Littérature scientifique sur le sujet « Mutantp53 »
Créez une référence correcte selon les styles APA, MLA, Chicago, Harvard et plusieurs autres
Sommaire
Consultez les listes thématiques d’articles de revues, de livres, de thèses, de rapports de conférences et d’autres sources académiques sur le sujet « Mutantp53 ».
À côté de chaque source dans la liste de références il y a un bouton « Ajouter à la bibliographie ». Cliquez sur ce bouton, et nous générerons automatiquement la référence bibliographique pour la source choisie selon votre style de citation préféré : APA, MLA, Harvard, Vancouver, Chicago, etc.
Vous pouvez aussi télécharger le texte intégral de la publication scolaire au format pdf et consulter son résumé en ligne lorsque ces informations sont inclues dans les métadonnées.
Articles de revues sur le sujet "Mutantp53"
Shi, Xu-Bao, Nancy J. Nesslinger, Arline D. Deitch, Paul H. Gumerlock et Ralph W. deVere White. « Complex functions of mutantp53 alleles from human prostate cancer ». Prostate 51, no 1 (19 mars 2002) : 59–72. http://dx.doi.org/10.1002/pros.10072.
Texte intégralde Kant, Eric, Immo Heide, Christian Thiede, Richard Herrmann et Christoph F. Rochlitz. « MDR1 expression correlates with mutantp53 expression in colorectal cancer metastases ». Journal of Cancer Research and Clinical Oncology 122, no 11 (novembre 1996) : 671–75. http://dx.doi.org/10.1007/bf01209030.
Texte intégralWyllie, Fiona S., Nick R. Lemoine, Claire M. Barton, Tim Dawson, Jane Bond et David Wynford-Thomas. « Direct growth stimulation of normal human epithelial cells by mutantp53 ». Molecular Carcinogenesis 7, no 2 (1993) : 83–88. http://dx.doi.org/10.1002/mc.2940070205.
Texte intégralKarlsson, Lena, Gunilla Leser, Ulla Delle et György Horvath. « Tumour Growth and Cell Kinetics in Variants of a Human Endometrial Adenocarcinoma Expressing Either Wild-Type or Mutantp53 ». Acta Oncologica 36, no 7 (janvier 1997) : 729–33. http://dx.doi.org/10.3109/02841869709001346.
Texte intégralDi Agostino, Silvia, Giancarlo Cortese, Olimpia Monti, Stefania Dell'Orso, Ada Sacchi, Miriam Eisenstein, Gennaro Citro, Sabrina Strano et Giovanni Blandino. « The disruption of the protein complex mutantp53/p73 increases selectively the response of tumor cells to anticancer drugs ». Cell Cycle 7, no 21 (novembre 2008) : 3440–47. http://dx.doi.org/10.4161/cc.7.21.6995.
Texte intégralKawashima, Kunihiro, Koichiro Mihara, Hisashi Usuki, Nobuyoshi Shimizu et Masayoshi Namba. « Transfected mutantp53 gene increases X-ray-induced cell killing and mutation in human fibroblasts immortalized with 4-nitroquinoline 1-oxide but does not induce neoplastic transformation of the cells ». International Journal of Cancer 61, no 1 (29 mars 1995) : 76–79. http://dx.doi.org/10.1002/ijc.2910610113.
Texte intégralCHEN, Hong-Lin, Yang-Hai XIANG, Ji-Ying ZHAO, De-Dong YIN, Guo-Hua LIANG, Wen-Xue ZHAI et Guang-Huai JIANG. « Genetic Analysis and Gene Fine Mapping of Rice Lesion Mimic Mutantc5 ». Acta Agronomica Sinica 39, no 7 (2013) : 1148. http://dx.doi.org/10.3724/sp.j.1006.2013.01148.
Texte intégralKanai, Nobuko, Theresa M. Vreeke et Charles J. Parker. « Paroxysmal nocturnal hemoglobinuria : Analysis of the effects of mutantPIG-A on gene expression ». American Journal of Hematology 61, no 4 (août 1999) : 221–31. http://dx.doi.org/10.1002/(sici)1096-8652(199908)61:4<221 ::aid-ajh1>3.0.co;2-#.
Texte intégralPothin, H. S., K. V. C. L. da Silva, M. Brendel et J. A. P. Henriques. « Genetic effects of photoactivated psoralens during meiosis in DNA repair mutantpso3-1 ofSaccharomyces cerevisiae ». Current Genetics 25, no 1 (janvier 1994) : 19–23. http://dx.doi.org/10.1007/bf00712961.
Texte intégralNeff, Anton W., F. Briggs et H. M. Chung. « Craniofacial development mutantpi (pinhead) in the Axolotl (Ambystoma mexicanum) which exhibits reduced interocular distance ». Journal of Experimental Zoology 241, no 3 (mars 1987) : 309–16. http://dx.doi.org/10.1002/jez.1402410305.
Texte intégralThèses sur le sujet "Mutantp53"
Marotta, Carolina. « The role of DEPDC1 (DEP domain containing 1) in breast cancer aggressiveness ». Doctoral thesis, Università degli studi di Trieste, 2013. http://hdl.handle.net/10077/8641.
Texte intégralMetastasis formation is the final step in a solid tumour progression and is the most common cause of death in cancer patients. Therefore novel therapeutic strategies to prevent development of metastases have a potential impact on cancer mortality. In the last years, work from our lab has identified that, following oncogenic signalling, the phosphorylation-dependent prolyl-isomerase Pin1 amplifies mutant p53 oncogenic functions. In particular, we have demonstrated the relevance of a Pin1/mutant p53 axis in controlling directly a transcriptional “ten genes signature” program relevant for tumour growth and invasion. This signature includes genes relevant for breast cancer progression, correlated to poor outcome of breast cancer patients. Among these, we have unveiled DEPDC1 as a potent promoter of invasiveness and migration in MDA MB231 triple negative breast cancer (TNBC) cells. This gene is has been found overexpressed in different mouse and human tumours, such as breast carcinoma, colorectal and lung adenocarcinomas. The aim of my PhD work was to investigate the role of DEPDC1 in the cancer progression that is linked to cell-biological traits associated with high-grade malignancy - including motility, invasiveness and loss of polarity. We found that the high DEPDC1 expression level positively correlates with clinical outcome and aggressiveness in breast cancer and we demonstrate that DEPDC1 regulates important phenotypes involved in tumour formation and progression. First, we identified a role of DEPDC1 in promoting aggressive cancer phenotypes in vitro by regulating cell motility, polarity and proliferation. Second, we have evaluated that the establishment of lung metastasis in vivo in mice was reduced upon inhibition of DEPDC1. Third, we demonstrate the tumorigenic potential of DEPDC1-V1 alone or cooperating with oncogenic H-Ras on induction of malignant cell transformation. Finally, a preliminary data shows that DEPDC1 is also able to increase the efficiency of mammosphere formation of breast cancer cells, implicating a role in cancer stemness. Until now, our results support the strong impact of DEPDC1 on tumour progression while molecular pathways perturbed by DEPDC1 and by which drive the cancer progression are still unknown. However, our analysis of RNA-seq data upon silencing of DEPDC1, suggests the mechanism by which DEPDC1 could induce an aggressive phenotype altering the gene expression profile of breast cancer cells. Future studies will address the molecular networks by which DEPDC1 drives the metastatic cancer progression that could be useful for discovering the novel therapeutic targets and diagnostic markers in breast cancer.
XXIV Ciclo
1983
Ndreu, Elma. « Aiming to identify protein co-factors contributing to eIF4E’s oncogenic potential ». Thèse, 2017. http://hdl.handle.net/1866/20400.
Texte intégralActes de conférences sur le sujet "Mutantp53"
Wainwright, John V., Jared B. Cooper, Anisha Chandy, Chirag D. Gandhi, Meic H. Schmidt et Meena Jhanwar-Uniyal. « Abstract 158 : Mutantp53, MAPK and STAT3 promote metastasis to the brain : Demonstrated by protein, gene, and functional analysis ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-158.
Texte intégralWainwright, John V., Jared B. Cooper, Anisha Chandy, Chirag D. Gandhi, Meic H. Schmidt et Meena Jhanwar-Uniyal. « Abstract 158 : Mutantp53, MAPK and STAT3 promote metastasis to the brain : Demonstrated by protein, gene, and functional analysis ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-158.
Texte intégral