Littérature scientifique sur le sujet « Tumor chemoresistance »
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Articles de revues sur le sujet "Tumor chemoresistance"
Yeldag, Gulcen, Alistair Rice et Armando Del Río Hernández. « Chemoresistance and the Self-Maintaining Tumor Microenvironment ». Cancers 10, no 12 (28 novembre 2018) : 471. http://dx.doi.org/10.3390/cancers10120471.
Texte intégralOplt, Alyssa, Elizabeth Stock, Hollie Noia, Patrick Cannon, Gregory Longmore et Katherine C. Fuh. « Abstract 3235 : The role of DDR2 in chemoresistant ovarian cancer ». Cancer Research 82, no 12_Supplement (15 juin 2022) : 3235. http://dx.doi.org/10.1158/1538-7445.am2022-3235.
Texte intégralGronlund, B., E. V. S. Høgdall, I. J. Christensen, J. S. Johansen, B. Nørgaard-Pedersen, S. A. Engelholm et C. Høgdall. « Pre-Treatment Prediction of Chemoresistance in Second-Line Chemotherapy of Ovarian Carcinoma : Value of Serological Tumor Marker Determination (Tetranectin, YKL-40, CASA, CA 125) ». International Journal of Biological Markers 21, no 3 (juillet 2006) : 141–48. http://dx.doi.org/10.1177/172460080602100302.
Texte intégralWu, Qitong, Sumit Siddharth et Dipali Sharma. « Triple Negative Breast Cancer : A Mountain Yet to Be Scaled Despite the Triumphs ». Cancers 13, no 15 (23 juillet 2021) : 3697. http://dx.doi.org/10.3390/cancers13153697.
Texte intégralBelisario, Dimas Carolina, Joanna Kopecka, Martina Pasino, Muhlis Akman, Enrico De Smaele, Massimo Donadelli et Chiara Riganti. « Hypoxia Dictates Metabolic Rewiring of Tumors : Implications for Chemoresistance ». Cells 9, no 12 (4 décembre 2020) : 2598. http://dx.doi.org/10.3390/cells9122598.
Texte intégralTrevino, J. G., S. R. Pillai et S. P. Chellappan. « Effect of nicotine on chemoresistant phenotype as mediated through Src-dependent Id1 expression in pancreatic adenocarcinoma cells. » Journal of Clinical Oncology 29, no 4_suppl (1 février 2011) : 216. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.216.
Texte intégralJi, Ping, Kristen M. Turner et Wei Zhang. « OverAKT3 : tumor progression and chemoresistance ». Cell Cycle 14, no 13 (4 juin 2015) : 1993–94. http://dx.doi.org/10.1080/15384101.2015.1046787.
Texte intégralBrown, Elizabeth, et Maurie Markman. « Tumor chemosensitivity and chemoresistance assays ». Cancer 77, no 6 (15 mars 1996) : 1020–25. http://dx.doi.org/10.1002/(sici)1097-0142(19960315)77:6<1020 ::aid-cncr3>3.0.co;2-l.
Texte intégralCree, Ian A., Russell D. Petty, Christian M. Kurbacher et Michael Untch. « Tumor chemosensitivity and chemoresistance assays ». Cancer 78, no 9 (1 novembre 1996) : 2031–32. http://dx.doi.org/10.1002/(sici)1097-0142(19961101)78:9<2031 ::aid-cncr27>3.0.co;2-x.
Texte intégralKern, David H. « Tumor chemosensitivity and chemoresistance assays ». Cancer 79, no 7 (1 avril 1997) : 1447–49. http://dx.doi.org/10.1002/(sici)1097-0142(19970401)79:7<1447 ::aid-cncr23>3.0.co;2-z.
Texte intégralThèses sur le sujet "Tumor chemoresistance"
Chau, Wing-ka, et 周穎嘉. « Characterization of ovarian tumor-initiating cells and mechanisms of chemoresistance ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/197834.
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Biological Sciences
Master
Master of Philosophy
Cox, Megan Christine. « Modeling the Heterogeneous Brain Tumor Microenvironment to Analyze Mechanisms of Vascular Development and Chemoresistance ». Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/95947.
Texte intégralPHD
BRIVIO, SIMONE. « Molecular mechanisms of cholangiocarcinoma progression : emphasizing the role of tumor-stroma interactions ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2018. http://hdl.handle.net/10281/199031.
Texte intégralCholangiocarcinoma (CCA) is an epithelial cancer arising from the biliary tree. CCA carries a poor prognosis, owing to early and pronounced invasiveness, and resistance to chemotherapy. The aggressiveness of CCA cells is exacerbated by the desmoplastic stroma developing in conjunction with tumor outgrowth, which mainly consists of cancer-associated fibroblasts (CAFs), tumor-associated macrophages, and lymphatic endothelial cells (LECs). During my PhD studies, I sought to dissect the nature and the biological relevance of the dense paracrine communications between stromal and cancer cells in CCA, in an effort to unveil the molecular mechanisms driving tumor progression. In a first study, we focused on a pleiotropic cytokine named leukemia inhibitory factor (LIF), which we found to be released not only by CCA cells, but also by inflammatory cells and CAFs within the tumor microenvironment. We showed that LIF hindered the induction of apoptosis in CCA cells treated with gemcitabine plus cisplatin, an effect dependent on the up-regulation of the anti-apoptotic protein myeloid cell leukemia (Mcl)-1, occurring downstream of PI3K activation. Therefore, targeting the LIF/PI3K/Mcl-1 axis may represent a feasible strategy to increase CCA responsiveness to chemotherapy. In a second study, we considered a classic readout of tumor-stroma interactions, i.e., the epithelial-to-mesenchymal transition (EMT) of cancer cells, a process underlying carcinoma invasion and metastasis. Previously, we had shown that S100A4, an EMT biomarker, acts as a mechanistic determinant of CCA invasiveness when expressed in the nucleus of cancer cells. We then demonstrated that the nuclearization of S100A4 was dependent on its SUMOylation, which could be inhibited by treating CCA cells with paclitaxel at nanomolar doses. Down-modulation of nuclear S100A4 hampered the activity of RhoA and Cdc42, the secretion of matrix metalloproteinase (MMP)-9, and the expression of membrane-type (MT)1-MMP. Moreover, low-dose paclitaxel significantly impaired CCA cell invasiveness, both in vitro and in a SCID mouse xenograft model, implying that a selective reduction in S100A4 nuclear expression may prevent tumor dissemination in CCA patients. In a third study, we aimed at clarifying whether the interplay between CCA cells and CAFs could drive tumor lymphangiogenesis, a process of utmost importance for CCA metastatization. We showed that, upon stimulation with platelet-derived growth factor (PDGF)-D, a major mediator of CAF recruitment by CCA cells, fibroblasts increased the secretion of vascular endothelial growth factor (VEGF)-A and VEGF-C, due to the activation of ERK1/2 and JNK. Consistently, conditioned medium from PDGF-D-treated fibroblasts promoted the recruitment of LECs, along with their assembly in 3-D vascular structures, and both effects could be prevented by antagonizing either PDGF receptor β on fibroblasts, or VEGF receptors 2 and 3 on LECs. The permeability of LEC monolayers was also increased by PDGF-D-treated fibroblasts, supporting the trans-endothelial migration of CCA cells. Overall, we unveiled the presence of a sequential cross-talk among CCA cells, CAFs and LECs, whose disruption may interfere with CCA metastatic spread. In conclusion, our results validate the notion that the tumor stroma strongly promotes the progression of CCA, both by directly shaping the behavior of cancer cells, and by setting up a microenvironment conducive to metastasis. Hopefully, a comprehensive understanding of the mutual interactions between cancer and stromal cells will lead to the development of innovative, multitargeted therapies that may more effectively eradicate the tumor.
Chauhan, Vikash Pal Singh. « Re-Engineering the Tumor Microenvironment to Enhance Drug Delivery ». Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10405.
Texte intégralEngineering and Applied Sciences
Kopp, Florian. « Novel insights into the role of microRNAs in chemoresistance, tumor progression and cancer therapy ». Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-163243.
Texte intégralHan, Chae Young. « The Role of Hexokinase II in the Regulation of Glycolysis and Cisplatin Sensitivity in Ovarian Cancer ». Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38574.
Texte intégralLi, Xia. « Role of tumor-surrounding adipocytes in breast cancer chemoresistance : molecular mechanisms and regulation by obesity ». Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30136.
Texte intégralBreast cancer is the most common cancer among women in France, as well as in the European Union and the United States. Although the number of cases observed each year has tended to decrease since 2005, notably due to organized screening, this disease remains the leading cause of cancer death in women. Many studies have shown that tumor progression is dependent on tumor cells but also on the "healthy" cells of the microenvironment (or stroma) that surround the tumor. In the case of breast cancer, adipocytes, the major cell type of the mammary stroma, represent emerging actors in tumor progression. My team is one of the first to have shown that peritumoral adipocytes were involved in the aggressiveness of breast cancers. From the bi-directional dialogue that takes place between adipocytes and mammary cancer cells results some changes in both cell types : (i) the tumor cells "educated" by the adipocytes have increased invasive capacities and greater resistance to treatments and (ii) the adipocytes co-cultured with the tumor cells acquire an activated phenotype with specific modifications such as delipidation, loss of adipocyte markers, overexpression of pro-inflammatory cytokines and secretion of proteins of the extracellular matrix, which led us to name them CAA for "Cancer-Associated Adipocytes". Interestingly, the paracrine dialogue between tumors and adipocytes could be amplified in obesity, where the normal balance of proteins secreted by adipose tissue is disrupted. In breast cancer, obesity is associated with an increased risk of occurrence after menopause and a worsening prognosis independent of menopausal status due to increased dissemination (local and remote) and decreased response to treatments, in particular by a greater resistance. The objective of my thesis was to evaluate the role of adipocytes in the chemoresistance of mammary tumor cells. Indeed, resistance is a major limit to the effectiveness of treatments and contributes to the onset of relapses, which are increased in obese patients. Using a 2D co-culture model, we have shown that adipocytes are able to promote pleiotropic resistance (doxorubicin, paclitaxel, 5-fluorouracil and cyclophosphamide) in various mammary tumor lines, irrespective of tumor type. By taking advantage of the fluorescence properties of anthracyclines, we have shown that this resistance implies an increase in the doxorubicin efflux, preventing it from acting at its site of nuclear action. This efflux mechanism implies an original process involving the major vault protein MVP / LRP (Major Vault Protein / Lung Resistance Protein), a nucleocytoplasmic transporter whose function remains poorly understood to date. Following nuclear drug efflux, it accumulates in cytoplasmic vesicles before before being expelled from the cell via extracellular vesicles. We also showed that this resistance mediated by MVP could be explained by the soluble factors secreted from adipocytes and is amplified in obesity conditions. In conclusion, our findings highlight that peritumoral adipocytes are able to influence tumor progression by promoting chemoresistance via an original mechanism involving the MVP protein, which could potentially become a marker of resistance to treatments. This work may explain, at least in part, the poor prognosis of breast cancers in obese patients and thus could provide interesting therapeutic perspectives, in order to interrupt the deleterious dialogue between adipocytes and tumor cells, particularly in obese patients
PAZIENZA, VALERIO. « Impact of engineered food on tumor growth and chemoresistance in the frame of pancreatic cancer ». Doctoral thesis, Università di Foggia, 2017. http://hdl.handle.net/11369/361941.
Texte intégralThe impact of nutrition (particularly associated with short term starvation (STS)) on major health benefits have been already demonstrated. These include amelioration of cardiovascular diseases, diabetes, insulin resistance, immune disorders, slowing of the aging process and in particular reduced risks of cancer. Recent studies in rodent and in in vitro models uncovered a potential link between STS and improved efficacy of chemotherapy which has already been demonstrated for some types of cancer. The broader objective of the research project developed during the PhD program was to elucidate the role of fasting (or short term starvation, STS) on the intracellular signaling events involved in the chemo-resistance of pancreatic cancer (PC) amidst the most aggressive types of cancer ranked as the fourth leading cause of cancer-related deaths worldwide, in order to implement a new diet formulation, mimicking calories restriction, in order to reverse chemoresistance or inhibit tumor growth. Taking advantage of in vivo xenograft mouse model for pancreatic cancer and in vitro PC cell lines, using biochemical and biomolecular approaches we first aimed to understand in depth the role of STS during the onset of pancreatic cancer in an ad hoc murine model and we then elucidate the molecular mechanisms involved in PC chemoresistance. It is important to systematically identify potential targets, which could serve as biomarkers for cancer prevention, prognosis and treatment. By elucidating the mechanisms involved in PC chemoresistance the results of this study will help scientists to identify new therapeutic targets.
Veaco, Jennifer Mitchell. « Prospective Detection of Chemoradiation Resistance in Patients with Locally Advanced Esophageal Adenocarcinoma ». Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/623577.
Texte intégralApproximately 25% of patients with locoregional esophageal adenocarcinoma (EC) are resistant (marked by minimal tumor regression; TRG 3) to preoperative chemoradiation, including 5FU‐based and CROSS regimens. Previously, an immunohistochemistry (IHC) test that accurately identifies patients as responders (TRG 0‐2) or non‐responders (TRG 3) to neoadjuvant CTRT was developed and validated. The current study was designed to identify gene expression profile (GEP) signatures able to predict response to preoperative treatment. Methods: Formalin‐fixed, paraffin‐embedded (FFPE) tumor tissue from 24 diagnostic biopsies (14 responders, 10 non‐responders) was collected. RNA was isolated, and RT‐PCR performed to assess the expression of 96 candidate genes chosen from in silicoanalysis. Genetic signatures incorporating genes with significant expression differences in pathologically determined responders versus non‐responders were identified, and linear and non‐linear predictive modeling methods were used to assess the accuracy of the signatures for predicting treatment response. Cross validation was performed to attain corrected accuracy values. Ten‐, 18‐, and 24‐gene signatures were identified with significantly different gene expression levels in responders compared to non‐responders (p < 0.05). Functional groups represented by the signatures included DNA damage repair, extracellular matrix remodeling, and 5FU metabolism. Partial Least Squares (PLS) prediction of treatment response was compared to pathologic TRG determined by blinded pathologic reading, and resulted in an area under the curve (AUC) of 0.99 and overall accuracy of 100% for the 24‐gene signature. Corrected AUC of 0.99 and accuracy of 95% resulted from five‐fold cross validation with 20 iterations. Heatmap analysis of the 24‐gene signature separated the EC cases into two distinct clusters, the first with 93% responders and the second with 90% non‐responders. The current study identifies novel gene signatures able to accurately predict EC patient response to preoperative treatment. The GEP may allow non‐responders to avoid unnecessary toxicities associated with chemoradiation therapy.
Kopp, Florian [Verfasser], et Ernst [Akademischer Betreuer] Wagner. « Novel insights into the role of microRNAs in chemoresistance, tumor progression and cancer therapy / Florian Kopp. Betreuer : Ernst Wagner ». München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1045153052/34.
Texte intégralLivres sur le sujet "Tumor chemoresistance"
Reader, Jocelyn, Sarah Lynam, Amy Harper, Gautam Rao, Maya Matheny et Dana M. Roque. Ovarian Tumor Microenvironment and Innate Immune Recognition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0004.
Texte intégralChapitres de livres sur le sujet "Tumor chemoresistance"
Kalir, Tamara A., et D. Stave Kohtz. « Chemoresistance, Dormancy and Recurrence in Platinum Drug Therapy of Ovarian Cancers ». Dans Tumor Dormancy, Quiescence, and Senescence, Vol. 3, 79–97. Dordrecht : Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9325-4_7.
Texte intégralBregenzer, Michael, Eric Horst, Pooja Mehta, Catherine Snyder, Taylor Repetto et Geeta Mehta. « The Role of the Tumor Microenvironment in CSC Enrichment and Chemoresistance : 3D Co-culture Methods ». Dans Methods in Molecular Biology, 217–45. New York, NY : Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1956-8_15.
Texte intégralCamaj, P., I. Ischenko, H. Seeliger, G. Arnold, K. W. Jauch et C. J. Bruns. « Overexpression of the gene IFIT3 enhances tumor growth, angiogenesis, metastasing and chemoresistance of the pancreas carcinoma cells ». Dans Deutsche Gesellschaft für Chirurgie, 17–18. Berlin, Heidelberg : Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_7.
Texte intégralIschenko, I., A. Renner, H. Seeliger, A. Kleespies, J. W. Ellwart, P. Camaj, M. E. Eichhorn, K. W. Jauch et C. J. Bruns. « Tumor stem cell targeted therapy with mTOR inhibitor RAD001 and hedgehog signalling inhibitor Cyclopamine reverts chemoresistance towards 5-Fluorouracil in human pancreatic carcinoma cells ». Dans Deutsche Gesellschaft für Chirurgie, 55–56. Berlin, Heidelberg : Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_22.
Texte intégralFabi, François, Pascal Adam et Eric Asselin. « Par-4 in Chemoresistant Ovarian and Endometrial Cancers ». Dans Tumor Suppressor Par-4, 41–58. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80558-6_3.
Texte intégralSée, Violaine, Barry Pizer et Daniel Meley. « Molecular Mechanisms of Chemoresistance in Medulloblastoma ». Dans Tumors of the Central Nervous System, Volume 8, 59–69. Dordrecht : Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4213-0_6.
Texte intégralLefranc, Florence, et Robert Kiss. « Glioblastoma : Role of Galectin-1 in Chemoresistance ». Dans Tumors of the Central Nervous System, Volume 2, 261–67. Dordrecht : Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0618-7_27.
Texte intégralShapiro, Joan R., Bipin M. Mehta, Salah A. D. Ebrahim, Adrienne C. Scheck, Paul L. Moots et Martin R. Fiola. « Tumor Heterogeneity and Intrinsically Chemoresistant Subpopulations in Freshly Resected Human Malignant Gliomas ». Dans Boundaries between Promotion and Progression during Carcinogenesis, 243–62. Boston, MA : Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5994-4_22.
Texte intégralThews, Oliver, Martin Nowak, Christoph Sauvant et Michael Gekle. « Hypoxia-Induced Extracellular Acidosis Increases p-Glycoprotein Activity and Chemoresistance in Tumors in Vivo via p38 Signaling Pathway ». Dans Oxygen Transport to Tissue XXXII, 115–22. Boston, MA : Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-7756-4_16.
Texte intégralAigner, Karl Reinhard, et Emir Selak. « Isolated Thoracic Perfusion with Carotid Artery Infusion for Advanced and Chemoresistant Tumors of the Parotid Gland ». Dans Induction Chemotherapy, 119–25. Berlin, Heidelberg : Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-18173-3_8.
Texte intégralActes de conférences sur le sujet "Tumor chemoresistance"
Lichtenfels, Martina, Camila Alves Silva, Caroline Brunetto Farias, Alessandra Borba Anton Souza et Antônio Luiz Frasson. « TIN VITRO BREAST CANCER CHEMORESISTANCE TEST ». Dans Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1058.
Texte intégralBai, Mingfeng, Yang Liu, Jing Cui, Meng Su et Dawei Zhang. « Overcoming chemoresistance using tumor mitochondria-targeted photodynamic therapy ». Dans Optical Methods for Tumor Treatment and Detection : Mechanisms and Techniques in Photodynamic Therapy XXVIII, sous la direction de David H. Kessel et Tayyaba Hasan. SPIE, 2019. http://dx.doi.org/10.1117/12.2508085.
Texte intégralKikuchi, Ryota, Takao Tsuji, Yuki Iwai, Hiroyuki Nakamura et Kazutetsu Aoshiba. « High CO2 tumor microenvironment confers chemoresistance in lung cancer cells ». Dans ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa4865.
Texte intégralYu, F., J. Wu, C. Gong, F. Su et E. Song. « Let-7 Inverts the Chemoresistance of Breast Tumor-Initiating Cells. » Dans Abstracts : Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009 ; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-1136.
Texte intégralOrzechowski, Amanda, et Haidong Dong. « Abstract 5026 : B7-H1 confers tumor chemoresistance by regulating MAPK/ERK activation ». Dans Proceedings : AACR Annual Meeting 2014 ; April 5-9, 2014 ; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5026.
Texte intégralLima, Paula Marynella Alves Pereira, Douglas Cardoso Brandão, Raquel Pereira Cruz, Priscila Capelari Orsolin, Wendell Guerra, Luiz Ricardo Goulart, Robson José de Oliveira Júnior et Thaise Gonçalves Araújo. « A NEW COPPER TERNARY COMPLEX IS A PROMISED COMPOUND FOR THE TREATMENT OF TRIPLE-NEGATIVE BREAST CANCER ». Dans Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2011.
Texte intégralRizvi, Imran, Emma A. Briars, Anne-Laure Bulin, Sriram R. Anbil, Daniela Vecchio, Ahmed Alkhateeb, William R. Hanna, Jonathan P. Celli et Tayyaba Hasan. « Designing PDT-based combinations to overcome chemoresistance in heterocellular 3D tumor models (Conference Presentation) ». Dans Optical Methods for Tumor Treatment and Detection : Mechanisms and Techniques in Photodynamic Therapy XXV, sous la direction de David H. Kessel et Tayyaba Hasan. SPIE, 2016. http://dx.doi.org/10.1117/12.2213436.
Texte intégralKyle, Alastair H., Jennifer H. E. Baker et Andrew I. Minchinton. « Abstract PR-7 : Overcoming chemoresistance in solid cancers by targeting quiescent tumor cells ». Dans Abstracts : AACR-NCI-EORTC International Conference : Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009 ; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-pr-7.
Texte intégralChaudhuri, Arnab Ray, Elsa Callen, Xia Ding, Ewa Gogola, Alexandra A. Duarte, Ji-Eun Lee, Nancy Wong et al. « Abstract IA09 : Replication fork stability confers chemoresistance in BRCA-deficient cells ». Dans Abstracts : AACR Special Conference on DNA Repair : Tumor Development and Therapeutic Response ; November 2-5, 2016 ; Montreal, QC, Canada. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3125.dnarepair16-ia09.
Texte intégralRizvi, Imran, Anne-Laure Bulin, Sriram R. Anbil, Emma A. Briars, Daniela Vecchio, Jonathan P. Celli, Mans Broekgaarden et Tayyaba Hasan. « PDT-based combinations in overcoming chemoresistance from stromal and heterotypic cellular communication (Conference Presentation) ». Dans Optical Methods for Tumor Treatment and Detection : Mechanisms and Techniques in Photodynamic Therapy XXVI, sous la direction de David H. Kessel et Tayyaba Hasan. SPIE, 2017. http://dx.doi.org/10.1117/12.2252685.
Texte intégralRapports d'organisations sur le sujet "Tumor chemoresistance"
Park, Jae-Hyun. Influence of the Tumor Microenvironment on Genomic Changes Conferring Chemoresistance in Breast Cancer. Fort Belvoir, VA : Defense Technical Information Center, avril 2013. http://dx.doi.org/10.21236/ada580419.
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