Дисертації з теми "Cancers poumon et sein"
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Soussan, Michaël. "Developpement et applications cliniques de methodes de quantification en TEP pour le pronostic et le suivi therapeutique des cancers." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA112135.
In the era of personalized medicine, genomics and targeted therapies, the availability of quantitative tools assisting the interpretation of medical images is essential. In Positron Emission Tomography (PET), beyond measurements of uptake intensity, it is possible to derive quantitative index characterizing the metabolic volume or the tumoral heterogeneity. The objective of this work was to investigate the value of new quantitative indices to enhance PET imaging, allowing for a more comprehensive analysis of the whole tumor. The first part of the work deals with methodological issues associated with the measurement of tumor heterogeneity using textural index. In particular, we identified the most robust and informative textural index for clinical applications. Two sets of patients have then been used to explore the contribution of metabolic volume and texture analysis in PET. In lung cancer patients, our results suggest that the measurement of tumor heterogeneity gives some information regarding the histological features of the tumor. A second set of results shows that metabolic volume is more relevant than conventional indices for evaluating the impact of neoadjuvant chemotherapy in locally advanced stages. A correlation between quantitative changes during treatment and post-treatment histology results was used to demonstrate the relevance of these indices. In breast cancer patients, our results suggest that tumors with aggressive immunohistological patterns, particularly triple-negative phenotype, have a more heterogeneous texture than other types. In summary, our results suggest that a more comprehensive quantitative characterization of the metabolic activity distribution in tumor using PET imaging improves the pre-therapeutic and prognostic evaluation of cancer
Chaisemartin, Luc de. "Etude de l’organisation et des fonctions des lymphocytes T au sein des structures lymphoïdes tertiaires dans le cancer pulmonaire." Paris 6, 2010. http://www.theses.fr/2010PA066684.
El, Kadiri Hanae. "Mise en évidence de l'activité antitumorale du taxol au moyen de tests in vitro sur cellules humaines : cancers bronchiques à petites cellules (lignée NCI-N 417), de l'ovaire et du sein." Université Joseph Fourier (Grenoble), 1988. http://www.theses.fr/1988GRE18002.
Toullec, Alexis. "Dispositif d’aiguille fibrée pour la spectroscopie de fluorescence endogène de lésions mammaires et pulmonaires ex vivo et in vivo ; vers le développement d'une méthode d’ histopathologie in situ." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS154/document.
The third Cancer Plan, launched in 2013, identifies early diagnosis as one of the major challenges for improving patient care. Despite the growth in medical imaging modalities and performance, challenges remain in diagnosis aid and optimizing the use of biopsy.Photonic imaging and especially spectrally resolved fluorescence has already been tested for the ex vivo characterization of breast and lung tumors, without contrast agent or sample processing. Our goal is to characterize the capabilities of an innovative medical device, developed in the laboratory, using a low-caliber fibered needle for the spectral analysis of the endogenous fluorescence of these lesions in situ. Our early work in preclinical and clinical studies showed significant differences in spectral signatures between benign and malignant tumors ex vivo and in vivo. Our results also highlighted the limits the device, in terms of specificity, for certain types of lesions.Another study was conducted on mammary tumors in order to identify the major tissue entities at the origin of the spectral signatures obtained with our fibered device. Spectral imaging in confocal and second harmonic microscopy (SHG), in multiphoton, has been implemented in order to establish a mapping of endogenous biomarkers of mammary tissues. We compare its results with the data obtained with the fibered needle device in order to position it not only as an aid to diagnosis but also as a promising method for in situ histopathology
Marchand, Anne. "Reconnaissance et occultation des cancers professionnels : le droit à réparation à l'épreuve de la pratique (Seine-Saint-Denis)." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLE005.
Cancerous pathologies, currently the leadingcause of death in France, are also one of the main causes of social inequalities before death. The importance of occupational factors in the onset of the disease remains largely under-estimated, particularly because very few cancr patients exercise their right to compensation for occupational diseases, a phenomenon officially described as "under-reporting" and "under-recognition". This research, which has benefited from data collected by a program designed to identify and support occupational-cancer patients implemented since 2002 in the French département of Seine-Saint-Denis by the the French "Groupement d'Intérêt Scientifique sur les Cancers d'Origine Professionnelle" (ie GISCOP93, a scientific association for occupational cancers), set out to monitor current and former workers and employees who have been diagnosed with broncho-pulmonary cancer as well as their families, as they go through the process of seeking and obtaining compensation, in order to identify the factors that determine whether they do or do not exercise their rights. This research, based on the data gathered during this phase of ethnographical research, on archival holdings and on observations in a French "Caisse primaire d'assurance maladie" (CPAM, ie local healthcare insurance office), comprises three parts. After describing the research protocol that was implemented, the first part focuses on identifying the conditions required for occupational-cancer patients, to exercise their rights: they need to learn to perceive themselves as "victims" of their occupational history and to find the resources necesary to start the compensation-seeking process. The second part focuses on retracing the history of the medical and legal category of occupational cancer, which was first defined in the early 20th century, and more specifically, on the history of broncho-pulmonary cancers. This part describes the conditions which led to creating the notion of "presumed origin" - a cornerstone of the occupational-harm reparation system - in the case of this specific type of cancer. By retracing the stages of evolution of a table of occupational diseases from the early 1920s to the early 1990s, it illustrates how fragile this last category can be. The third section records what happens when the right to compensation is enforced by the institution in charge of investigating claims, revealing what takes place behind the scènes during the investigation of a claimand the conditions that define whether and when a case of cancer is recognized as an occupational disease
Bennis, Fai͏̈za. "Etude de la 3-hydroxy-3-méthylglutaryl coenzyme à réductase dans la lignée d'adénocarcinome pulmonaire humain A5449 : régulation et implication dans la croissance cellulaire." Toulouse 3, 1993. http://www.theses.fr/1993TOU30263.
Ortholan-Nègre, Cécile. "Approche translationnelle du concept de cible en cancérologie : étude de l'effet combiné du Docetaxel et du Bevacizumab sur la boucle autocrine VEGF / VEGF-R2 dans des modèles cellulaires de cancer du sein et de la prostate : étude d'une signature microARN pronostique dans les adénocarcinomes du poumon de stade I." Nice, 2010. http://www.theses.fr/2010NICE4083.
Targeted therapies are and important part of cancer treatment. Oncologist may have an overview of potential targets, and may understand the synergic effect of chemotherapies and targeted therapies. Tumor neoangiogenesis represent a critical step in tumor development. Main anti angiogenesis targeted therapy is Bevacizumab, which is a monoclonal antibodies inhibiting the binding VEGF (vascular endothelial growth factor) to its receptor. Docetaxel is one of the most important chemotherapy in cancer treatment. It inhibits microtubule depolymerisation. In breast and prostate cancer, Docetaxel delivered in association with Bevacizumab increases tumor response compared with Docetaxel alone. In this work, we investigated the combined effect of both treatments on the VEGF / VEGF-R2 autocrine loop, in breast and prostate cancer cells. We have demonstated that, in standard condition, the VEGF / VEGF-R2 loop is redundant in terms of cell survival. However, when cells are treated with Docetaxel, main growth pathways are inhibited: then, the VEGF / VEGF-R2 autocrin,e loop is useful for cell survival. The addition of Bevacizumab to Docetaxel inhibits the autocrine loop by decreasing extracellular VEGF and membrane expression of VEGF-R2, leading to cell proliferation arrest. Then, inthis work, we propose a new explanation for the synergiec effect of Taxane and Bevacizumab on tumor cells. Another approach in the understanding of targeted therapy action is the identification of prognostic and therapeutic targets. In the second part of this work, we have investigated the microRNA expression pattern of 27 stage I lung adenocarcinomas. By screening microRNA expression on microchip, we have highlighted the presence of a prognostic signature, predicting cancer outcome : under expression of mir99a and mir30a, over expression of mir 297 and mir 21. The signature is under validation on a large series of patient. As a conclusion, both parts of this work investigate two aspects of the target concept in oncology, by studying mechanism of synergy between a targeted therapy and chemotherapy, and by searching new targets such as microRNA
Ducrot, Lucas. "Réseaux bayésiens et analyse de survie pour l’estimation de courbes de pénétrance du cancer broncho-pulmonaire lié à des prédispositions génétiques." Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS055.
This thesis focuses on estimating penetrance curves of genetic diseases from pedigree data, with a particular interest in the genetic predisposition to bronchopulmonary cancer. In this context, it aims to provide clinical and epidemiological results, as well as methodological findings.Genetic counselling is offered to patients with severe family histories of genetic diseases. Geneticists must select from these patients who should be offered genetic testing, and assess the disease risks for these patients and their families. Advances in genetics are rapid, and the number of identified pathogenic variants for different diseases increases each year. This necessitates significant predictive and risk assessment tools, especially in the context of bronchopulmonary cancer. Indeed , the links between the latter and pathogenic variants (such that SFTPA1/SFTPA2 and the genes TP53 and EGFR) are known but still poorly described.Existing methods for assessing the risk of disease occurrence rely on penetrance curves, but their estimation faces challenges due to the small number of patients and the omnipresent selection bias in genetics-collected datasets. To overcome these obstacles, the thesis explores the use of familial data, employing a set of statistical tools including Bayesian networks, mixture models, survival analysis, as well as existing models, for which it attempts to weaken certain assumptions.Chapter 1 provides an overview of the medical context of the thesis, introducing the concepts of genetic diseases and genetic counseling. Chapter 2 serves as a methodological introduction, presenting and illustrating concepts such as survival analysis, Bayesian networks, sum-product algorithm, mixture models and EM algorithm, using examples. It also offers a state-of-the-art review of penetrance curve estimation for genetic diseases and highlights the selection bias in genetics. The chapter concludes with a summary of the addressed research questions.Then, the thesis revolves around four projects. The first two projects, corresponding to chapters 3 and 4, offer predominantly clinical and epidemiological results. The first project, described in Chapter 3, compares different methods for predicting pathogenic variants for breast/ovarian cancers (Manchester Score and family models like BOADICEA). The second project, addressed in Chapter 4, provides estimates of penetrance for interstitial lung disease and bronchopulmonary cancer for carriers of pathogenic variants SFTPA1 and SFTPA2.The last two projects, corresponding to chapters 5 and 6, are more methodological. Chapter 5 is dedicated to developing a new method for estimating the penetrance curve of a genetic disease from pedigree data when the disease presents sporadic cases. It is based on an incidence constraint of the disease in the general population and a parameterization of the relative hazard between carriers and non-carriers of pathogenic variants. Chapter 6 focuses on highlighting the bias introduced by selection in genetics and its consequences on the results of the method developed in Chapter 5. Known correction methods, such as Proband's Phenotype Exclusion Likelihood (PEL) and Genotype-Restricted Likelihood (GRL), combined with our method, are applied to simulated data
Mombelli, Sarah. "Cancers du sein et immunité anti-tumorale." Thesis, Reims, 2014. http://www.theses.fr/2014REIMS041/document.
With around 49 000 new affected women each year, breast cancer is the most common of feminine cancers. Breast cancer screening, and treatments improvements make mortality decreased but it stays the most murderous of feminine cancers in France.Breast cancer being a heterogeneous disease, individualizing patients' treatments is now one of first goals of practitioner. It is around of this common aim that my 2 thesis projects are turned on.On the one side, for clinical study, I designed a database on the neoadjuvant strategy of operable breast cancers, assembling 318 patients treated at Jean Godinot institute. This database allow us to compare our results with literature ones, to highlight the interest of neoadjuvant chemotherapy to determine new prognostic factors, and to validate evaluation of residual disease in breast and nodes by RDBN index.On the other side experimental study allowed us to improve our knowledge on molecular mechanisms of tumor escape. We demonstrated pro-tumoral role of IL-17A but also of IL-17E, these two cytokines can be presents in tumoral microenvironment, and evidenced their implication in cell cycle dysregulation through generation of LMW-E and acquisition of chemoristance mechanisms
Martin, Marie-Claude. "Cancers broncho-pulmonaires primitifs chez les sujets de 75 ans et plus." Bordeaux 2, 1999. http://www.theses.fr/1999BOR2M111.
Bigras, Gilbert. "Corrélation entre sociologie cellulaire et cycle cellulaire dans les cancers du poumon." Université Joseph Fourier (Grenoble), 1997. http://www.theses.fr/1997GRE19006.
DRAOUI, AHMED. "Metastases pulmonaires et osseuses des cancers differencies de la thyroide : aspects diagnostique, therapeutique et pronostique." Lille 2, 1990. http://www.theses.fr/1990LIL2M318.
Delpous, Stéphanie. "Interêt de TFF1 et TFF3 dans les cancers du sein." Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ049.
The breast cancer adjuvant treatment decision is often difficult. Currently, it is necessary to develop new prognostic and predictive markers in oncology. Trefoil factor 1 (TFF1) and trefoil factor 3 (TFF3) are two related small secreted proteins induced by estradiol in mammary epithelial cancer cells. Studied in isolation, their value as prognostic markers was controversial and contradictory results were reported. The aim of our study was to evaluate the prognostic value of combined TFF1 and TFF3 dosages in a prospective breast cancer series. ln agreement with the literature, we found that TFF1 and/or TFF3 expressions were specific to estrogen-receptor positive tumours ("luminal-like"). ln contrast with previous reports, TFFi and TFF3 were expressed independently from each other in some tumors. Of interest, the presence of bath TFF1 and TFF3 was associated with poor prognosis elements, distinguishing a high-risk subtype within luminal breast cancers.Therefore, TFF1 +/TFF3+ breast cancers should be considered for adjuvant therapy. TFF1 andTFF3 are secreted under distinct molecular forms, monomers, homodimers and heterodimers.These distinct molecular forms are supposed to have different functions. By using proximity ligation assay (PLA), we found TFF1/TFF3 heterodimers in double-positives cancer samples. These data suggest that TFF1/TFF3 heterodimer may contribute to the aggressive phenotype observed in double positive tumors
Bonsang-Kitzis, Hélène. "Caractérisation moléculaire et immunité des cancers du sein triple-négatifs." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS162.
Triple negative breast cancer (TNBC) is the most heterogeneous and pejorative subtype of breast cancer. The cornerstone of the treatment of such tumors is based on systemic chemotherapy, more and more frequently administered before surgery, since no targeted therapy has been validated to date. Obtaining a pathological complete response (PCR) is a major favorable prognostic marker as well as an in vivo test of anti-tumor drug susceptibility. The objective of our thesis work was therefore to provide elements of understanding of this heterogeneity through the clinical, biological and molecular dissection of these tumors.We analyzed gene expression profiles of TNBCs and identified 6 distinct molecular subtypes with different biologies and prognoses. This classification used an original methodology based on both classical bioinformatic tools and biological networks. The enrichment of immunity genes from the stromal compartment of the tumor represents a major determinant of the prognosis of these tumors: a strong expression of the immunity genes is associated with a significantly more favorable prognosis.Our main contribution is based on a better understanding of immunity and tumor infiltrated lymphocytes (TILS) of these TNBCs. It is probably the most immunogenic subgroup of breast cancers with the highest TILs levels pre-NAC with HER2-positive tumors. TILS levels are also highly correlated with genes of our immune prognosis module. The predictive and prognostic value of stromal TILS is different according to the molecular subtype of breast cancer, suggesting a completely different immunity of these tumors. The rate of TILS also varies differentially within each subgroup under the influence of the NAC, indicating a complex interaction between TILS and treatments. We show that the kinetics of TILS levels with NAC is a relevant indicator of response to NAC with a response that is all the more important that a decrease in the TILS rate will be important. The most immunogenic tumors with an important immune activity are therefore the most favorable triple-negative tumors. One of the challenges of the coming years will therefore be to identify, as soon as possible, the least immunogenic TNBC that can best benefit from immunotherapies alone or in combination with chemotherapeutic treatment in order to activate or restore early a deficient immunity.Under the same denomination of TILS there are probably different phenotypic populations of lymphocytes. Indeed, after CNA, their prognostic value is opposite between the TNBC and the HER2-positive tumors: high levels of TILS are associated with an unfavorable prognosis in HER2-positive tumors whereas they have a tendency to be associated with a better prognosis for TNBC tumors. The interactions are complex between cytotoxic agents and the tumor and / or its microenvironment. The analysis of the breast or axillary lymph node residual disease represents an underutilized material that could lead to a better understanding of the mechanisms of sensitivity or resistance to treatment.Beyond the key role immunity for these tumors, our work identifies some TNBCs for which the hormonal environment, through the body mass index or the menopausal status, could play a role. Thus, the exploration of the metabolome, immune features in overweight / obese patients or the analysis of the androgen-receptor pathway (and its connections with the estrogen and progesterone-receptor pathways) of the TNBC must also be explored. This opens up possible treatment perspectives for some patients
CHARET, JEAN-CHRISTOPHE. "La biologie dans les cancers broncho-pulmonaires : statut et index simplifie." Amiens, 1993. http://www.theses.fr/1993AMIEM071.
Van, Den Broeck Arnaud. "Aspects épigénétiques des cancers broncho-pulmonaires et implication de l'histone acétyltransférase Tip60." Grenoble 1, 2009. http://www.theses.fr/2009GRE10150.
Epigenetic defines reversible and inheritable modifications of gene expression without change in nucleotide sequence. It is now well-known that epigenetic modifications such as DNA methylation contribute to the development of cancer. Tip60 protein is a transcriptional co-regulator which possesses an histone acetyltransferase (HAT) activity. Tip60 is also a key component of the DNA damage response (DDR) and plays a crucial role in the control of genome stability through its ability to acetylate proteins. We have previously shown that Tip60 is a key component of DDR pathways activation induced by tobacco carcinogens and have hypothesized that a modification of histone and/or non histone proteins acetylation pattern could constitute a new epigenetic hallmark of lung cancer. We have shown for the first time in lung cancer a global alteration of the “epigenetic landscape” of histone H4, which is the main Tip60 target. Our results show that some epigenetic modifications (H4K20me3) might be candidate biomarkers for early detection and therapeutic approaches of lung cancer. Furthermore, we identify Tip60 as a new regulator of expression and biological properties of the E2F1 transcription factor. We also demonstrate that both proteins play a coordinated role in the DDR induced by cisplatine, by working on DNA repair pathways. Finally, we observe the frequent loss of Tip60 protein expression in these cancers, suggesting that Tip60 might be a candidate biomarker for the response to treatment with platinium based chemotherapies
Baudier, Philippe. "Les cancers du sein de type III traités par radiothérapie et chirurgie partielle." Montpellier 1, 1990. http://www.theses.fr/1990MON11276.
Beffy, Céline. "Les cancers bronchopulmonaires : données fondamentales et prise en charge thérapeutique." Paris 5, 1997. http://www.theses.fr/1997PA05P200.
Roche, Olivier. "Forme kystique des cancers broncho-pulmonaires primitifs : 5 observations cliniques et revue de la litterature." Université Louis Pasteur (Strasbourg) (1971-2008), 1990. http://www.theses.fr/1990STR1M189.
Leclercq, Guy. "Base moléculaire de la sensibilité oestrogénique des cancers du sein." Doctoral thesis, Universite Libre de Bruxelles, 1993. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212861.
Thibaut, Béatrice. "Suivi thérapeutique de cancers pulmonaires inopérables et/ou polymétastasés : essai préliminaire chez vingt trois patients traités par polychimiothérapie." Paris 5, 1990. http://www.theses.fr/1990PA05P014.
Loriot, Yohann. "Influence de l’inhibition des signaux de survie et radiosensibilisation des cancers pulmonaires." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T072/document.
Targeted therapies are drugs that block a specific molecular target involved in following alterations in cell physiology: growth signal self-sufficiency, insensitivity to growth-inhibitory signals, evasion of apoptosis, an unlimited replicative potential, sustained angiogenesis, tissue invasion, and metastasis. Although these compounds showed efficacy when given alone, there is now a rationale to combine these agents with other antitumor therapies such as chemotherapy, radiation and surgery. In this context, there is compelling data supporting the association between targeted therapies and radiation. The better understanding of mechanisms of sensitivity or resistance to radiation may help to envision new strategies to improve its efficacy. The primary goal of this work was to assess new strategies of radiosensitization based on molecular characteristics of both small cell lung cancer (by targeting Bcl-2 and Bcl- XL proteins as well as IGF-I pathway) and non-small cell lung cancer (by targeting EGFR pathway). The second objective was also to assess new methods to better investigate combination of radiation with new targeted therapies. In the first part of the work, we evaluated the impact of the inhibition of BCL-2 in small cell lung cancer cell lines with oblimersen, an antisense BCL-2 oligodeoxynucleotide and with a small peptide BH3 mimetic, S44563 which targets both Bcl-2 and Bcl- XL proteins. We showed that inhibiting anti-apoptotic mechanisms could enhance radiosensitivity of SCLC cells. S44563 caused SCLC cells to acquire hallmarks of apoptosis through activation of the mitochondrial pathway in Bcl2 and Bcl- XL overexpressing cell lines. S44563 markedly enhanced the sensitivity of SCLC cells to radiation in both in vitro and in vivo assays through apoptosis induction. This positive interaction was explained by the induction of radiation-induced anti-apopototic proteins, mainly Bcl- XL by the NF-κB pathway. These data were confirmed by in vivo experiments showing that the radiosensitization was greater when S44563 was given after the completion of the radiation in the context of radiation-induced oncogenic addiction. In the second part of the work, we showed that IGF-1R targeting increases the antitumor effects of DNA-damaging agents in SCLC model. R1507 (a monoclonal antibody directed against IGF-1R), exhibited synergistic effects with both cisplatin and IR in SCLC cell lines through IGF-IR downregulation and reduced activation of downstream AKT. However, we observed a transient reduction of IGF-1R staining intensity in vivo, concomitant to the activation of multiple cell surface receptors and intracellular proteins involved in proliferation, angiogenesis, and survival. These data underscore the challenge of the combination of concomitant radiotherapy and chemotherapy and support the early use of targeted therapies to improve the antitumor efficacy
Paridaens, R. "Caractérisation et exploitation thérapeutique des propriétés d'hormonodépendance des cancers du sein." Doctoral thesis, Universite Libre de Bruxelles, 1987. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213511.
GUILLET, PIERRE. "Valeur et imperfections de l'examen clinique dans les cancers du sein." Aix-Marseille 2, 1989. http://www.theses.fr/1989AIX20037.
BONNIER, PASCAL. "Aspects epidemiologiques et pronostiques recents des cancers du sein. La tumeur et son environnement." Aix-Marseille 2, 1997. http://www.theses.fr/1997AIX20667.
JOLY, DE MICHELI ANNICK. "Les cancers du sein impalpables : analyse morphologique et evolution de 114 cas." Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX2O240.
Adam, Julien. "Création de biomarqueurs à visée pronostique et prédictive dans les cancers broncho-pulmonaires." Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS260.
Non-small cell lung cancers (NSCLC) remain a leading cause of cancer-related death despite the advent of targeted therapies and immunotherapies. At advanced stages, patient survival remains limited and establishment of new biomarkers, either prognostic for patient stratification or predictive of response to various therapies, is an important goal for patient’s treatment.Development of biomarkers is dependent on many components among which: knowledge of cancer cell biology in complex cellular processes such as DNA repair, characteristics of tools available to create biomarkers and applicability in daily medical practice.In this thesis, expression of PARP1 has been evaluated as a prognostic biomarker in NSCLC, in the broader context of DNA repair biomarkers. The biological and clinical relevance of MMS19 protein, identified in gene expression analysis , as a biomarker for cisplatin sensitivity in NSCLC has also been studied. Finally, the use of circulating tumor cells for biomarker development has been studied through the detection of ALK gene rearrangment, an oncogenic targetable alteration in NSCLC
Falque, Laurent. "Cancers broncho-pulmonaires primitifs chez les sujets de 40 ans et moins." Bordeaux 2, 1997. http://www.theses.fr/1997BOR23098.
Beauchamp, Thierry. "Les métastases hypophysaires : aspects cliniques et revue de la littérature : à propos de 3 cancers bronchopulmonaires." Bordeaux 2, 1988. http://www.theses.fr/1988BOR25385.
Descotes, Françoise. "Oncogenes et cancers : interet de l'etude de her-2/neu dans les cancers du sein et de c-ha-ras-1 et c-k1-ras-2 dans les tumeurs de la vessie." Besançon, 1992. http://www.theses.fr/1992BESA3717.
GOMEZ, FREDERIC. "Suivi epidemiologique des cancers du sein : description et analyse des perdues de vue." Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20860.
Petit-Gaillard, Stéphanie. "Les cancers mammaires bilatéraux synchrones et métachrones chez la femme." Montpellier 1, 2001. http://www.theses.fr/2001MON11004.
BALDUIN, MARIE-THERESE. "Radiotherapie a visee curative des cancers broncho-pulmonaires non a petites cellules t1n0 et t2n0 : a propos de 53 observations." Lyon 1, 1989. http://www.theses.fr/1989LYO1M169.
LEVY-NEUMAND, OLIVIER. "Les metastases pleuro-pulmonaires et mediastinales des cancers colorectaux : a propos de 19 observations en milieu pneumologique." Lyon 1, 1989. http://www.theses.fr/1989LYO1M158.
Gligorov, Joseph. "Polymorphismes et traitements néoadjuvants des cancers du sein : efficacité du docétaxel et polymorphisme d’ABCB1/MDR1." Paris 6, 2012. http://www.theses.fr/2012PA066082.
In non-metastatic breast cancer, neoadjuvant treatment allows to study the parameters influencing their effectiveness, related to the tumor and / or the host. The MDR family proteins, especially ABCB1 are involved in the mechanisms of resistance to anthracyclines and taxanes. The correlations between efficiency (histological response), ABCB1 polymorphism (patients and tumors) and pharmacokinetics of doxorubicin and docetaxel have been studied in the context of a therapeutic trial. In this study, polymorphism in exon 26 of ABCB1 (rs1045642) is the only that influences the pharmacokinetics of docetaxel and this only in premenopausal patients. Patients carrying CC genotype (40%) have an average value of the AUC of docetaxel significantly lower than those carrying genotypes CT (45%) and TT (15%) (p <0. 0001). Moreover it was found in premenopausal patients a statistically significant correlation between low rates of docetaxel AUC and diplotype 2677GG-3435CC and 1236CC haplotype-61AA-2677GG-3435CC. It has not been found a link between ABCB1 polymorphisms and the pharmacokinetics of doxorubicin. There is also a negative relationship between AUC of docetaxel and pathological response. There seems therefore that a minimum value of AUC of docetaxel is necessary to obtain a response. Furthermore, we found an association between tumor response and polymorphism of ABCB1 (C3435T genotype, CT and TT vs. CC)
Gligorov, Joseph. "Polymorphismes et traitements néoadjuvants des cancers du sein : efficacité du docétaxel et polymorphisme d'ABCB1/MDR1." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2012. http://tel.archives-ouvertes.fr/tel-00829467.
Negulescu, Ana-Maria. "Caractérisation des récepteurs à dépendance Notch3 et Kremen1 dans les cancers." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1265.
Membrane receptors are major actors of the interaction between a cell and its environment. They are able to trigger different types of signals such as survival, differentiation, migration or cell death. The work presented in this manuscript has been done on a particular family of receptors called dependence receptors. They are characterized by their function rather than by their structure. In the presence of their ligand they induce a survival signal whereas in the absence of the ligand they induce an active signal of cell death. Two new dependence receptors have been studied: Notch3 and Kremen1, in the context of homeostasis control, and more particularly in the control of breast cancer tumorigenesis. We show that Notch3 dependence receptor is lost in breast cancer, because of a significant gain of methylation observed between the normal tissu and the tumoral tissue within the same patient. Notch3 plays also a pro-apoptotic role in endothelial cells of lung cancer. Experiences carried on cancer cohorts have allowed us to notice that the Dickkopf (Dkk1) ligand, which links the Kremen1 receptor, is over-expressed in several cancers whereas the receptor is lost in different cancers. Restoring Kremen1 expression or disabling Dkk1 in breast cancer basal type MDA-MB 231 cells, leads to large autophagic cell death. Concerning therapeutic approaches, we selected several antibodies against Kremen1 extra-cellular domain, which induce the death of cancer cells
ESSAFI, NAJET. "Place et role du ca 15-3 : dans les cancers du sein metastases." Nice, 1989. http://www.theses.fr/1989NICE6587.
Quemener, Cathy. "Rôle de la glycoprotéine EMMPRIN dans l'invasion et l'angiogenèse des cancers du sein." Paris 7, 2008. http://www.theses.fr/2008PA077232.
The metastatic process is related to tumor invasion and angiogenesis and depends largely on the degradation of the basal membrane and the extracellular matrix by proteases such as matrix proteases (MMP) and serine proteases (uPA, plasmin). EMMPRIN is a membrane glycoprotein overexpressed in many cancer tissues and is known for its ability to stimulate MMP expression both in tumor and stromal cells. In this work, we showed that EMMPRIN also regulates the System of urokinase plasminogen activator (uPA) and its receptor (uPAR) in stromal cells and in various tumor models, thus participating to the increase of the overall proteolytic function of the cancer cells in vitro and in vivo. We also showed that EMMPRIN induces the expression of VEGF in endothelial cells, and more specifîcally the expression of VEGF soluble isoforms and their receptor VEGF-R2. These isoforms specifîcally induced are involved in the processes of tubulogenesis and survival of endothelial cells. We also suggest that this VEGF upregulation by EMMPRIN could involve the transcription factor HIFI-a in normal conditions of oxygen pressure. All this work will validate the role of the glycoprotein EMMPRIN in the development of metastasis and tumor angiogenesis in breast cancer and contribute to target its optimal pharmacological inhibition for a future clinical application
Guérard, Marie. "Signalisation nucléaire de l'IGF-1R et résistance aux thérapies anti-EGFR dans les cancers du poumon." Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV085/document.
Responsible of 1.6 million deaths each year worldwide, lung cancer is today the leading cause of cancer mortality in the world. Non-small-cell lung cancers account for about 85% of lung cancer and have a very bad prognosis (5-year survival rate inferior to 10%). EGFR-TKI (EGFR tyrosine kinase inhibitors, gefitinib) are a real medical advance for lung cancers treatment. However, these treatments are efficient in a small subgroup of patients. So, one of the current issues is to identify primary resistance mechanisms involved in tumors.Tyrosine kinase receptors (RTK) activate intracellular signaling pathways from the plasma membrane. These last years, a nuclear translocation of the RTK was shown. Recent works suggest that RTK nuclear signaling could contribute to tumors resistance in response to anti-cancerous therapies.In our team, it was shown that activation of IGF-1R signaling is associated with lung adenocarcinoma progression and that gefitinib induces IGF-1R nuclear accumulation in a mucinous adenocarcinoma cell line. On the basis of these results, we hypothesize that nuclear IGF-1R could play a role in the resistance of mucinous lung adenocarcinoma to EGFR-TKI.Our results indicate that more than 70% lung adenocarcinoma tumors present a positive IGF-1R nuclear staining. Thanks to EGFR-TKI-resistant cell lines, we show that gefitinib induces the nuclear accumulation of IGF-1R in mucinous adenocarcinoma. This nuclear translocation involves clathrin-mediated endocytosis and a complex between IGF-1R, importin β1 and pro-amphiregulin. Amphiregulin silencing prevents IGF-1R nuclear translocation in response to gefitinib and restores gefitinib-induced apoptosis in vitro and in vivo. Our whole results identify that IGF-1R intracellular trafficking is a new component of response to EGFR-TKI and strongly suggest that a nuclear IGF-1R/amphiregulin signaling contributes to mucinous lung adenocarcinoma progression in response to EGFR-TKI
Vandewalle, Brigitte. "Oestrogènes et catécholoestrogènes dans les cancers du sein : effets sur la croissance et la différenciation cellulaires." Lille 1, 1987. http://www.theses.fr/1987LIL10209.
Bigos, Sylvie, and Évelyne Cempel. "Cancers broncho-pulmonaires primitifs : suivi de 195 patients recrutes de 1985 a 1989 dans la region miniere d'henin beaumont." Lille 2, 1992. http://www.theses.fr/1992LIL2M027.
Pierga, Jean-Yves. "Recherche et caractérisation phénotypique et génotypique des cellules tumorales médullaires et sanguines dans les cancers du sein." Paris 11, 2003. http://www.theses.fr/2003PA11TO26.
Espitalier, Marion. "Les cancers inflammatoires du sein PEV3 (ou mastites carcinomateuses) : méthodes et résultats thérapeutiques de 1976 à 1981 au CLRC de Montpellier." Montpellier 1, 1988. http://www.theses.fr/1988MON11050.
Bertholon, Jacques. "Instabilité chromosomique dans les cancers du sein et du côlon : implication des gènes CHRF et p21WAFI." Lyon 1, 2006. http://www.theses.fr/2006LYO10272.
In order to study the connection between the perturbation of the microtubule network, the chemoresistance to anticancer therapeutic agents and the phenotype CIN, we first studied the role of Chfr. We did not observe any direct relationship between the loss of the Chfr expression and the CIN phenotype in colon and breast cancer samples. We also investigated the mechanisms responsible for drug resistance to Paclitaxel and their relationship with the CIN phenotype. For this purpose, we have developed a model of human mammary epithelial cells resistant to Paclitaxel. A thorough analysis of the Paclitaxel-resistant clones suggests that p21WAF1 inactivation may play an important role in the acquisition of chemoresistance and CIN phenotypes observed in these cells
Vandewalle, Brigitte. "Oestrogènes et catécholoestrogènes dans les cancers du sein effets sur la croissance et la différenciation cellulaires /." Grenoble 2 : ANRT, 1987. http://catalogue.bnf.fr/ark:/12148/cb37610560t.
Cabelguenne, Arnauld. "GSTP1 et p53 : marqueurs prédictifs de la réponse à la chimiothérapie associant le 5-Fluorouracile et le Cisplatine dans les cancers des voies aérodigestives supérieures." Paris 5, 2003. http://www.theses.fr/2003PA05N109.
Optimization of therapeutic strategy requires prior determination of predictive parameters of patients' response to anti-cancer drugs. In head and neck cancer patients treated by induction chemotherapy based on Cisplatin and 5-Fluorouracil, we showed a link between the presence of allelic GSTP1105val and the more important presence of mutations in p53 gene, that GSTM1 gene deletion was a risk factor of laryngeal cancers (2,6 times), that chemotherapy response is associated with a low plasma level of GSTP1. Presence of p53 mutations led to a decrease of chemo-sensibility to CDDP and to 5-FU. We identified a significant difference between the presence of p53 mutations in responder patients and non-responder patients (61% versus 81%). Predict the response to chemotherapy is now possible
Rigaill, Guillem. "Développements statistiques et algorithmiques pour l'analyse des cancers du sein de type triple négatif." Phd thesis, AgroParisTech, 2010. http://pastel.archives-ouvertes.fr/pastel-00593939.
Molist, Romain. "Caractérisation cytogénétique et moléculaire d' un nouveau sous-type de cancers du sein canalaires." Paris 7, 2005. http://www.theses.fr/2005PA077111.
TORCHARD, DELPHINE. "Recherches sur la predisposition aux cancers du sein et de l'ovaire : le gene brca1." Paris 7, 1997. http://www.theses.fr/1997PA077306.