Relevant bibliographies by topics / Endocryne tumour / Dissertations / Theses
To see the other types of publications on this topic, follow the link: Endocryne tumour.

Dissertations / Theses on the topic 'Endocryne tumour'

Author: Grafiati
Published: 11 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 dissertations / theses for your research on the topic 'Endocryne tumour.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.

1

BRAGANTINI, Emma. "Prognostic significance of cytokeratin 19 in pancreatic endocrine tumours." Doctoral thesis, Università degli Studi di Verona, 2009. http://hdl.handle.net/11562/337410.

Full text
Abstract:
Presupposti. La prognosi delle neoplasie endocrine pancreatiche è difficile da stabilire nonostante la recente classificazione dell’OMS. Studi recenti hanno evidenziato il potenziale ruolo prognostico di alcuni marcatori come CK19, CD99 e P27. Scopo. Valutare il ruolo prognostico dell’espressione di CK19 nelle neoplasie endocrine pancreatiche. Materiali e metodi. Sono state analizzate 149 neoplasie endocrine pancreatiche per l’espressione immunoistochimica di CK19 utilizzando tissue array. Risultati. La presenza di CK19 è stata riscontrata in 100/149 (67,1%) e in 26 su 35 (74.2%) corrispondenti metastasi sia linfonodali che viscerali. E’ stata evidenziata una correlazione statisticamente significativa tra espressione di CK19 e le dimensioni del tumore, lo stato linfonodale, la presenza di metastasi, la sopravvivenza a cinque anni, e con i sottogruppi della classificazione OMS che mostrano una prognosi peggiore (carcinomi endocrini ben differenziati e carcinomi endocrini poco differenziati) Conclusioni: Il presente studio conferma l’associazione dell’espressione di CK19 con le dimensioni del tumore, lo status linfonodale, la presenza di metastasi, la sopravvivenza a cinque anni, e con i sottogruppi della OMS2004 che mostrano una prognosi peggiore. L’analisi multivariata non ha confermato il ruolo della CK19 come marcatore prognostico indipendente. Possiamo quindi concludere che CK19 può essere utilizzato come marcatore di malignità ma non come marcatore prognostico indipendente.
Aim: Pancreatic endocrine tumours are rare neoplasm, whose behaviour is difficult to predict. Recent 2004 WHO classification gives clear criteria to define prognosis of PET, but despite these criteria some tumours show a more aggressive course. Recent studies lighted the role of some immunohistochemical markers as CK19, CD99, P27 as prognostic marker in pancreatic endocrine. The aim of this study was to evaluate the prognostic value of CK19 expression in PETs. Methods and results: 149 PETs and 35 mached metastases were studied using tissue array technology and evaluating immunohistochemical expression of CK19. The presence of CK 19 was detected in a total of 100/149 primitive tumours (67.1%) and 26/35 (74.2%) metastases both in lymph node and in other sites. The difference between the prevalence of CK 19 in metastasis and primitive tumours was not significant. There was a strong correlation between presence of CK 19 in the primitive and its matched metastasis (Fisher's test; P = 0.0012). The results were statistically compared with follow up data, showing a significant correlation with with tumour dimension, lymph node status, presence of metastasis, 5 years survival, and with the subgroups of WHO 2004 classification that have a worse prognosis (WDEC and PDEC). When the WHO parameter was added to the model, ck19 was no longer significantly associated with survival. Furthermore, ck19 expression was not significantly associated with survival when evaluated in single WHO subgroups. Conclusions: We conclude that ck19 can be used as a malignancy marker and index but they are not an independent prognostic markers
APA, Harvard, Vancouver, ISO, and other styles
2

Restany, Alain. "Les tumeurs endocrines du pancréas à sécrétions multiples : considérations pathogéniques et thérapeutiques." Montpellier 1, 1988. http://www.theses.fr/1988MON11263.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Bonnavion, Rémy. "Study of the effects of Men1 disruption in mouse pancreatic endocrine progenitors during development and adult life." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10144/document.

Full text
Abstract:
Le syndrome des Néoplasies Endocriniennes Multiples de type I (NEM1) est une maladie tumorale héréditaire rare caractérisée par l'apparition de tumeurs notamment du pancréas endocrine. Le gène de prédisposition est le suppresseur de tumeur MEN1, généralement retrouvé muté sur un des 2 allèles au niveau germinal chez les patients NEM1. Les tumeurs endocrines pancréatiques sont rares mais souvent métastatiques lors du diagnostic. Ces tumeurs forment un groupe hétérogène de par le type d'hormone qu'elles peuvent sécréter. Le développement et l'évolution de ces tumeurs sont encore très mal compris. L'origine cellulaire des différents types de tumeurs endocrines pancréatiques reste énigmatique, notamment en ce qui concerne les tumeurs exprimant des hormones non pancréatiques tels que les gastrinomes. Mon projet de thèse s'est articulé autour de la caractérisation d'un nouveau modèle murin d'invalidation du gène Men1 spécifiquement dans les cellules progénitrices endocrine pancréatiques Ngn3+ (PEPs), le modèle PancEndoMen1 KO. Ces travaux nous ont permis de démontrer que les gastrinomes pancréatiques liés à l'inactivation du gène Men1, avaient pour origines les cellules pancréatiques endocrines elles-mêmes. De plus, les souris PancEndoMen1 KO, développent des altérations de prolifération différentes suivant les lignages endocrines. De surcroît, l'invalidation du gène Men1 soit dans les cellules progénitrices pancréatiques, soit dans les cellules PEPs conduit au développement de tumeurs caractérisées par une altération de leur différentiation endocrine. Ainsi, mes travaux de thèse ont permis de mieux renseigner l'histogenèse des tumeurs endocrines pancréatiques en adressant le rôle dans la tumorigenèse de l'invalidation de Men1 dans les cellules PEPs au cours du développement
Multiple Endocrine Neoplasia Type I syndrome (MEN1) is a rare hereditary tumoral disease characterized by the apparition of tumors in multiple endocrine organs including the endocrine pancreas. MEN1 patients generally carry a germinal mutation on one allele of the predisposing gene to the disease, the tumor suppressor MEN1. Pancreatic endocrine tumors are rare, slowly evolving and often present with metastasis at diagnosis. These tumors constitute a heterogeneous group defined by their hormonal secretions. Evolution and development of these tumors is far from being understood. The cell of origin of the different pancreatic endocrine tumor types is enigmatic, notably for tumors secreting non-pancreatic hormones such as gastrinomas. My thesis project was structured toward the characterization of a new murine model allowing the specific disruption of the Men1 gene in Ngn3+ pancreatic endocrine progenitors, the PancEndoMen1 KO model. The combined study of this new model and previous model generated in the team, allowed us to demonstrate that pancreatic gastrinomas related to Men1 inactivation, originate from the endogenous pancreatic endocrine cells. In parallel, our results demonstrated that the mutant mice having Men1-deficient Ngn3+-progenitors resulted in differential cell proliferation alterations in different pancreatic endocrine cells. Importantly, Men1-disruption in either pancreatic endocrine or pan-pancreatic progenitors displayed tumors with impaired differentiation features. Thus, this thesis works allowed to better characterize pancreatic endocrine tumors histogenesis by addressing the role of pancreatic endocrine progenitors targeted Men1 disruption during development in tumorigenesis
APA, Harvard, Vancouver, ISO, and other styles
4

Kaboré, Moussa. "Contribution à l'étude des tumeurs neuro-endocrines : à propos d'un cas de "tumeur carcinoi͏̈de" de l'ovaire, avec dissémination péritonéale." Bordeaux 2, 1989. http://www.theses.fr/1989BOR25283.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

L', Hopital François. "Tumeur endocrine pancréatique secrétant calcitonine et glucagon." Clermont-Ferrand 1, 1987. http://www.theses.fr/1987CLF11048.

Full text
Abstract:
Après urappel sur les tumeurs endocrines du pancréas, la somatostatine, la calcitonine et le calcitonine gene related peptide (CGRP), l' auteur décrit une observation de tumeurs endocrines pancréatiques sécrétant calcitonine et glucagon (dosages radio-immunologiques et immunocytochimie), s' exprimant sous la forme : d' un processus tumoral hépatique (métastases), de diarrhée, de flushs, d' épisodes d' hypoglycémie, et traitées par la somatostatine retard. Il s' agit de la première observation décrite de tumeur pancréatique associant calcitonine et glucagon, les épisodes d' hypoglycémie sont expliqués par une sécrétion inappropriée d' insuline. L' auteur note enfin l' absence d' efficacité de la somatostine retard sur l' hyperglucagonémie (en opposition avec les données de la littérature) et sur l' hypercalcitoninémie (en accord avec les données de la littérature).
APA, Harvard, Vancouver, ISO, and other styles
6

Cuny, Thomas. "New regulatory mechanisms in the growth of endocrine tumors : digestive neuroendocrine tumors, pitiutary adenomas." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5061.

Full text
Abstract:
Bien que rares, les tumeurs endocrines développées chez l'Homme demeurent problèmatiques. Une meilleure compréhension des mécanismes qui régulent leur croissance constitue un objectif essentiel pour identifier des cibles thérapeutiques nouvelles.Dans la première partie de cette thèse, nous avons étudié l'impact du microenvironnement tumoral (MeT), définit par l'ensemble des facteurs qui encerclent la niche tumorale primitive, sur la croissance des tumeurs endocrines digestives. In vitro, nous observons un effet prolifératif réciproque entre des fibroblastes, l'une des cellules pivots du MeT, et des lignées cellulaires humaines de tumeurs endocrines pancréatiques, tel qu'il est susceptible d'exister in situ. Dans une seconde partie, nous avons montré que le pegvisomant, un antagoniste du récepteur de l'hormone de croissance utilisé chez des patients atteint d'adénome hypophysaire somatotrope, n'a pas d'effet prolifératif in vitro sur les cellules somatotropes adénomateuses
Although rare, endocrine tumors developed in Humans remain problematic, such as a better understanding of their regulatory mechanisms of growth represent a step forward to identify new therapeutical targets.In the first part of this thesis, we investigated the impact of the tumor microenvironment (TME), as defined by the factors surrounding the tumor primitive niche, on the growth of human digestive endocrine tumors. We, here, showed the occurrence of a reciprocal proliferation between human fibroblasts, a key cell within the TME, and human pancreatic neuroendocrine tumor cell lines, suggesting that human fibroblasts may constitue a new therapeutical target of interest in the TME of digestive endocrine tumors. In a second part, we showed that pegvisomant (PEG), a growth hormone receptor antagonist currently used in patients with GH-secreting pituitary adenoma, did not impact in vitro the proliferation rate of GH-secreting adenoma cells and therefore is suitable in patients with a persisting GH-secreting pituitary adenoma residue after surgery
APA, Harvard, Vancouver, ISO, and other styles
7

Villaume, Karine. "Mécanismes de l'angiogenèse associée aux tumeurs endocrine digestives : rôle du VEGF." Thesis, Lyon 1, 2009. http://www.theses.fr/2009LYO10189/document.

Full text
Abstract:
Les tumeurs endocrines digestives sont des tumeurs hypervasculaires, ce qui suggère l'existence d'un processus d'angiogenèse tumorale actif. Les mécanismes de l'angiogenèse tumorale associée aux tumeurs endocrines digestives sont complexes. Deux processus semblent coexister : les tumeurs les mieux différenciées sont capables de récapituler les propriétés pro-angiogéniques des cellules endocrines normales alors que les tumeurs moins différenciées et plus agressives sont associées à un processus d angiogenèse non spécifique, développé en réponse à l'hypoxie. Dans ces deux processus, le VEGF joue vraisemblablement un rôle important, dans la mesure où il fait partie intégrante du programme de différenciation endocrine. L'objectif de notre travail a été de mieux comprendre les mécanismes de sa régulation dans les cellules endocrines digestives tumorales et d'analyser son rôle dans la croissance tumorale, à travers une double approche expérimentale, in vitro et in vivo ; Nos résultats nous ont permis de : (a) montrer la complexité de la régulation de la synthèse et de la sécrétion du VEGF par les cellules endocrines néoplasiques, qui implique plusieurs voies de signalisation (PI3K/Akt/mTOR et p38/MAPK), dont les rôles respectifs varient selon le type de cellule étudiée ; (b) confirmer expérimentalement la dissociation entre expression du VEGF et capacités angiogéniques d'une part, propriétés invasives et métastatiques d'autre part ; (c) montrer expérimentalement que l'inhibition de l'angiogenèse peut contribuer à l'effet antitumoral de substances d'intérêt thérapeutique dans les tumeurs endocrines digestives
Digestive endocrine tumors are hypervascular tumors, likely to be associated with an active angiogenic process. The mechanisms of tumor angiogenesis in digestive endocrine tumors are complex. Two processes seem to coexist: well differentiated tumors are able to recapitulate the pro-angiogenic capacities of normal endocrine cells whereas less differentiated and more aggressive tumors are associated with a non specific angiogenic process, in response to hypoxia. In both processes, VEGF is likely to play an important role, since it is constitutively expressed by normal peptide-secreting endocrine cells, as part of their specific differentiation program. Our aim was to evaluate the mechanisms of regulation of VEGF synthesis and secretion by neoplastic digestive endocrine tumors and to analyze its role in tumor progression, through an in vitro and in vivo experimental approach. We were able to demonstrate that: (a) the regulation of VEGF synthesis and secretion is complex and involves several pathways (PI3K/Akt/mTOR and p38/MAPK), with different roles according to the cell studied; (b) there is a dissociation between VEGF expression and angiogenic capacities, on one hand, and invasive and metastatic properties, on the other hand; (c) the inhibition of angiogenesis may contribute to the anti-tumoral effect of several drugs of therapeutic interest in digestive endocrine tumors
APA, Harvard, Vancouver, ISO, and other styles
8

Hessman, Ola. "Genetic studies of endocrine abdominal tumors." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5026-1/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Larsson, Gunnel. "Quality of Life in Patients with Endocrine Gastrointestinal Tumours." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4916-6/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Tsolakis, Apostolos V. "Characterization of Endocrine Cells and Tumours in the Stomach." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8804.

Full text
APA, Harvard, Vancouver, ISO, and other styles
11

Johansson, Térèse A. "Pancreatic Endocrine Tumourigenesis : Genes of potential importance." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9294.

Full text
Abstract:

Understanding signalling pathways that control pancreatic endocrine tumour (PET) development and proliferation may reveal novel targets for therapeutic intervention. The pathogenesis for sporadic and hereditary PETs, apart from mutations of the MEN1 and VHL tumour suppressor genes, is still elusive. The protein product of the MEN1 gene, menin, regulates many genes. The aim of this thesis was to identify genes involved in pancreatic endocrine tumourigenesis, with special reference to Notch signalling.

Messenger RNA and protein expression of NOTCH1, HES1, HEY1, ASCL1, NEUROG3, NEUROD1, DLK1, POU3F4, PDX1, RPL10, DKK1 and TPH1 were studied in human PETs, sporadic and MEN 1, as well as in tumours from heterozygous Men1 mice. For comparison, normal and MEN1 non-tumourous human and mouse pancreatic specimens were used. Nuclear expression of HES1 was consistently absent in PETs. In mouse tumours this coincided with loss of menin expression, and there was a correlation between Men1 expression and several Notch signalling factors. A new phenotype consisting of numerous menin-expressing endocrine cell clusters, smaller than islets, was found in Men1 mice. Expression of NEUROG3 and NEUROD1 was predominantly localised to the cytoplasm in PETs and islets from MEN 1 patients and Men1 mice, whereas expression was solely nuclear in wt mice. Differences in expression levels of Pou3f4, Rpl10 and Dlk1 between islets of Men1 and wt mice were observed.

In addition, combined RNA interference and microarray expression analysis in the pancreatic endocrine cell line BON1 identified 158 target genes of ASCL1. For two of these, DKK1 (a negative regulator of the WNT/β-catenin signalling pathway) and TPH1, immunohistochemistry was performed on PETs. In concordance with the microarray finding, DKK1 expression showed an inverse relation to ASCL1 expression.

Altered subcellular localisation of HES1, NEUROD1 and NEUROG3 and down-regulation of DKK1 may contribute to tumourigenesis.

APA, Harvard, Vancouver, ISO, and other styles
12

Guy, Laurent. "LES Tumeurs neuro-endocrines de la prostate." Clermont-Ferrand 1, 1994. http://www.theses.fr/1994CLF1MS06.

Full text
APA, Harvard, Vancouver, ISO, and other styles
13

Nord, Brita. "Endocrine tumour development : with special focus on chromosome arms 1p and 11q /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-166-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
14

Bassett, John Howard Duncan. "Positional cloning studies of multiple endocrine neoplasia type 1 (MEN1)." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391265.

Full text
APA, Harvard, Vancouver, ISO, and other styles
15

Simon, Jean-Claude. "Tumeurs endocrines duodeno-pancreatiques non fonctionnelles : a propos de 20 cas cliniques de 1980 a 1990." Lyon 1, 1992. http://www.theses.fr/1992LYO1M007.

Full text
APA, Harvard, Vancouver, ISO, and other styles
16

Magen-Kunzelmann, Valérie. "Expression de la chromogranine A et de ses sous-unités dans les tumeurs endocrines du pancréas : à propos de 21 cas." Montpellier 1, 1999. http://www.theses.fr/1999MON11030.

Full text
APA, Harvard, Vancouver, ISO, and other styles
17

CHANVRY, DOMINIQUE. "Les somatostatinomes : a propos d'un cas et revue de la litterature." Rennes 1, 1992. http://www.theses.fr/1992REN1M027.

Full text
APA, Harvard, Vancouver, ISO, and other styles
18

MAKLOUF, MOISE. "Radiologie des tumeurs endocrines du pancreas." Lille 2, 1990. http://www.theses.fr/1990LIL2M027.

Full text
APA, Harvard, Vancouver, ISO, and other styles
19

Arthur, Laura Margaret. "Tumour evolution over time : treatment and progression : exploring the molecular heterogeneity of oestrogen receptor positive breast cancer." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29581.

Full text
Abstract:
Introduction Recent advances in microarray technology have allowed more understanding of the complex molecular biology of breast cancer. The traditional prognostic information afforded by hormone receptor status and pathology variables is being supplemented and superseded by gene signatures predictive of risk of recurrence and response to treatments. Approximately 75% of breast cancers are oestrogen receptor positive (ER+) and can be treated by drugs that block oestrogen production such as letrozole. However not all ER+ tumours respond and even those that initially respond can develop resistance. Treating patients with neoadjuvant letrozole affords a unique opportunity to sample the same tumour in vivo at different time points reducing any potential inter-patient and inter-tumour variability. The molecular effects of drugs can be assessed long before clinical outcome is apparent. Underlying genetic differences or characteristics of the patient, tumour or sample may affect the molecular response to treatment. This project set out to use sequential patient-matched samples to evaluate molecular changes in breast tumours in the presence or absence of endocrine treatment in different subtypes, defined by histology or mutation status and to assess molecular variation between primary tumour and nodal metastasis. Methods RNA was extracted and processed to generate whole transcriptome Illumina Beadarray gene expression data from four unique cohorts of patients. Clinical data on treatments, recurrence and survival was collected from medical records. The first cohort compared 25 breast cancer patients with matched samples at diagnosis and at surgery, 14-35 (median 23) days later, with no intervening treatment; with 36 patients treated with neoadjuvant letrozole. A PCR assay to detect 8 known PIK3CA mutations and assessment of PTEN status was performed at both the primary and secondary event in a second cohort of 120 patients with endocrine treated disease who relapsed with either recurrence, lymph node metastases, a new second primary or progression of disease on primary endocrine therapy. The third cohort compared the molecular response to neoadjuvant letrozole in 14 patients with invasive lobular cancer (ILC) and 14 patients with invasive ductal cancer (IDC). A fourth cohort of women with node positive disease at diagnosis were assessed for variations in gene expression profiles between primary tumour and synchronous metastatic axillary lymph nodes (68 samples from 31 patients). Results The genomic profile of the no intervening treatment cohort did not differ significantly. Some changes in inflammatory genes were evident. This reassures us that changes seen during treatment are truly due to drug effect. This validates the use of a second biopsy to explore prediction of response. PIK3CA mutation status is maintained in the majority of patients with endocrine resistant disease and changed in only 15.7%. Where there was a change in PIK3CA this was significantly more likely to be a second primary breast cancer rather than a recurrence or progression of the primary cancer. PTEN status was also maintained in most patients. This does not support the theory that acquisition of a PIK3CA mutation is responsible for developing endocrine resistance. Novel PI3K inhibitor drugs may still be suitable in endocrine-resistant disease if activation of the pathway develops by other mechanisms. Consistent with previous studies, significant molecular differences were observed between ILC and IDC pre-treatment. Over half of these molecular differences were maintained after 3 months of letrozole. However, changes over time in individual tumours in response to letrozole were highly consistent in both ILC and IDC. When comparing primary with synchronous metastatic nodes only 39% of tumours clustered together with their matched primary or node. The molecular subtype of the node was often a poorer prognosis than the primary. There were also differences in subtype between nodes in a small cohort of patients with 2 involved nodes. Conclusions We have demonstrated that neoadjuvant window studies are a valid model for assessment of drug effects and evaluated differences in histology and mutation status. Endocrine resistance in breast cancer is rarely related to acquisition of PIK3CA mutations. Synchronous lymph node metastases can differ greatly from their matched primary. These findings are highly relevant when considering prescribing (neo)/adjuvant therapy and have significantly improved our understanding of breast cancer as we strive towards personalised medicine.
APA, Harvard, Vancouver, ISO, and other styles
20

Newey, Paul J. "The role of the tumour suppressor proteins, parafibromin and menin, in endocrine tumourigenesis." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.711613.

Full text
APA, Harvard, Vancouver, ISO, and other styles
21

Eeden, Susanne van. "Endocrine tumors of the pancreas and gastrointestinal tract." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2005. http://dare.uva.nl/document/78589.

Full text
APA, Harvard, Vancouver, ISO, and other styles
22

Abou, El Fadil-Nicol Fatima. "Distribution de la sorbine dans le tractus digestif du porc, du rat et de l'homme." Lyon 1, 1997. http://www.theses.fr/1997LYO1T167.

Full text
APA, Harvard, Vancouver, ISO, and other styles
23

TANGUY, CAROFF ELISABETH. "Les tumeurs endocrines apparemment non-secretantes du pancreas : a propos de 7 observations." Angers, 1992. http://www.theses.fr/1992ANGE1017.

Full text
APA, Harvard, Vancouver, ISO, and other styles
24

RODDE, MARIE-HELENE. "A propos de deux observations de tumeurs endocrines non fonctionnelles du pancreas : strategies diagnostiques et therapeutiques." Aix-Marseille 2, 1989. http://www.theses.fr/1989AIX20243.

Full text
APA, Harvard, Vancouver, ISO, and other styles
25

Micallef, Rachel Antonia. "Wnt signalling in endocrine resistant breast cancer." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/41274/.

Full text
Abstract:
Wnt signalling components are reported to be deregulated in breast cancer but the contribution of this pathway in endocrine resistance is less clearly defined. Endocrine resistance is an important clinical challenge affecting up to a quarter of all breast cancer patients and is associated with a poorer clinical prognosis. This project focussed on exploring the role of Wnt signalling in endocrine resistant breast cancer cell models. Wnt pathway elements were deregulated in the acquired tamoxifen resistant cell line (Tam-R) compared to tamoxifen sensitive parental cells (MCF-7), with changes supportive of Wnt signalling activation in this tamoxifen resistant model apparent from Affymetrix HGU-133A gene microarray data and Western blot analysis. In contrast, Wnt signalling appeared to be suppressed based on Affymetrix data for MCF-7 cells treated with oestradiol for 10 days, with equivocal changes in MCF-7 cells treated with tamoxifen for 10 days or a faslodex resistant cell model (Fas-R). Excitingly, Tam-R cells were also more sensitive than MCF-7 cells to pharmacological manipulation of Wnt signalling. While Wnt activation using Wnt3a and LiCl did not affect cell growth or migration, inhibition of Wnt signalling usingIWP2, PNU 74654 and iCRT14 suppressed Tam-R cell growth and migration. There is mounting evidence of cross talk between Wnt and EGFR signalling in breast cancer, and EGFR activity is upregulated in Tam-R cells. The project’s findings tentatively supported cross-talk between the two signalling pathways in this model. Thus, targeting of the Wnt pathway alongside EGFR blockade was superior in suppressing cell growth and migration in Tam-R cells. The effect appeared to be more pronounced when Wnt signalling was inhibited at the nuclear level using iCRT14. Collectively, these data suggest that Wnt signalling may play an important role in tamoxifen resistance where it may offer an opportunity for more effective therapeutic intervention to control relapse and associated tumour aggressiveness.
APA, Harvard, Vancouver, ISO, and other styles
26

Lackie, Peter Mar. "Peptide containing endocrine cells and endocrine tumours in the respiratory tract : investigated by cell culture, immunocytochemistry and electron microscopy." Thesis, Imperial College London, 1987. http://hdl.handle.net/10044/1/46993.

Full text
APA, Harvard, Vancouver, ISO, and other styles
27

Bergman, Lee Melissa. "Molecular and cellular biology of the multiple endocrine neoplasia type 1 tumour suppressor gene /." St. Lucia, Qld, 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16539.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
28

Picon, Aline. "Syndrome de Cushing paranéoplasique et tumeurs neuro-endocrines pulmonaires : pièges et difficultés diagnostiques à propos de trois cas." Montpellier 1, 1996. http://www.theses.fr/1996MON11143.

Full text
APA, Harvard, Vancouver, ISO, and other styles
29

Sandgren, Johanna. "Array-based Genomic and Epigenomic Studies in Healthy Individuals and Endocrine Tumours." Doctoral thesis, Uppsala universitet, Institutionen för kirurgiska vetenskaper, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-129533.

Full text
Abstract:
The human genome is a dynamic structure, recently recognized to present with significant large-scale structural variation. DNA-copy number changes represent one common type of such variation and is found both between individuals and within the somatic cells of the same individual, especially in disease states like cancer.  Apart from DNA-rearrangements, epigenomic changes are increasingly acknowledged as important events in the maintenance of genomic integrity. In this thesis, different array-based methods have been applied for global genomic and epigenomic profiling of both normal and cancer cells. In paper I, a genomic microarray was established and used to determine DNA-copy number variants (CNVs) in a cohort of 76 healthy individuals from three ethnic populations. We identified 315 CNV regions that in total encompassed ~3,5% of the genome. In paper II, the array was utilized to discover CNVs within several differentiated tissues from the same subject. Six variants were identified providing evidence for somatic mosaicism. In paper III and IV we studied pheochromocytomas and paragangliomas, rare endocrine tumours that most often present as benign and sporadic with unclear genetic/epigenetic cause. Genome-wide DNA-copy number analysis of 53 benign and malignant samples in paper III revealed numerous common and novel chromosomal regions of losses and gains. High frequencies of relatively small overlapping regions of deletions were detected on chromosome 1p arm, encompassing several candidate tumour suppressor genes. In paper IV, an epigenomic map for two histone modifications associated with silent (H3K27me3) or active (H3K4me3) gene transcription, was generated for one malignant pheochromocytoma. Integrated analysis of global histone methylation, copy number alterations and gene expression data aided in the identification of candidate tumour genes. In conclusion, the performed studies have contributed to gain knowledge of CNVs in healthy individuals, and identified regions and genes which are likely associated with the development and progression of pheochromocytoma/paraganglioma.
APA, Harvard, Vancouver, ISO, and other styles
30

Magnus, Jeanne Marie Léonie. "Études cliniques des tumeurs adénoïdes." Paris : BIUM, 2003. http://www.bium.univ-paris5.fr/histmed/medica/cote?TPAR1895x360.

Full text
APA, Harvard, Vancouver, ISO, and other styles
31

Walls, Gerard V. "Studies of tumourigenesis in the multiple endocrine neoplasia type 1 and hyperparathyroidism-jaw tumour syndromes." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.711626.

Full text
APA, Harvard, Vancouver, ISO, and other styles
32

Quesney-Tison, Christine. "Tumeur neuro-endocrine carcinoïde du larynx : à propos d'un cas, revue de la littérature." Caen, 1990. http://www.theses.fr/1990CAEN3091.

Full text
APA, Harvard, Vancouver, ISO, and other styles
33

Boelaert, Kristien. "Pituitary tumor transforming gene (PTTG) and related growth factors in endocrine tissues." Thesis, University of Birmingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424097.

Full text
APA, Harvard, Vancouver, ISO, and other styles
34

Fjällskog, Marie-Louise. "Current Medical Treatment of Endocrine Pancreatic Tumors and Future Aspects." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2709.

Full text
Abstract:

We treated 16 patients with somatostatin analogs combined with α-interferon and achieved a biochemical and/or radiological response in 56% (median duration 22 months). We consider this treatment a good alternative for patients who fail during chemotherapy or who do not want to/cannot receive cytotoxic drugs.

Thirty-six patients with neuroendocrine tumors were treated with cisplatin combined with etoposide. Of 14 patients with evaluable EPTs, 50% responded radiologically and/or biochemically (median duration 9 months). We consider this treatment useful as first-line medical treatment in aggressive EPTs or in patients failing prior chemotherapy.

Twenty-eight tumor tissues from EPTs were examined with immunohistochemistry regarding expression of somatostatin receptors (ssts) 1 to 5 on tumor cells and in intratumoral vessels. We found that sst2 and sst4 were highly expressed on tumor cells and in vessels. However, sst3 and sst5 were lacking in half of the tumor tissues and in most of the vessels. Because of the variability in sst expression, we recommend analysis of each individual’s receptor expression before starting treatment.

Endocrine pancreatic tumors (EPTs) are rare with an incidence of 4 per million inhabitants. In the majority of cases they grow slowly, but there are exceptions with very rapidly progressing malignant carcinomas. First-line medical treatment is streptozotocin combined with 5-fluorouracil.

We examined 38 tumor samples regarding expression of tyrosine kinase receptors platelet-derived growth factor receptors (PDGFRs), c-kit and epidermal growth factor receptor (EGFR). We found that the receptors were expressed in more than half of the tumor tissues. Further studies will reveal if tyrosin kinase antagonists can be part of the future treatment arsenal.

APA, Harvard, Vancouver, ISO, and other styles
35

Ekeblad, Sara. "Pancreatic Endocrine Tumors and GIST - Clinical Markers, Epidemiology and Treatment." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7937.

Full text
APA, Harvard, Vancouver, ISO, and other styles
36

Walter, Thomas. "Métastases hépatiques de tumeurs endocrines digestives : développement de modèles animaux pour l’étude des mécanismes biologiques et l’évaluation préclinique des thérapeutiques." Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10241.

Full text
Abstract:
Les métastases hépatiques de tumeurs endocrines digestives sont hypervasculaires et hétérogènes. Les mécanismes de développement de ces métastases hépatiques, en particulier le rôle de l’angiogenèse tumorale associée à ces tumeurs, sont complexes. Ceci explique la difficulté de prédire le profil évolutif de ces tumeurs et de trouver des facteurs prédictifs de réponses aux traitements médicaux utilisés. L’objectif de notre travail a été de mieux comprendre : le rôle de l’angiogenèse dans le développement des métastases hépatiques de tumeurs endocrines digestives ; les mécanismes d’actions et en particulier leur activité anti-angiogénique, de deux types de molécules (analogue de la somatostatine et inhibiteur de mTOR). Nos résultats nous ont permis à travers une double approche expérimentale, in vitro et in vivo de : (a) montrer la complexité de la régulation de la synthèse et de la sécrétion du VEGF par les cellules endocrines néoplasiques ; (b) confirmer expérimentalement la dissociation entre expression du VEGF et capacités angiogéniques d’une part, propriétés invasives et métastatiques d’autre part, dans les tumeurs endocrines digestives ; (c) montrer expérimentalement que l’inhibition de l’angiogenèse peut contribuer à l’effet anti-tumoral de substances d’intérêt thérapeutique dans les tumeurs endocrines digestives
Liver metastases of digestive endocrine tumors are hypervascular and heterogeneous. The mechanisms of development of these metastases, especially the role of angiogenesis, are complex. This explains the difficulty to predict the natural history of these tumors and to find predictive factors of response to medical treatments. Our aim was to evaluate: the role of angiogenesis in the development of liver metastasis from digestive endocrine tumors; mechanisms of action, especially antiangiogenic activity, of two drugs (somatostatin analogues and mTOR inhibitor). We were able to demonstrate through an in vitro and in vivo experimental approach that: (a) the regulation of VEGF synthesis and secretion is complex, with different roles according to the cell studied; (b) there is a dissociation between VEGF expression and angiogenic capacities, on one hand, and invasive and metastatic properties, on the other hand; (c) the inhibition of angiogenesis may contribute to the anti-tumoral effect of several drugs of therapeutic interest in digestive endocrine tumors
APA, Harvard, Vancouver, ISO, and other styles
37

MAZZA, SYLVIO. "Syndrome de cushing paraneoplasique et tumeur endocrine du pancreas : a propos d'un cas." Reims, 1989. http://www.theses.fr/1989REIMM052.

Full text
APA, Harvard, Vancouver, ISO, and other styles
38

Teunissen, Jacobus Johannes Maria. "Endocrine tumours molecular radiation on target peptide receptor radionuclide therapy with lutetium-octreotate." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/14119.

Full text
APA, Harvard, Vancouver, ISO, and other styles
39

Takeda, Kazuna. "MRI evaluation of residual tumor size after neoadjuvant endocrine therapy vs. neoadjuvant chemotherapy." Kyoto University, 2012. http://hdl.handle.net/2433/157449.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

Ertefai, Benyamin. "Resistance mechanisms during endocrine treatment in breast cancer." Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/95393/.

Full text
Abstract:
Prolonged endocrine therapy is the mainstay of treatment for ER+ breast cancer patients. However, resistance develops in many patients which leads to more aggressive disease. Understanding the mechanisms of acquired resistance that emerge as a consequence of prolonged endocrine treatment remains critical. This study aimed to use gene expression profiling to discover induced mechanisms shared by a panel of MCF7-derived acquired resistant cells that underpin endocrine resistant growth. The in vitro panel represents resistance to oestrogen deprivation, tamoxifen or fulvestrant and includes long-term (3year) models to better-mimic clinical endocrine exposure. Affymetrix 1.0ST microarrays detected 572 genes induced in all resistant models versus MCF7. Over-represented ontologies, pathways and functional classification for these genes revealed induction of oxidative phosphorylation (OxPhos) and TCA cycle enzymes in the resistant models, a finding further confirmed by mass spectrometry. Increased oxygen consumption, NADH dehydrogenase and/or cytochrome C oxidase activity was detected in resistant cells, and targeting with OxPhos inhibitors Metformin or Antimycin A confirmed growth-dependency on OxPhos. Western blotting for AMPK (energy sensor) activity and its downstream anabolic targets (ACC, mTOR/P70S6K) showed Metformin reduced fatty acid and protein synthesis in growth-sensitive endocrine resistant cells. In silico analysis inferred clinical relevance since many TCA/OxPhos genes associated with earlier relapse in ER+ and/or tamoxifen treated patients. Monitoring basal glycolysis (extracellular lactate) and growth impact of 2DG or glutamine restriction demonstrated glycolysis and glutaminolysis also contribute to endocrine resistance. The microarrays furthermore revealed that metabolic kinases PCK2, ALDH18A1 and PFKFB2, and components of cell response to Zn were commonly-induced which may additionally help endocrine resistant growth. This study has revealed increased OxPhos arises as a consequence of prolonged endocrine treatment and is a key bioenergetic pathway sustaining resistance. Since resistant growth is Metformin-sensitive, such targeting of this energy pathway (alongside further antihormones or glycolysis/glutaminolysis inhibitors) could help treat resistance.
APA, Harvard, Vancouver, ISO, and other styles
41

Lindberg, Daniel. "Molecular Genetic Studies of Sporadic and MEN1-Associated Endocrine Pancreatic Tumors." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7595.

Full text
APA, Harvard, Vancouver, ISO, and other styles
42

Martin, Denis. "Le vipome pancréatique : à propos d'un cas." Montpellier 1, 1988. http://www.theses.fr/1988MON11373.

Full text
APA, Harvard, Vancouver, ISO, and other styles
43

Ranaivoson, Ilse. "Expression endocrine des tumeurs germinales sécrétant HCG : à propos de 9 observations." Caen, 1994. http://www.theses.fr/1994CAEN3019.

Full text
APA, Harvard, Vancouver, ISO, and other styles
44

Raynaud, Jean. "Les lésions tumorales du pancréas endocrine avec syndrome d'insulinome : étude de 10 cas par les techniques immunocytochimiques." Bordeaux 2, 1989. http://www.theses.fr/1989BOR25185.

Full text
APA, Harvard, Vancouver, ISO, and other styles
45

Benchekroun, Ghita. "Caractérisation morphologique et fonctionnelle des tumeurs corticotropes du chien et du chat." Thesis, Paris Est, 2016. http://www.theses.fr/2016PESC0070/document.

Full text
Abstract:
La maladie de Cushing résulte du développement de tumeurs hypophysaires corticotropes d’agressivité variable. Cette forme d'hypercorticisme dépendante de l’ACTH se distingue des formes indépendantes de l’ACTH, souvent consécutives à une tumeur surrénalienne. Les outils de distinction entre ces deux formes ainsi que les marqueurs d’agressivité des tumeurs hypophysaires ont été peu documentés ; ils seraient pourtant précieux pour les cliniciens. Un premier objectif, atteint, de notre travail a visé à identifier sur des cohortes cliniquement caractérisées de chiens atteints de syndrome de Cushing, des marqueurs sanguins et morphologiques qui soient distinctifs des deux formes de syndromes de Cushing (concentration plasmatique en ACTH, échographie et examen tomodensitométrique des glandes surrénales). Un second objectif de notre travail a visé à identifier des paramètres cliniques et biologiques susceptibles de refléter l'agressivité des tumeurs corticotropes. Nous avons ainsi montré chez le chien qu'une hypothermie ou une bradycardie peut signer une tumeur de grande taille. Chez le chat, atteint d'adénomes corticotropes généralement agressifs, nous avons démontré que le dosage de la POMC plasmatique est pertinent pour diagnostiquer la maladie de Cushing. La valeur élevée de la concentration plasmatique en POMC chez l'homme, le chien et le chat, a suggéré que ces tumeurs induisent un défaut de maturation de la POMC. L'analyse par western-blot des acteurs protéiques de cette maturation chez le chien a en effet révélé une diminution de la quantité d'enzyme pro-convertase 1/3 au sein des tumeurs corticotropes de grande taille
Cushing’s disease or hyperadrenocorticism (HAC) is one of the most frequent endocrine diseases in dogs. Most cases are ACTH-dependent HAC and are associated with pituitary tumors of variable aggressiveness. The other form of HAC is known as ACTH-independent. The present work was carried out on cohort of dogs and cats presented with HAC. The first objective of this work was to assess the accuracy of diagnostic investigations (such as adrenal glands ultrasonography, computed tomodensitometry scan of adrenal glands and pituitary gland and basal ACTH measurement) in a large cohort of dogs with HAC and to identify the best thresholds that allow a correct classification of HAC (ACTH dependent vs ACTH independent). The second objective was to demonstrate that clinical information such as bradycardia or hypothermia reflect the aggressiveness of the pituitary tumor. We also demonstrated that plasma proopiomelanocortin (POMC) concentration was elevated in cats with Cushing’s disease. This observation, previously reported in dogs and humans, suggests a physiopathological implication of ACTH loss of maturation in aggressive pituitary tumour. We investigated if proconvertase 1/3 (PC1/3) could be involved in this alteration through western blot detection of POMC, pro-ACTH, ACTH and PC1/3 in corticotropic tumors. This work showed a difference in PC1/3 protein levels between large and small corticotroph tumours, PC1/3 signal being weak to undetectable in large pituitary tumours
APA, Harvard, Vancouver, ISO, and other styles
46

PACCHIONI, CATHERINE. "Tumeurs neuro-endocrines du thymus : a propos de 4 cas avec revue de la litterature depuis 1972." Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX20334.

Full text
APA, Harvard, Vancouver, ISO, and other styles
47

Ollivier, Stéphane. "Chimiothérapie systémique des tumeurs neuro-endocrines par Fluoro-Uracile, Dacarbazine et Acide folinique : étude de phase 2 chez 18 patients à l'institut Bergonié, 1991-1994." Bordeaux 2, 1995. http://www.theses.fr/1995BOR23034.

Full text
APA, Harvard, Vancouver, ISO, and other styles
48

El, Hajj Diab Darine. "Nano-thérapie ciblée des tumeurs endocrines par hyperthermie magnétique intra-lysosomale." Thesis, Toulouse 3, 2015. http://www.theses.fr/2015TOU30038/document.

Full text
Abstract:
Les tumeurs endocrines sont habituellement diagnostiquées grâce à l'emploi d'une technique d'imagerie utilisant un peptide radio-marqué (somatostatine ou Osteoscan) dont le récepteur est présent dans 80% des tumeurs. Le récepteur à sept domaines transmembranaires RCCK2 est également sur-exprimé avec une forte incidence dans les tumeurs endocrines. De plus, notre équipe a montré que la gastrine et la CCK, les deux ligands agonistes naturels du RCCK2, induit une internalisation massive du RCCK2 ; le récepteur est ensuite orienté majoritairement avec ses ligands vers les lysosomes pour y être dégradé. Notre équipe a alors formulé l'hypothèse que la surexpression de RCCK2 dans les tumeurs endocrines comparativement aux tissus sains et sa capacité d'internalisation massive pouvaient être avantageusement utilisées pour développer une nouvelle approche diagnostique et thérapeutique. Mon projet de thèse présentaient plusieurs objectifs : 1°) optimiser une nanoplateforme magnétique permettant le ciblage efficace de cellules tumorales surexprimant le RCCK2 ; 2°) valider la stratégie de nanothérapie ciblée par hyperthermie magnétique afin d'éradiquer spécifiquement des cellules tumorales surexprimant le RCCK2, puis étudier les mécanismes cellulaires impliqués dans la signalisation de mort ; 3°) élaborer des stratégies permettant d'augmenter l'efficacité thérapeutique anti-tumorale. Dans un premier temps, j'ai développé une nano-plateforme constituée d'une nanoparticule magnétique (NPM) d'oxyde de fer de type SPION (superparamagnetic iron oxide nanoparticles). J'ai élaboré différents lots de NPM présentant différentes densités en ligand à leur surface et analysé leur capacité de liaison, d'internalisation et d'accumulation dans les lysosomes. Les nanoparticules vectorisées s'accumulent dans les cellules de façon dépendante du récepteur (2.2pg de fer/cellule). J'ai ensuite cherché à valider la stratégie de nanothérapie ciblée par hyperthermie magnétique. Pour cela, j'ai appliqué un champ magnétique alternatif à haute fréquence (275 kHz, 40 mT) sur des cellules ayant ou non internalisé des NPM. L'application du champ magnétique, induit la mort de 30% des cellules tumorales ayant internalisé des NPM, sans élévation détectable de température du milieu extracellulaire, suggérant que l'hyperthermie magnétique serait probablement induite très localement à l'échelle du lysosome. Nous avons appelé ce phénomène : hyperthermie magnétique intra-lysosomale. Ensuite, j'ai cherché à préciser les mécanismes cellulaires pouvant être impliqué dans l'induction de la mort des cellules. Mes résultats montrent que l'application du champ magnétique sur des cellules ayant accumulé des NPM dans leur lysosome induit une production de radicaux libres oxygénés (ROS) responsables de la perméabilisation de la membrane lysosomale et conduisant à la fuite des cystéines protéases lysosomales dans le cytosol, impliqués ainsi dans le mécanisme de mort par hyperthermie magnétique intra-lysosomale. Enfin, dans le but d'augmenter l'efficacité thérapeutique, j'ai combiné ce traitement d'hyperthermie magnétique intra-lysosomale à un traitement chimiothérapeutique, la doxorubicine. Les résultats montrent un effet additif des traitements hyperthermique et chimiothérapeutique. Une telle stratégie de combinaison d'approches thérapeutiques présente l'avantage d'utiliser des doses faibles d'agent chimiothérapeutique, afin de limiter les effets secondaires vis-à-vis des cellules saines
Endocrine tumors are usually diagnosed through the use of an imaging technique using a radiolabeled peptide (somatostatin or Osteoscan) whose receptor is present in 80% of tumors. The CCK2R which belongs to the seven transmembrane domains receptor family is also overexpressed with a high incidence in endocrine tumors. In addition, our team has shown that gastrin and cholecystokinin (CCK), both natural agonists of the CCK2R, induce a massive CCK2R internalization; then the receptor is directed with the ligand to lysosomes to be degraded. Our team hypothesized that CCK2R overexpression in endocrine tumors compared to healthy tissue and its ability to internalize could advantageously be used to develop a new diagnostic and therapeutic approach. My thesis project had several objectives: 1) To optimize a magnetic nano-platform for an effective targeting of tumor cells overexpressing the CCK2R; 2) To validate the targeted nanotherapy strategy by magnetic hyperthermia to specifically eradicate tumor cells overexpressing the CCK2R, and study the mechanisms involved in cell death; 3) To develop strategies in order to increase the anti-tumor therapeutic efficiency. Firstly, I have developed a nano-platform composed of a SPION (superparamagnetic iron oxide nanoparticles) type magnetic nanoparticle (MNP). I developed different batches of MNP with different ligand densities at their surface and analyzed their binding capacity, internalization and lysosomal accumulation. Targeted nanoparticles uptake is receptor dependent, reaching a rate of 2.2 pg iron/cell, after 24 hours of incubation. Thus, I validated the strategy of targeted nanotherapy by magnetic hyperthermia. For this, I applied a high frequency alternating magnetic field (275 kHz, 40 mT) on cells with or without internalized MNPs. The application of the magnetic field induces the death of 30% of tumoral cells having internalized MNPs, without any perceptible temperature rise in the incubation medium, suggesting that the magnetic hyperthermia would probably be induces very locally at the scale of the nanoparticules or the lysosome. We called this phenomenon intra-lysosomal magnetic hyperthermia. Then, I studied the cellular mechanisms involved in the induction of cell death by intra-lysosomal magnetic hyperthermia. My results showed that the application of a magnetic field increased the production of reactive oxygen species (ROS), leading to lysosomal membrane permeabilization and to the leakage of lysosomal enzymes in the cytosol of cells having internalized MNPs, indicating that ROS production and lysosomal cysteine proteases are involved in the mechanisms of cell death. Finally, in order to increase the therapeutic efficacy, I combined this intra-lysosomal magnetic hyperthermia treatment to a chemotherapeutic treatment, the doxorubicin. The results showed an additive effect of hyperthermia and chemotherapy treatments. This combining therapeutic strategy presents the advantage of using low doses of chemotherapeutic agent, in order to decrease the side effects towards healthy cells
APA, Harvard, Vancouver, ISO, and other styles
49

CHAUDRON, FRANCOIS. "Interet des chemoembolisations dans le traitement des metastases hepatiques des tumeurs endocrines digestives." Lyon 1, 1991. http://www.theses.fr/1991LYO1M241.

Full text
APA, Harvard, Vancouver, ISO, and other styles
50

Biondi, Christine A. "Mouse models of multiple endocrine neoplasia type 1 (MEN 1)." Thesis, Queensland University of Technology, 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Endocryne tumour' for other source types:
Journal articles Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography