans l'évolution du TGT. Néanmoins, la revue de littérature ne permettait pas d'identifier de facteurs de risque environnementaux avérés, mais montrait un manque d'études investiguant les expositions prénatales sur le risque de TGT. L'étude NORD-TEST menée sur les données de registre de quatre pays nordiques est l'étude la plus puissante à ce jour et ne montre aucune association entre l'exposition parentale professionnelle aux pesticides en période prénatale et le TGT<br>Testicular germ cell tumours (TGCT) are the most common cancer diagnosed among young European men aged between 15 and 39 years. TGCT incidence rates have doubled in most European countries over the last 30 years. This rapid increase in incidence, the geographical variations and the studies in migrant populations suggest a role of environmental factors in TGCT aetiology. This thesis aims to contribute to the knowledge of TGCT evolution by studying the impact of environmental and occupational exposures, especially during the prenatal period. The objectives are: 1. To estimate the proportion of the increased incidence due to overall changes in risk patterns compared to the proportion due to demographic changes, by predicting the future testicular cancer trends in Europe 2. To summarize and evaluate the current knowledge on environmental and occupational exposures related to TGCT risk by means of a systematic literature review 3. To investigate the association between the prenatal parental occupational exposure to pesticides and TGCT risk in the offspring. The results show that the TGCT incidence continues to increase, supporting an environmental impact on TGCT evolution. From the epidemiological literature to date no specific environmental risk factors emerge; however, there have clearly been a lack of studies investigating prenatal exposures on TGCT risk. The NORD-TEST study, based on registry data from four Nordic countries, is the largest study to date. No association was found between parental occupational exposure to pesticides during prenatal period and TGCT risk
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Aguilar, Roberto III. "Development of A Testicular Cancer Vaccine." Cleveland State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=csu1461270103.
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Garner, Michael J. "Dietary risk factors for testicular cancer." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/26333.
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Although testicular cancer is a relatively rare cancer in Canada, accounting for only 1.1% of all malignant neoplasms in males, it is the most common cancer among men 20 to 45. Understanding of the causes of testicular cancer risk in general, and the association with diet in particular, remains limited. Data from the National Enhanced Cancer Surveillance System were used to explore the relationship of diet and testicular cancer risk. There were 601 cases of testicular cancer and 744 controls available for study. We systematically examined 17 food groups, 15 nutrients, and 7 individual foods based on data collected through a 69-item food-frequency questionnaire. Our results suggest that higher dairy product intake, specifically cheese, is associated with a higher risk of testicular cancer in Canadian males. Risk differences were observed between histological subtypes of testicular cancer. This thesis provides a basis for future studies designed to address testicular cancer etiology.
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QUESNEL, THIERRY. "Contribution a l'etude des tumeurs bilaterales du testicule : a propos de 9 cas originaux et d'une revue de la litterature." Lyon 1, 1988. http://www.theses.fr/1988LYO1M085.
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Drianno, Nicolas. "Le traitement des tumeurs non séminomateuses du testicule stade I : à propos de 22 cas : analyse et revue de la littérature." Montpellier 1, 1996. http://www.theses.fr/1996MON11043.
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Lakhdari, Nadjem. "Programmation néonatale de l’infertilité mâle : rôle de la dérégulation de l’expression des microARNs dans l’apoptose des cellules germinales." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T096/document.
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Un certain nombre d’études épidémiologiques font état d’une augmentation de l’infertilité masculine durant ces cinquante dernières années, en particulier dans les pays industrialisés, mais aussi d’une augmentation des malformations de l’appareil reproducteur masculin telles que la cryptorchidie (absence de migration des testicules dans les bourses) ou l’hypospadias (malformation du pénis), et des cancers testiculaires. Des données expérimentales suggèrent que ces anomalies du tractus génital mâle sont liées. Ces symptômes forment le syndrome de dysgénésie testiculaire. Les causes d’apparition ce syndrome semblent être d’origine environnementale. En effet, les évolutions relativement rapides de ce syndrome suggèrent des facteurs dynamiques, en lien avec le mode de vie ou l’environnement. Une des hypothèses est que, l’exposition durant la vie fœtale ou néonatale à des composés présents dans l’environnement capables d’interférer avec le système hormonal (perturbateurs endocriniens environnementaux, PEEs), serait responsable de l’augmentation de l’incidence de ces pathologies. Au banc des principaux accusés, les molécules qui possèdent des activités de type estrogénique ou antiandrogénique. A ce jour, les mécanismes d’action à l’origine du syndrome de dysgénésie testiculaire sont encore mal connus. Certaines études suggèrent des mécanismes de type épigenétique dans les effets à long terme des PEEs. L’objectif de notre travail était d’identifier et caractériser les mécanismes d’action de type épigenétique impliqué dans l’infertilité mâle. Pour cela, nous avons utilisé un modèle expérimental (rats nouveau-nés) reposant sur une exposition développementale à un estrogène (estradiol benzoate). Ce modèle induit chez le rat adulte un phénotype d’hypospermatogenèse liée à une à apoptose chronique des cellules germinales testiculaires. Nous montrons que ce phénotype est lié à l’altération de deux voies, impliquant en amont des effecteurs épigénétiques. La première voie implique la famille des miR-29s. Ainsi, nous observons une augmentation de l’expression des miR-29a, b, c qui provoque une diminution de deux de ses cibles: la protéine antiapoptotique MCL-1 et les enzymes de méthylation de l’ADN DNMTs. La chute des DNMTs entraine une hypométhylation globale (estimée à travers le gène Line-1) et spécifique du facteur de choc thermique HSF1. Ceci provoque une réexpression de ces facteurs entrainant l’apoptose des cellules germinales adultes. La deuxième voie implique le miR-18a. L’augmentation de son expression provoque une chute de l’expression de sa cible HSF2 qui régule la protéine de choc thermique HSP70/HSPA2. Le faible taux d’HSPA2 est une autre explication de l’apoptose des cellules germinales dans notre modèle. Nous montrons aussi que ce phénotype est irréversible lorsque l’exposition à lieu chez le nouveau-né alors qu’il est réversible quand l’exposition à lieu à l’âge adulte. Ces données suggèrent que l’exposition néonatale à l’estradiol benzoate induit une programmation développementale de l’hypospermatogenèse.Enfin, les anomalies tissulaires d’expression des miRNAs se retrouvent au niveau sanguin, suggérant leur utilisation potentielle comme biomarqueurs. Nous avons validé cet aspect chez l’homme en montrant que l’expression des miR29s et du miR-18a était plus élevée chez les patients oligo- ou azoospermiques que les chez patients normospermiques.En conclusion, nos résultats indiquent que l’hypospermatogenèse due à une apoptose chronique des cellules germinales observée chez l’animal adulte après exposition néonatale à l’EB met en jeu une modification d’expression de plusieurs effecteurs épigénétiques clés: miR-29s, miR-18a et DNMTs. De plus, les miR-29s et miR-18a pourraient être de nouveaux biomarqueurs circulants non invasifs de la stérilité masculine dans le contexte d’une oligo ou azoospermie chez l'homme<br>Epidemiological studies have reported an increase in male infertility over the past fifty years, especially in industrialized countries, but also an increase in malformations of the male reproductive tract such as cryptorchidism (no migration of the testes into the scrotum) and hypospadias (malformation of the penis), and testicular cancers. Experimental data suggest that these abnormalities of the male genital tract are related. These symptoms form the testicular dysgenesis syndrome. The causes of the occurrence of this syndrome appear to be environmental in origin. Indeed, the relatively rapid evolution of this syndrome suggests dynamic factors related to lifestyle or environment. One hypothesis is that exposure during fetal or neonatal life to compounds present in the environment can interfere with the hormonal system (environmental endocrine disruptors), would be responsible for the increased incidence of these pathologies. Bench of the main accused, molecules that have estrogenic or anti-androgenic activity types. To date, the mechanisms of action behind the testicular dysgenesis syndrome are poorly understood. Some studies suggest that epigenetic mechanisms are at playThe objective of our work was to identify and characterize the epigenetic mechanisms of action involved in male infertility induced by neonatal exposure to xenoestrogen. For this, we used an experimental model based on a developmental exposure to estrogen (estradiol benzoate). This model induced in adult rats a hypospermatogenesis phenotype due to chronic apoptosis of germ cells.We show that this phenotype is related to an alteration of two pathways, involving upstream effectors epigenetic. The first pathway involves the family of miR- 29s. Thus, we observe an up-regulation of miR -29a, b, c, which causes a decrease in two of his targets: the anti-apoptotic protein MCL- 1 and the enzymes of DNA methylation DNMTs. Falling DNMTs leads to a global hypomethylation (estimated through the Line -1 gene) and to specific hypomethylation of the heat shock factor, HSF1. This causes a re-expression of factors that induce apoptosis in adult germ cells. The second pathway involves up-regulation of miR -18a that causes a down-regulation of its target HSF2 which regulates the heat shock protein HSP70/HSPA2. The down-regulation of HSPA2 is another explanation of germ cell apoptosis in our model. We also show that this phenotype is irreversible when the estrogen exposure takes place in the newborn whereas it is reversible when exposure takes place in adulthood, suggesting that neonatal exposure to estradiol benzoate induced a developmental programming of hypospermatogenesis.Finally, abnormal tissue expressions of miRNAs are found in the blood, suggesting their potential use as biomarkers. We validated this aspect in humans showing that the expression of miR29s and miR-18a was higher in patients with decrease or no sperm counts compared to normal sperm count. In conclusion, our results indicate that hypospermatogenesis due to chronic germ cell apoptosis observed in adult animals after neonatal exposure to EB involves a change in expression of several key epigenetic effectors: miR-29, miR-18a and DNMTs. In addition, miR-29 and miR-18a could be new non invasive circulating biomarkers of men infertility
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Akre, Olof. "Etiological insights into the testicular cancer epidemic /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3689-7/.
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Lam, Man-Yee Josephine. "Genetic Control of Susceptibility to Testicular Cancer." Case Western Reserve University School of Graduate Studies / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=case1112676217.
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Pee, Barbel Christel Giesela. "Health promotion : social cognitions and testicular self examination." Thesis, University of Surrey, 1997. http://epubs.surrey.ac.uk/844306/.
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Testicular self-examination (TSE) is an important behaviour to prevent the development of testicular cancer. This thesis examined the stages of decision making, emotions, perceived costs and benefits of screening, the self perceptions, social influences, and health routines in samples of adult males and adolescent school boys. A multi-method approach was adopted involving qualitative and quantitative methods of study. The qualitative part of the investigation comprised a series of studies including focus groups, in-depth interviews, programme evaluation and survey studies. The aim was to elucidate the meanings associated with health and illness and preventive cancer screening. Such information formed the bases for developing a survey measure and a health promotion programme to promote TSE. A comparative cross-sectional approach, including the components of three social cognition models was then carried out revealing a hybrid model (HSCM) to be most effective in explaining TSE. Acknowledging traditional social cognitions as predictors of TSE decision making, it also stresses the importance of emotional cognitions, self perceptions and routine behaviours. Using a five-stage model building approach, a longitudinal examination of stages of decision making was also carried out. Logistic analysis revealed that much of the variation in TSE practice was explained by a planning stage, implicating a two-stage motivation and volition stage rather than a five-stage model. In addition to explaining the characteristics associated with TSE practice and elucidating a stage approach to decision making, a draft health promotion programme was developed and evaluated. Two forms of the programme, a booklet and a seminar, were appraised and deemed effective as motivators of preventive action. Findings are discussed in terms of theory and practice of health education. The implications of the findings for health psychology are also discussed.
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LALANNE-BERDOUTICQ, LACAILLE D'ESSE DOMINIQUE. "Les formes familiales du cancer du testicule : a propos d'une serie de 14 cas." Lyon 1, 1990. http://www.theses.fr/1990LYO1M169.
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WILLIAUME, DANIELE. "Fertilite et cancer du testicule : etude clinique a partir des dossiers selectionnes au cecos de rennes (1982-1990)." Rennes 1, 1993. http://www.theses.fr/1993REN1M140.
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Keller, Jean-Michel. "Cancers du testicule stade 1 : à propos de 74 cas." Université Louis Pasteur (Strasbourg) (1971-2008), 1992. http://www.theses.fr/1992STR1M227.
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Roach, Sherry L. "The molecular analysis of the differentiation of human testicular teratocarcinoma." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239291.
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Richiardi, Lorenzo. "New evidence on germ-cell testicular cancer aetiology /." Stockholm, 2003. http://diss.kib.ki.se/2004/91-7349-733-9/.
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Pearce, Hayden. "Understanding the mechanism of cure in testicular cancer." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/5106/.
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The expression of cancer testis antigens (CTAgs) is normally restricted to spermatogenic cells of the testis but is also present in many cancers including testicular germ cell tumours (TGCTs). CTAg-specific T cell responses have been identified in patients with other solid tumours, and here we identified CTAg-specific T cells in TGCT patients. MAGEA-family specific T cell responses were detected in 21/49 patients with a magnitude of up to 0.149% of total peripheral blood mononuclear cells. Responses to multiple MAGEA antigens were frequently detected in seminoma patients irrespective of tumour stage. Conversely, NSGCTT patients only developed responses towards MAGEA3, which were strongly associated with disease progression. Longitudinal analysis revealed that the magnitude of MAGE-specific immune responses diminished over time by up to 95%, which correlated with the removal of tumour antigens. MAGE-specific CD8 T cells demonstrated cytotoxic potential against endogenously presented antigen. Tumour infiltrating T cells were antigen experienced, recently activated, oligoclonal populations; many of which expressed the inhibitory molecules, TIM-3 and PD-1. Proliferation and cytokine secretion was suppressed in vivo but was rescued with in vitro stimulation, indicative of an exhausted T cell phenotype. Our findings have significant implications in the development of novel CTAg-specific immunotherapy in patients with cancer.
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Odhah, M. S. "Cisplatin : Pharmacokinetic and biochemical studies in cancer patients." Thesis, Cardiff University, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372341.
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List, Penelope Anne Denman. "Individual differences associated with adults' self-examination for breast cancer and testicular cancer." Thesis, Keele University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558321.
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Designs and Samples. Four questionnaire-based studies were conducted: one prospective study with 67 adults, followed up at three months; and three cross-sectional studies with sample sizes of 136, 147 and 283. Each study included female and male participants, who were aged 20 or over and lived in Great Britain. Measures. A range of individual differences were measured within the four studies. These included health locus of control beliefs, coping responses, general anxiety, anxiety in relation to health and to performing self-examinations, worry about breast or testicular cancer, perceived breast or testicular cancer risk, dispositional optimism, health optimism, and socially desirable responding. In addition, female participants provided self-reports of their breast self-examination behaviour and in the final study, whether or not they were ‘breast aware’; while male participants gave self-reports of their testicular self-examination behaviour. Results. Multiple regression analyses revealed that worry about breast or testicular cancer and anxiety about performing self-examinations operated as the most consistent independent predictors of self-examination behaviour. In addition, ANCOVAs showed that perceived breast or testicular cancer risk and dispositional optimism were significantly associated with self-examination frequency. Across the four studies, associations between the individual differences and adults’ self-examination behaviour were generally evidenced as being similar for females and males. Utilising data from the final study, a model of individual differences and breast or testicular self-examination behaviour was constructed and proposed. Conclusions. The present research has demonstrated associations between a number of individual differences and breast or testicular self-examination. These findings indicate the potential impact of individual differences on adults’ self-examination behaviour.
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Weir, Hannah Kate. "Endocrine factors and risk of testicular germ cell cancer." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ28312.pdf.
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Mostafa, M. M. I. "Clinical pharmacokinetic studies on cisplatin in testicular cancer patients." Thesis, Cardiff University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380195.
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Wahed, I. A. "Testicular toxicity of standard and investigational anti-cancer drugs." Thesis, University of Bradford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380578.
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Lakhdari, Nadjem. "Programmation néonatale de l'infertilité mâle : rôle de la dérégulation de l'expression des microARNs dans l'apoptose des cellules germinales." Phd thesis, Université Paris Sud - Paris XI, 2013. http://tel.archives-ouvertes.fr/tel-01061771.
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Un certain nombre d'études épidémiologiques font état d'une augmentation de l'infertilité masculine durant ces cinquante dernières années, en particulier dans les pays industrialisés, mais aussi d'une augmentation des malformations de l'appareil reproducteur masculin telles que la cryptorchidie (absence de migration des testicules dans les bourses) ou l'hypospadias (malformation du pénis), et des cancers testiculaires. Des données expérimentales suggèrent que ces anomalies du tractus génital mâle sont liées. Ces symptômes forment le syndrome de dysgénésie testiculaire. Les causes d'apparition ce syndrome semblent être d'origine environnementale. En effet, les évolutions relativement rapides de ce syndrome suggèrent des facteurs dynamiques, en lien avec le mode de vie ou l'environnement. Une des hypothèses est que, l'exposition durant la vie fœtale ou néonatale à des composés présents dans l'environnement capables d'interférer avec le système hormonal (perturbateurs endocriniens environnementaux, PEEs), serait responsable de l'augmentation de l'incidence de ces pathologies. Au banc des principaux accusés, les molécules qui possèdent des activités de type estrogénique ou antiandrogénique. A ce jour, les mécanismes d'action à l'origine du syndrome de dysgénésie testiculaire sont encore mal connus. Certaines études suggèrent des mécanismes de type épigenétique dans les effets à long terme des PEEs. L'objectif de notre travail était d'identifier et caractériser les mécanismes d'action de type épigenétique impliqué dans l'infertilité mâle. Pour cela, nous avons utilisé un modèle expérimental (rats nouveau-nés) reposant sur une exposition développementale à un estrogène (estradiol benzoate). Ce modèle induit chez le rat adulte un phénotype d'hypospermatogenèse liée à une à apoptose chronique des cellules germinales testiculaires. Nous montrons que ce phénotype est lié à l'altération de deux voies, impliquant en amont des effecteurs épigénétiques. La première voie implique la famille des miR-29s. Ainsi, nous observons une augmentation de l'expression des miR-29a, b, c qui provoque une diminution de deux de ses cibles: la protéine antiapoptotique MCL-1 et les enzymes de méthylation de l'ADN DNMTs. La chute des DNMTs entraine une hypométhylation globale (estimée à travers le gène Line-1) et spécifique du facteur de choc thermique HSF1. Ceci provoque une réexpression de ces facteurs entrainant l'apoptose des cellules germinales adultes. La deuxième voie implique le miR-18a. L'augmentation de son expression provoque une chute de l'expression de sa cible HSF2 qui régule la protéine de choc thermique HSP70/HSPA2. Le faible taux d'HSPA2 est une autre explication de l'apoptose des cellules germinales dans notre modèle. Nous montrons aussi que ce phénotype est irréversible lorsque l'exposition à lieu chez le nouveau-né alors qu'il est réversible quand l'exposition à lieu à l'âge adulte. Ces données suggèrent que l'exposition néonatale à l'estradiol benzoate induit une programmation développementale de l'hypospermatogenèse.Enfin, les anomalies tissulaires d'expression des miRNAs se retrouvent au niveau sanguin, suggérant leur utilisation potentielle comme biomarqueurs. Nous avons validé cet aspect chez l'homme en montrant que l'expression des miR29s et du miR-18a était plus élevée chez les patients oligo- ou azoospermiques que les chez patients normospermiques.En conclusion, nos résultats indiquent que l'hypospermatogenèse due à une apoptose chronique des cellules germinales observée chez l'animal adulte après exposition néonatale à l'EB met en jeu une modification d'expression de plusieurs effecteurs épigénétiques clés: miR-29s, miR-18a et DNMTs. De plus, les miR-29s et miR-18a pourraient être de nouveaux biomarqueurs circulants non invasifs de la stérilité masculine dans le contexte d'une oligo ou azoospermie chez l'homme.
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Jaillon, Christine. "Tumeurs germinales non seminomateuses du testicule avec métastases ganglionnaires rétropéritonéales : analyse de 51 patients traités à l'Institut Bergonié et à l'Hôpital Pellegrin et étude des facteurs prédictifs de réponse complète à la chimiothérapie et de fibrose-nécrose des masses résiduelles." Bordeaux 2, 1995. http://www.theses.fr/1995BOR23077.
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Srivastava, Anil. "The relationship of physical activity to risk of testicular cancer." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0003/MQ40724.pdf.
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Jackson, Mark B. "The aetiology of cryptorchidism and its relationship to testicular cancer." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236296.
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Russell, Kathleen Sheridan. "Psychosocial concerns and individual anxieties for fathers with testicular cancer." Thesis, University of East London, 2015. http://roar.uel.ac.uk/4592/.
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The purpose of this qualitative study was to explore the major areas of psychosocial concerns, individual anxieties and coping responses for fathers with testicular cancer. While numerous studies have been carried out with mothers with cancer, research from the perspective of fathers with cancer is sparse. This study attempts to identify and explore their specific concerns and priorities. The study was approved by the Royal Marsden Hospital (RMH) Committee for Clinical Research (CCR) and the Local Research Ethics Committee (LREC). Men were recruited from the RMH Testicular Clinic. All of the men had two or three school age children and were from a range of ethnic backgrounds, professions and education levels. The Biographical Narrative Interpretive Method (BNIM) of interviewing was used and the Interpretative Phenomenological Analysis (IPA) method was employed to analyze the data. Psychodynamic concepts were utilized as the theoretical framework to develop interpretations for each participant. Theories of masculinity were also incorporated. A set of themes emerged which was supported by the current literature. The psychosocial concerns included: lack of adequate medical information, concerns for children and wife and work concerns. The individual anxieties included: concerns around self concepts and masculinity, physical changes and self-image, challenges to faith and finding meaning, fear of recurrence, fear of death and annihilation. The participants employed specific coping responses including: intellectualization, minimizing, maintaining stoic façade and idealization which helped them to cope with the impact of their disease AND allowed them to maintain their sense of masculinity. This phenomenon was labeled “The Masculine Way of Handling Illness”. Additionally, the men split their cancer into the “good one to get”. The findings suggest that men need more reliable information, preferably on a reputable UK site, about talking to their children, the physical effects of treatment and the options of having a prosthesis.
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Sandén, Inger. "Att drabbas av testikelcancer : en studie av män med behandlad testikelcancer och deras anhöriga /." Linköping : Univ, 2000. http://www.bibl.liu.se/liupubl/disp/disp2000/arts217s.htm.
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Hollings, Jerrelee, and Rebecca Zullo. "The Burden of Illness for Inpatient Testicular Cancer in the United States." The University of Arizona, 2010. http://hdl.handle.net/10150/623793.
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Class of 2010 Abstract<br>OBJECTIVES: The purpose of this study was to determine the number of inpatient discharges and burden of illness due to testicular cancer with data from the national database Healthcare Cost and Utilization Project (HCUP).
METHODS: This retrospective study looked at hospital discharge records to obtain information regarding the inpatient burden of illness of testicular cancer patients. The study looked at procedures, co-‐morbidities, hospital characteristics, case-‐mix control, and the Deyo-‐Charlson to see how they were associated with the charges, length of stay, and inpatient mortality. Also included in the study was information regarding patient age, method of payment, and hospital type and size. A linear multivariate regression was performed to estimate determinates of hospital costs.
RESULTS: During the 5-‐year time frame of the study, 28,985 inpatient admissions with testicular cancer were identified. For the overall sample, the average total charges per hospitalization were $29,857. For the 717 patients that died while receiving inpatient treatment, the associated charges averaged $73,800, more than double that associated with the overall sample. The gamma regression of charges for the overall sample showed an association between increased charges and age, length of stay, number of procedures, all admission years in reference to 2002, admission to a large-‐sized hospital in reference to a small hospital, admission to an urban hospital in reference to a rural hospital, admission to a teaching in reference to a nonteaching hospital and the Deyo-‐Charlson score.
CONCLUSIONS: Testicular cancer is on the rise worldwide and is associated with a high inpatient burden of illness.
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Vignal, Rodolphe. "L'autoconservation du sperme dans le cancer du testicule : à propos de 110 patients." Bordeaux 2, 2001. http://www.theses.fr/2001BOR2M007.
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Badcock, Graeme Leslie. "Characterisation of the TRA-1-60 antigen, a marker for testicular germ cell tumours." Thesis, University of Sheffield, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268286.
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Robinson, David S. "Men's experiences of testicular cancer and its treatment : a grounded theory study." Thesis, University of Ulster, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432814.
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Watterson, Jeanette Debbie. "Germline and novel double p53 mutations in canine skin and testicular cancer." Thesis, University of York, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247026.
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GARY, DESRUMAUX CHRISTINE. "Risque de second cancer apres traitement par chimiotherapie pour une tumeur germinale non seminomateuse du testicule." Lille 2, 1993. http://www.theses.fr/1993LIL2M215.
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Chevalier, Nicolas. "GPR30/GPER, récepteur aux estrogènes couplé aux protéines G : un nouvel acteur dans la carcinogenèse germinale testiculaire, impliqué dans l'action des perturbateurs endocriniens environnementaux ?" Nice, 2012. http://www.theses.fr/2012NICE4103.
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Le cancer germinal testiculaire (CGT), cancer le plus fréquent de l’homme jeune, a vu son incidence tripler en cinquante ans. Sa physiopathologie demeure inconnue mais des données épidémiologiques suggèrent le rôle d’une exposition foetale ou périnatale à des perturbateurs endocriniens environnementaux (PEE) à activité estrogénique, associés à des facteurs de prédisposition génétique. Grâce à la lignée séminomateuse humaine (JKT-1), l’estrogéno-dépendance du CGT a été mise en évidence par l’équipe d’accueil en décrivant sur la prolifération des cellules germinales malignes : une voie génomique et mitochondriale via le récepteur classique ER béta exerçant un rôle suppresseur tumoral; et une voie non génomique, via un récepteur membranaire couplé aux protéines G, exerçant un rôle promoteur tumoral. Nous avons pu identifier (antagoniste, siRNA) que ce récepteur membranaire était GPR30/GPER. Localisé à la membrane plasmique dans notre modèle, il est capable de lier, avec une forte affinité, le bisphénol A, un PEE à activité estrogénique, et d’induire la prolifération des cellules séminomateuses humaines. Nous avons pu mettre en évidence que GPR30/GPER est exprimé par les cellules germinales humaines adultes normales et qu’il était surexprimé dans les cellules séminomateuses JKT-1. Cette surexpression a été confirmée dans une collection tumorale multicentrique de séminomes et reliée à deux polymorphismes spécifiques situés dans la région promotrice de GPR30/GPER, qui pourraient constituer un facteur de susceptibilité génétique de CGT, à rechercher chez des patients à haut risque de développer de telles tumeurs. Ces résultats nous amènent à formuler l’hypothèse qu’une surexpression de GPR30/GPER par polymorphismes (et/ou modification épigénétique), associée à l’extinction d’ER béta par modification épigénétique, pourrait être impliquée dans l’action des PEE sur le contrôle de la prolifération germinale maligne et/ou la carcinogenèse testiculaire<br>Testicular germ cell tumours (TGCT) are the most frequent cancer of young men with an increasing incidence all over the world since fifty years. Pathogenesis remains unknown but fetal or perinatal exposure to environmental endocrine disruptor compounds (EDC) with estrogenic affinity, together with genetic susceptibility, have been suggested. Using the JKT-1 cell line, which is derived from a human testicular seminoma, the lab has previously shown that estrogens are involved in human seminoma cell proliferation in vitro through two signalling pathways: the one through nuclear and mitochondrial ER beta, which acts as a tumoural suppressor; the other one through a membrane G protein coupled receptor (GPCR), with a proliferative effect. Using selective antagonist and siRNA, we identified this GPCR as GPR30/GPER, a widely conserved orphan GPCR, which is located at the cell membrane in JKT-1 cells. Bisphenol A, an estrogenic EDC, induces JKT-1 cells proliferation in vitro through GPR30/GPER. GPR30/GPER is expressed both in normal adult and tumoural human germ cells, and selectively overexpressed in seminoma tumours. We demonstrated that this overexpression is associated with two polymorphisms, which are located in the 5’ regulatory region of GPR30/GPER gene. Thus, overexpression of GPR30/GPER due to genetic polymorphisms is involved in testicular carcinogenesis and could be a genetic susceptibility factor of TGCT, which might be screened in high-risk TGCT patients. Both overexpression of GPR30/GPER by genetic polymorphisms (and/or epigenetic modifications) and silencing of ER beta by hypermethylation could also participate in the effects of EDC during the control of malignant germ cell proliferation and/or testicular carcinogenesis
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Sen, Sumitra. "Cellular and Molecular Effects of Mono-(2-ethylhexyl) phthalate (MEHP) in Testicular Cancer." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36844.
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Phthalates are endocrine-disrupting chemicals (EDCs) that are known testicular toxicants, used commonly as industrial plasticizers that are found in everyday items. Di-(2-ethylhexyl) phthalate (DEHP) is the most abundant phthalate in the environment, and its primary metabolite mono-(2-ethylhexyl) phthalate (MEHP) is ten-fold more potent. The purpose of this study is to examine the cellular and molecular effects of MEHP in the development of testicular cancer. Proliferation was measured for NT2 cells exposed to 10µM and 100µM MEHP at 24 and 48 hours and for cells under controlled conditions. Methylation-specific PCR (MSP) was used to determine the methylation status of the promoter region of key testicular genes post exposure to MEHP. MEHP caused a dose-dependent negative effect on proliferation and significantly altered methylation levels for key testicular genes following exposure to 10µM MEHP and 100µM, as compared to controls. This suggests that MEHP alters proliferation and methylation of testicular tumour cells in a time- and dose-dependent manner.
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Colbourne, Linda Claire. "Testicular and prostate cancer : explaining the treatment and post treatment experience of couples." Thesis, University of Southampton, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419165.
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Lodyga, Marc. "The Relationship Between Health Belief Model Constructs and Factors Influencing Cancer Self-Examinations in College Students." OpenSIUC, 2013. https://opensiuc.lib.siu.edu/dissertations/767.
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The purpose of this study is to explore college students' breast and testicular cancer self-examination beliefs and practices using constructs of the Health Belief Model. Over a 1.6 million Americans are diagnosed each year with cancer. With that, over 200,000 women will be diagnosed with breast cancer while nearly 8,000 men will develop testicular cancer. If cancer is diagnosed and treated in the early stages, it will greatly increase the chance of survival and quality of life. One of the easiest methods to discover cancer early is to perform self-examinations. Self-examinations are safe, quick, private, and do not require a visit to the doctor. This study will explain reasons why some college students perform breast (for women) and testicular (for men) self-examinations while others choose not to perform self-examinations. A survey of 386 (202 female and 184 male) college students was conducted at a midsize university located in the Midwest. Participants were asked to complete Champion's Health Belief Model Scale. In addition, participants were asked to complete two open-ended survey questions regarding their self-examinations beliefs and behaviors. Overall, 129 (34%) participants performed self-examinations. Of those 129, females were more likely to perform self-examinations than males. In addition, females were also more likely to be taught how to perform self-examinations. Participants were more likely to perform self-examinations if felt susceptible to developing cancer and if they felt comfortable in their ability to properly perform one. Finally, participants were also more likely to perform self-examinations if they were given a cue to action (i.e. their doctor told them to or a relative had cancer). The significance of the data will help educators and health care professionals develop health programming to address the barriers that keep college students from performing self-examinations. In particular, there needs to be tailored programming for males because they are more susceptible to developing testicular cancer during their college years than any other time in their lives. Finally, a social marketing campaign could be an easy intervention to reach the masses. A Social marketing campaign would be a beneficial way to raise awareness, educate students on cancer in college, and show the simple steps in performing self-examinations.
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Camacho, Moll Maria Elena. "Germ cell neoplasia in situ (GCNIS) and the pathogenesis of testicular germ cell cancer." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28807.
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Testicular germ cell cancer (TGCC) has been increasing in incidence over recent decades, and is currently the most common malignancy amongst young men resulting in significant morbidity. These tumours are believed to arise from premalignant germ cell neoplasia in situ (GCNIS) cells, which originate from the aberrant germ cell differentiation from gonocyte to spermatogonia during fetal/early postnatal life. GCNIS cells remain dormant in the testis until puberty when they are activated to become tumours. Therefore, GCNIS cells remain in a pre-invasive stage during early childhood and early adulthood prior to the development of a seminoma or non-seminoma TGCC. GCNIS cells are phenotypically similar to gonocytes with expression of stem cell/early germ cell markers including OCT4, PLAP and LIN28. Furthermore, proteins which are expressed in more mature germ cells (spermatogonia) such as MAGE-A4 have also been shown to be expressed in GCNIS cells and these studies have indicated that GCNIS cells are a heterogeneous population in terms of protein expression profile. The relationship between the protein expression profile of individual GCNIS cells populations and their oncogenic potential has not been fully explored. GCNIS cells are located in the seminiferous tubules supported by somatic Sertoli cells. These cells have been previously reported to exhibit an immature protein expression profile in GCNIS tubules from patients with testis cancer, suggesting that the germ stem cell niche in GCNIS tubules resembles that of a fetal one. Associations between Sertoli cell maturation and GCNIS progression into tumour formation has not been fully investigated. Oncogenes are key players in the regulation of oncogenic potential of cancer cells. Gankyrin is an oncogene that has been shown to down-regulate OCT4, and interact with MAGE-A4 in hepatocellular carcinoma and colorectal cancer, where Gankyrin interaction with MAGE-A4 reduces the oncogenic potential of tumour cells. In this study I aimed to investigate the heterogeneity of GCNIS in relation to disease stage and Sertoli cell development. We also aimed to determine the role of Gankyrin in TGCC cell survival and invasion. The co-expression of early germ cells proteins such as OCT4, LIN28 and PLAP was characterized in GCNIS cells during childhood and adulthood pre-invasive TGCC and in invasive disease characterized by the presence of a testicular tumour. These results show that LIN28 was expressed in 95% of OCT4 GCNIS cells, whereas PLAP expression in GCNIS cells increased as the disease progressed from childhood pre-invasive disease to invasive seminoma (32.3% v 76%; p < 0.05). In contrast there was a reduction in the proportion of MAGE-A4 expressing GCNIS cells with disease progression. The MAGE-A4 expressing population was also less proliferative than the MAGE-A4 negative GCNIS population. The methylation status of GCNIS cells was then investigated. EZH2 a methyltransferase previously reported to be important for TGCC development, was expressed in GCNIS cells at all stages of disease, however the histone 3 modification H3K27me3 (mediated by EZH2) was expressed in a significantly higher percentage of the proliferative OCT4+/MAGE-A4- GCNIS cells compared with the OCT4+/MAGEA4+ population (11.7% v 1.1%; p < 0.01) which could indicate a repressive role for H3K27me3 over MAGE-A4 expression. Next, it was determined whether an association between Sertoli cell maturation status and progression of TGCC could be observed. The maturation status of Sertoli cells was studied using proteins indicative of immature (desmin, cytokeratin, fibronectin and AMH) and mature (vimentin and androgen receptor) Sertoli cells. These studies demonstrated heterogeneity of Sertoli cells maturation in GCNIS-containing tubules. Desmin, fibronectin, AMH and vimentin expression did not show any association with TGCC progression. Cytokeratin was expressed in Sertoli cells of human fetal testis up to second trimester of fetal life, absent in tubules with active spermatogenesis but heterogeneously present in GCNIS, demonstrating that cytokeratin expression is indicative of the presence of GCNIS. Androgen receptor was weakly present in Sertoli cells from human fetal testis and pre-pubertal pre-invasive TGCC testis whereas in GCNIS of adult pre-invasive testis and invasive samples, androgen receptor was abundantly expressed in Sertoli cells of GCNIS-containing tubules. These combined results for cytokeratin and androgen receptor suggest that Sertoli cells from GCNIS-containing tubules, in pre-invasive and invasive TGCC patients are partially differentiated. Gankyrin expression was characterised in fetal germ cells, GCNIS cells and TGCC tissue. In fetal testis nuclear Gankyrin was absent in OCT4+/MAGE-A4- (gonocyte) population whereas it was present in a subpopulation of OCT4-/MAGE-A4+ (spermatogonia) germ cells. In GCNIS cells from TGCC patients nuclear Gankyrin was expressed in 87%, 63.3%, 91.5% and 79% in childhood pre-invasive, adult pre-invasive, seminoma and non-seminoma GCNIS cells respectively. Finally, in seminoma cells, Gankyrin was expressed in the cytoplasm indicating a change in localisation as the GCNIS cells become invasive. We used siRNA to knockdown Gankyrin in NT2 (a TGCC cell line) cells in-vitro and demonstrated a decrease in cell number, suggesting that Gankyrin might play a role in TGCC progression and invasiveness. Gankyrin down-regulation also resulted in an increase in p53 and p21 mRNA level. Given the role of P53 and p21 in cisplatin cytotoxic effect in TGCC we went on to investigate the role of Gankyrin in cisplatin resistance using NT2 cells. We demonstrate that Gankyrin mediated cisplatin resistance through the p53/p21 pathway, upregulating apoptosis rates through BAX and FAS, whilst there was no effect on cell proliferation, cell cycle or cell migration. In conclusion, we have shown that GCNIS cells are heterogeneous and their phenotype can determine their oncogenic potential. We also show that Sertoli cells from GCNIS-containing tubules undergo partial differentiation displaying markers of immature and mature Sertoli cells, with a heterogeneous association of cytokeratin with GCNIS presence. We also demonstrate that the oncogene Gankyrin has a role in NT2 cells survival and cisplatin resistance indicating that manipulation of Gankyrin may have a role in the treatment of TGCC.
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Wraith, Anita Elizabeth. "The psychological implications of surviving testicular cancer : impact on body image, sexuality and masculinity." Thesis, University of Leeds, 2005. http://etheses.whiterose.ac.uk/455/.
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INTRODUCTION: Men's health generally and testicular cancer in particular are neglected areas of research. This particular malignancy is the most common among young men in the western world (Champion, 1996), and its prevalence is on the increase, however, so too are cure rates. As a consequence there are an increasing number of young male survivors. Impact on sexual function of survivors is well documented in the literature, yet little is mentioned about the impact on the sexuality and masculinity of the young man following treatment. The objective of the research therefore was to explore the impact on survivor's self-perceptions,in particular focusing on the areas of sexuality, masculinity and body image. METHOD: The research followed a cross-sectional design, comparing men at four different stages post-illness. Repertory grid technique was utilised for data collection purposes, which combined qualitative and quantitative methods. Semi-structured interviews (n = 10) were analysed using content analysis, which formed the basis of a generic repertory grid. Quantitative data from subsequent grid completion (n = 37)were analysed using a beta version of SPSS to carry out 3-way 3-mode multidimensional unfolding. RESULTS: The results suggest that men's self-perceptions change as a consequence of testicular cancer, and that sexuality, masculinity and body image play a part in these changes for some, but not all men. The constructs rated in this study all contribute to the differences in patterns across groups. Results suggest the occurrence of an adjustment process, showing current perceptions of the self as more aligned with retrospective pre-illness perceptions by 24 months post-illness. The majority of men judged repertory grid technique to be a satisfactory means of evaluating self-perceptions relating to the illness experience. DISCUSSION: The results of the study have implications for the level of professional support received by men with testicular cancer, both generally and with specific reference to issues of sexuality, masculinity and body image. However the innovative style of this research and the absence of pre-existing evidence in support of the findings, mean that further research will be required to gain a thorough understanding of the psychological implications of surviving testicular cancer with regards to these issues. Specific recommendations are made for further research
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Kaijser, Magnus. "Does cancer originate in utero? : epidemiological evaluation of a hypothesis /." Stockholm : Karolinska Univ. Press, 2002. http://diss.kib.ki.se/2002/91-7349-151-9.
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Yakoub, Sadok. "Un rôle protecteur contre le stress oxydant pour l’E3-Ubiquitine ligase c-Cbl : utilité comme marqueur pronostic des carcinomes." Thesis, Lyon 1, 2009. http://www.theses.fr/2009LYO10220.
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Le travail présenté a porté sur l’analyse in vivo du proto-oncogène c-cbl, dont la forme connue est c-Cbl (p120cbl). Il s’agit d’une E3-Ubiquitine ligase et un poly-adaptateur moléculaire. Nous avons montré l’androgéno-dépendance de l’expression de c-Cbl dans les cellules germinales testiculaires et les cellules épithéliales de la prostate de rats et de souris. Nous avons montré la régulation anti-apoptotique exercée in vivo par la c-Cbl dans la prostate par comparaison des souris c-cbl invalidées ou non pour c-cbl (KO ou WT). L’effet exercé par c-cbl dans le testicule est pro-apoptotique (J.Cell Biol, 2005), que nous avons ultérieurement attribué à une nouvelle isoforme testiculaire de c-Cbl (Δ-c-Cbl). La comparaison des MEF KO et WT après induction d’apoptose par l’étoposide, a conforté l’effet anti-apoptotique exercée in vivo par c-Cbl dans la prostate. Elle a aussi montré la forte apoptose des MEF KO au peroxyde d’hydrogène : c-Cbl peut être considérée comme un protecteur du stress oxydant. L’intensité du stress oxydant associé aux cancers et leur forte résistance à l’apoptose sont des propriétés qui pourraient être reliées à c-Cbl. L’analyse in situ effectuée à partir de tumeurs congelées et de Tissue Microarrays (TMA) a montré une expression élevée de c-Cbl dans certains cancers, dont l’intensité pourrait correspondre à la gravité de l’atteinte anatomo-pathologique. La protéine c-Cbl est apparue être un marqueur d’agressivité du cancer de la prostate, probablement de l’ovaire, de l’utérus, du cerveau, du poumon, du colon et du rectum. Nous la considérons aussi comme une cible thérapeutique car, protecteur du stress oxydant, elle prendrait part à la résistance à l’apoptose des cellules tumorales. Un brevet a été déposé (2009, co-inventeurs : S.Yakoub et al). Un article rapportant ces résultats est en cours de soumission (S. Yakoub et al)<br>This work has focused on the in vivo analysis of the proto-oncogene c-cbl, coding for c-Cbl (p120cbl). We demonstrated the androgen-dependency of c-Cbl in the testicular germ cells and the prostatic epithelial cells of rats and mice. We then identified the anti-apoptotic regulation exerted by p120cbl in the prostate, comparing mouse c-cbl KO and WT, unlike this exerted in the testis (J.Cell Biol, 2005). We reported this difference to the high expression in testis of a new c-Cbl isoform, Δc-Cbl. The comparison of MEF KO and WT allowed confirming the anti-apoptotic regulation to etoposide exerted by c-Cbl. A very high apoptotic effect was observed in MEF KO with H2O2: c-Cbl is a strong stress oxidative protector. Knowing the intensity of oxidative stress in several cancers and their particular resistance to apoptosis as well, the in situ analysis of these malignancies was made from frozen tumours and tissue microassays (TMA). c-Cbl was indeed highly expressed and its intensity appears to reflect the aggressiveness of the pathology. c-Cbl could then be considered as a marker of severity of prostate cancer but probably also ovary, uterus, brain, lung, colon and rectum. It can also be considered as a therapeutic target involved in resistance to apoptosis as a stress oxidative protector. A patent was filed in the United States (2009, co-inventors: S. Yakoub et al)
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Karlsson, Lisa, and Julina Thorin. "Patienters upplevelser av testikelcancer : En litteraturstudie." Thesis, Högskolan i Halmstad, Akademin för hälsa och välfärd, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-41290.
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Bakgrund: Testikelcancer uppkommer främst hos män under 35 års ålder. Mortaliteten har minskat i de flesta länder samtidigt som incidensen beräknas att öka. Orsaken till insjuknandet av testikelcancer är okänd. En knöl i testikeln är oftast det vanligaste symtomet på testikelcancer. Sjuksköterskor beskrev en brist i kunskap angående testikelcancer. Syfte: Syftet var att beskriva patienters upplevelser av testikelcancer. Metod: Arbetet genomfördes som en allmän litteraturstudie. Datainsamlingen utfördes i tre databaser med inriktning på omvårdnadsforskning. Vetenskaplig kvalitet bedömdes och innehållsgranskningar genomfördes vilket genererade i tio resultatartiklar. Databearbetningen genomfördes som en innehållsanalys i fem steg. Resultat: Resultatet presenterades genom följande huvudteman: En vändpunkt i livet, Behandlingen gav besvär, Känslorna av maskulinitet påverkades och Oro inför framtiden. Det framkom i resultatet att få ett cancerbesked var en chockartad upplevelse. Fatigue, hårförlust och kirurgiska ärr upplevdes vara de mest besvärande biverkningarna. Patienterna upplevde att sin maskulinitet påverkades på olika sätt och fertilitet betraktades som en viktig aspekt. Det framkom att patienterna upplevde oro inför framtida förhållande och att återinsjukna i cancer. Slutsats: Sjuksköterskor behöver förståelse för patienternas upplevelser utav testikelcancer och därmed behövs mer forskning för att kunna bedriva en god evidensbaserad omvårdnad.<br>Background: Testicular cancer occurs primarily in men under the age of 35. The mortality has decreased in most countries and at the same time is the incidence expected to increase. The cause of testicular cancer is unknown. A lump in the testicle is the most common symptom of testicular cancer. Nurses has described a lack of knowledge about testicular cancer. Aim: The aim of the study was to describe patients experiences of testicular cancer. Method: The study was conducted as a general literature study. The datacollection was from three databases who had focus on nursing science. The research quality was assessed and content reviews was conducted which generated in ten resultarticles. The data processing was performed as a content analysis in five steps. Result: The result is presented through the following main themes: A turning point in life, The treatment caused problems, The feelings of masculinity were affected and Concerns about the future. It appeared in the results that receving cancer was a shocking experience. Fatigue, hair loss and surgical scars were found to be the most bothersome side effects. The patients felt that their masculinity was affected in different ways and fertility was considered an important aspect. It emerged that patients experienced worries about future relationships and to re-illness in cancer. Conclusion: Nurses need to understand patients experiences of testicular cancer and with that more research is required to able to conduct a good evidence-based nursing.
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Siddeek, Bénazir. "Exposition in utero aux antiandrogènes et rôle des IAPs et de PARP-1 dans le testicule adulte." Lyon 1, 2007. http://www.theses.fr/2007LYO10135.
Full textAbstract:
Le syndrome de dysgénésie testiculaire (SDT) a été lié à une exposition fœtale ou néo-natale à des perturbateurs endocriniens. Dans ce contexte, nous avons développé un modèle expérimental de rats exposés in utero à l'antiandrogène flutamide qui développe chez l'adulte une hypospermatogenèse due à une apoptose chronique des cellules germinales. Cette apoptose est liée à une diminution d'expression des IAP et au fait que les cellules de Sertoli n'assurent plus leur fonction de protection. Une autre anomalie du SDT est le cancer testiculaire (CT). Sur des biopsies humaines, nous montrons une forte expression des IAP dans le tissu tumoral dont XIAP. L'étude de son rôle in vitro montre que la diminution de son expression sensibilise les cellules de CT à l'apoptose induite par le cisplatine. Enfin, l'analyse de souris dont PARP-1 est invalidé montre dans le testicule, une diminution de l'apoptose et une augmantation de la prolifération céllulaire qui pourrait être un terrain propice au CT<br>Testicular dysgenesis syndrome (TDS) has been linked to a fetal or neo-natal exposure to endocrine disruptors. In this context, we developed an experimental model of rats exposed in utero to the anti androgen flutamide, which develop at the adult age, a hypospermatogenesis due to a chronic germ cell apoptosis. This apoptosis is linked to an increase in the IAPs expression and to the fact that Sertoli cells do not longer protect the germ cells. Another abnormality of the TDS is the testicular cancer (TC). Using human biopsies, we show a high expression level of IAPs in the tumoral tissues including XIAP. The in vitro study of XIAP role show that the decrease of its expression sensitizes CT cells to apoptosis induced by cisplatin. Finally, using invalidated PARP-1 male mice, we show a decrease in the apoptosis rate and an increase in the proliferation process, which could be a favourable ground for TC