Littérature scientifique sur le sujet « Acidic tumor microenvironment »
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Articles de revues sur le sujet "Acidic tumor microenvironment"
Böhme, Ines, et Anja Katrin Bosserhoff. « Acidic tumor microenvironment in human melanoma ». Pigment Cell & ; Melanoma Research 29, no 5 (5 juillet 2016) : 508–23. http://dx.doi.org/10.1111/pcmr.12495.
Texte intégralFeng, Liangzhu, Ziliang Dong, Danlei Tao, Yicheng Zhang et Zhuang Liu. « The acidic tumor microenvironment : a target for smart cancer nano-theranostics ». National Science Review 5, no 2 (24 juin 2017) : 269–86. http://dx.doi.org/10.1093/nsr/nwx062.
Texte intégralJin, Haojie, Ning Wang, Cun Wang et Wenxin Qin. « MicroRNAs in hypoxia and acidic tumor microenvironment ». Chinese Science Bulletin 59, no 19 (12 avril 2014) : 2223–31. http://dx.doi.org/10.1007/s11434-014-0273-y.
Texte intégralLiu, Yu-Cheng, Zhi-Xian Wang, Jing-Yi Pan, Ling-Qi Wang, Xin-Yi Dai, Ke-Fei Wu, Xue-Wei Ye et Xiao-Ling Xu. « Recent Advances in Imaging Agents Anchored with pH (Low) Insertion Peptides for Cancer Theranostics ». Molecules 28, no 5 (26 février 2023) : 2175. http://dx.doi.org/10.3390/molecules28052175.
Texte intégralBoedtkjer, Ebbe, et Stine F. Pedersen. « The Acidic Tumor Microenvironment as a Driver of Cancer ». Annual Review of Physiology 82, no 1 (10 février 2020) : 103–26. http://dx.doi.org/10.1146/annurev-physiol-021119-034627.
Texte intégralSharma, Vishal, et Jagdeep Kaur. « Acidic environment could modulate the interferon-γ expression : Implication on modulation of cancer and immune cells’ interactions ». Asian Biomedicine 17, no 2 (1 avril 2023) : 72–83. http://dx.doi.org/10.2478/abm-2023-0047.
Texte intégralXu, Jingyong, Yao Li, Zhe Li, Weiwei Shao, Jinghai Song et Junmin Wei. « Acidic Tumor Microenvironment Promotes Pancreatic Cancer through miR-451a/MEF2D Axis ». Journal of Oncology 2022 (12 janvier 2022) : 1–12. http://dx.doi.org/10.1155/2022/3966386.
Texte intégralNoack, Anne-Kathrin, Henrike Lucas, Petr Chytil, Tomáš Etrych, Karsten Mäder et Thomas Mueller. « Intratumoral Distribution and pH-Dependent Drug Release of High Molecular Weight HPMA Copolymer Drug Conjugates Strongly Depend on Specific Tumor Substructure and Microenvironment ». International Journal of Molecular Sciences 21, no 17 (21 août 2020) : 6029. http://dx.doi.org/10.3390/ijms21176029.
Texte intégralMbugua, Simon Ngigi. « Targeting Tumor Microenvironment by Metal Peroxide Nanoparticles in Cancer Therapy ». Bioinorganic Chemistry and Applications 2022 (16 décembre 2022) : 1–20. http://dx.doi.org/10.1155/2022/5041399.
Texte intégralVernucci, Enza, Jaime Abrego, Venugopal Gunda, Surendra K. Shukla, Aneesha Dasgupta, Vikrant Rai, Nina Chaika et al. « Metabolic Alterations in Pancreatic Cancer Progression ». Cancers 12, no 1 (18 décembre 2019) : 2. http://dx.doi.org/10.3390/cancers12010002.
Texte intégralThèses sur le sujet "Acidic tumor microenvironment"
Audero, Madelaine. « Acidic tumor microenvironment and Ca2+ signaling interplay in Pancreatic Ductal Adenocarcinoma (PDAC) progression ». Electronic Thesis or Diss., Université de Lille (2022-....), 2023. http://www.theses.fr/2023ULILS105.
Texte intégralPancreatic ductal adenocarcinoma (PDAC) is the most common cancer affecting the pancreas, characterized by an unsatisfactory 5-year survival rate of around 10%, and to date, there are no effective therapeutic options for PDAC. This is in part due to a highly desmoplastic and immunosuppressive microenvironment that contributes to therapeutic failure. Moreover, the PDAC tumor microenvironment is featured by high acidosis (˂ pHe 6.5), a result of the metabolic reprogramming ("Warburg effect"), and hypoxic conditions, which offers important cues for its aggressiveness by selecting cancer cell phenotypes with competitive benefits for PDAC progression. In this context, Ca2+-permeable ion channels are known to regulate several hallmarks of cancer, including in PDAC. Therefore, they represent good target candidates due to their ability to integrate signals from the TME. Ca2+ channels are indeed pH and hypoxia sensors able to transduce TME signals to activate intracellular downstream pathways linked to PDAC progression. Although the roles of tumor acidosis and Ca2+ signaling in cancer progression are well established, the hypothesis of acidic TME employing Ca2+ signaling as a preferential route for sustaining tumor progression has not yet been sufficiently explored.My Ph.D. work aimed to study the phenotypic and genetic changes of PDAC cells upon acidic stress along the different stages of selection and to evaluate how tumor acidosis modulates Ca2+ signals and phenotypes in the PDAC cell lines, with a particular focus on Ca2+ oscillations and Store-Operated Ca2+ entry (SOCE). To this end, PANC-1 and Mia PaCa-2 cells were subjected to short- and long-term acidic pressure and recovery to pHe 7.4. The latter treatment was to mimic PDAC edges and consequent cancer cell escape from the tumor. The impact of acidosis was assessed for cell morphology, proliferation, adhesion, migration, invasion, invadopodia activity, and epithelial-mesenchymal transition (EMT) via functional in vitro assays and RNA sequencing, and for intracellular Ca2+ signals using Fura-2. Our results indicate that short acidic treatment limits the growth, adhesion, invasion, and viability of PDAC cells. As the acid treatment progresses, it selects cancer cells with enhanced migration and invasion abilities induced by EMT, thereby further enhancing their metastatic potential when re-exposed to pHe 7.4. RNA-seq analysis of PANC-1 cells exposed to short-term acidosis and pHe-selected recovered to pHe 7.4 revealed distinct transcriptome rewiring. We noted an enrichment of genes relevant to proliferation, migration, EMT, and invasion in acid-selected cells. Interestingly, PANC-1 cells are characterized by slower Ca2+ oscillations during short-term acid exposure compared to control cells and a tendency of ORAI1 downregulation at mRNA levels, while long-term acidosis and recovery to neutral pHe determine the recovery of fast Ca2+ oscillations and upregulation of ORAI1. In all our cell models, Ca2+ oscillations are SOCE-dependent, as ORAI1 blockade with Synta66 and siORAI1 results in impaired Ca2+ oscillations' initiation and maintenance. These data correlate with SOCE in PANC-1 cells, which is decreased during the short-term acid treatment, and increased in acid-selected cells with and without recovery to pHe 7.4. Finally, ORAI1-mediated Ca2+ entry might be involved in the activation of signaling cascades that lead to the increased migration and invasion of all the cell models exposed to acidic pHe, as Synta66 treatment and siORAI1 didn't affect control cells' invasion and migration.In conclusion, our findings show that acid-induced selection contributes to the acquisition of a more aggressive phenotype in PDAC cells, characterized by upregulation of SOCE, required for the generation of fast Ca2+ oscillations which may trigger Ca2+-dependent signaling pathways involved in PDAC progression
Schnipper, Julie. « The impact of the acidic tumor microenvironment on ion channel expression and regulation, in the progression of pancreatic ductal adenocarcinoma ». Electronic Thesis or Diss., Amiens, 2022. http://www.theses.fr/2022AMIE0071.
Texte intégralThe transient receptor potential canonical 1 channel (TRPC1) is one of the most prominent nonselective cation channels involved in several diseases, including cancer progression. TRPCs can be activated by different physio-chemical stimuli of their surroundings, for instance, pH. Another hallmark of cancer is the variable extracellular pH landscape, notably in epithelial cancers such as pancreatic ductal adenocarcinoma (PDAC). PDAC progression and development are linked to the physiology and microenvironment of the exocrine pancreas. There are strong indications that PDAC aggressiveness is caused by the interplay between the tumor acidic microenvironment and ion channel dysregulation. However, this interaction has never been studied before. Here, we investigate if TRPC1 is involved in PDAC progression in the form of proliferation and migration and if the pH fluctuations of the acidic tumor microenvironment affect these processes. We found that TRPC1 was significantly upregulated in PDAC tumor tissue compared to adjacent normal tissue, and in the aggressive PDAC cell line PANC-1, compared to a duct-like cell line, hTERT-HPNE. To investigate if fluctuations of the acidic tumor microenvironment affect TRPC1 dysregulation, PANC-1 cells were incubated in a medium with a pH of 7.4 or 6.5 over 30 days, where after cells were recovered in pH 7.4 for 14 days (7.4R). Acid adaptation (6.5) reduced TRPC1 protein expression but favored its membrane localization compared to the control (7.4). pH recovery treatment (7.4R) resulted in an upregulation of TRPC1 expression with a high membrane localization, both in 2D and 3D models. We found that pH fluctuations and the siRNA-based knock-down (KD) of TRPC1 affected 2D and spheroid PANC-1 proliferation, respectively. In our 2D model, flow cytometry and cell cycle regulating protein immunoblotting showed that TRPC1 KD affected the progression through G0/G1 phase under all conditions and S-phase under control pH 7.4, which shifts to the G2/M phase in pH 6.5 and 7.4R. In addition, pH 6.5 enhanced, and the KD of TRPC1 decreased cell migration, respectively. Furthermore, we found that TRPC1 interacted strongly with PI3K under acidic conditions and CaM under all conditions, and a KD of TRPC1 decreased both this interaction and the activation of AKT and ERK1/2. Finally, basal Ca2+ entry was significantly reduced upon the KD of TRPC1 in pH 6.5 and 7.4R, where the entry was enhanced. The reduction of extracellular Ca2+ concentration resulted in an additional decrease in proliferation and migration of cells transfected with siTRPC1 growing in pH 6.5 and 7.4R, but not in normal pH 7.4 conditions.Collectively, our results show that TRPC1 is upregulated in PDAC tissue and cell lines. The acidic tumor microenvironment favors its plasma membrane localization, and its interaction with PI3K/CaM and Ca2+ entry leads to PDAC cells proliferation and migration. In addition, we performed an expression profile screening of ORAI channels, their partner STIM1, and a voltage-activated sodium channel (Nav1.6), and an acid-sensing ion channel (ASIC1) in PDAC tissues and cell lines, and investigated whether the acidic tumor microenvironment affects epigenetic regulation of ion channel expression. We found that ORAI3 was upregulated in PDAC tissue compared to normal tissue, where STIM1 and NaV1.6 were significantly downregulated. Moreover, ORAI3 was more localized in the plasma membrane in tumor tissue. Acid-adaptation had a differential effect on Ca2+ channel expression. Furthermore, our preliminary results show that the acidic tumor microenvironment does not affect the methylation levels of the ASIC1 or TRPC1 promoter region, but so some extend the SCN8A gene promoter
Assi, E. « ROLE OF ACID SPHINGOMYELINASE IN THE TUMOUR MICROENVIRONMENT ». Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/229416.
Texte intégralAl-Husari, Maymona. « Mathematical modelling of the tumour microenvironment : the causes and consequences of tumour acidity ». Thesis, University of Strathclyde, 2012. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=18965.
Texte intégralTimosenko, Elina. « Tryptophan catabolism and amino acid transporter reprogramming in the tumour microenvironment ». Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:33745777-7aab-4342-b997-fc4317ec34fb.
Texte intégralSilva, Lídia [Verfasser], et Rüdiger [Akademischer Betreuer] Hell. « Branched-chain amino acid metabolism in the tumor microenvironment interaction / Lidia Silva ; Betreuer : Rüdiger Hell ». Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1177148897/34.
Texte intégralAlruwaili, Waad A. « Conjugated Bile Acid and Sphingosine 1-phosophate prompt Cholangiocarcinoma Cell Growth via Releasing Exosomes ». VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5715.
Texte intégralDong, Jihu. « Physiopathologie de cellules souches cancéreuses isolées de glioblastomes primitifs et évaluation pré-clinique de molécules "tête de série" par une approche de biologie et de chimie médicinale ». Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ036/document.
Texte intégralGlioblastomas are the most malignant primary brain tumors. The identification of glioblastoma stemcells (GSCs) has transformed our comprehension of those tumors by revealing a hierarchical organization. GSCs can self-renew, differentiate and enter into a quiescent state. They are considered as cells which fuel and as the main culprits of tumor relapse. The discovery of GSCs triggered a change in paradigm for cancer therapy. Indeed to gain in efficacy, therapies need to target, not only the cells forming the bulk of the tumor, but also GSCs particularly resistant and endowed with a high tumorigenic potential. Chemical screening of the Prestwick chemical library in our laboratory, unveiled bisacodyl with a specific activity on quiescent GSCs.This thesis presents work on the characterization of GSCs, study of the mode of action of bisacodyl on GSCs, as well as a preclinical evaluation of bisacodyl on a 3D model in vitro and animal models in vivo
Sadiq, Barzan A. « A dissection of class I phosphoinositide 3-kinase signalling in mouse embryonic fibroblasts and prostate organoids ». Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/278056.
Texte intégralTang, Ching-Chun, et 湯景鈞. « Study on Acidic Tumor Microenvironment in Oral Cancer ». Thesis, 2019. http://ndltd.ncl.edu.tw/handle/m37yv5.
Texte intégral國立臺灣大學
口腔生物科學研究所
107
The microenvironment of cancer cells is considered to be an important indicator of cancer progression. Studies have shown that due to the specific metabolic mechanisms of cancer cells, the extracellular matrix of cell has a higher hydrogen ion concentration than the cytoplasm. Exposure of cancer cells to this environment has an effect on their function, including changing in the metabolic system, mediating the growth processes, and expression of autophagy proteins. Compared with cancer within other parts of the body, the oral cavity is the only access to the digestive system. The cancer cells that grow in are more frequently affected by the external environment, especially with acidic environment due to food digestion of secreting seliva. Therefore, Oral cancer cells are not only influenced by endogenous micro-acidification, but also by the exogenous oral digestive system, we presumed that oral cancer should have higher research value in related field about how the microenvironment acidosis changing cell performance. However, there are few related studies using oral cancer as a subject. In this thesis, the influence of the slightly acidic environment on the growth of cancer cells is taken as the main story. We collaboration in vivo and in vitro experiment. Observing the performance of stemness and extented to drug resistance, proofing that both in vivo and in vitro test can show consistent results. The results show that acidification has significant impact on different types of oral cancer cells line. For tongue cancer (SAS), long-term acid stimulation its ability to upregulate stemness and further have its influence on proliferation and chemoresistance, at the meanwhile acidosis cancer cell can also improve its vasculogenic mimicry ability. But the acidosis stimulation has totally different influence on oral squamous cell carcinoma (OECM1), stemness of the OEMC1 was down regulation after acid treated but proliferation and chemoresistance ability was same as SAS. Nevertheless, OECM1 in vivo tumor incident rate showed dramatic different from in vitro side population data that OECM1 had much more lower tumor incident rate than SAS. Leak of vasculogenic mimicry ability may be one of the reason that tumor couldn’t form enough vascular-like tube to gain nutrient and lead awful in vivo tumor incident rate.
Livres sur le sujet "Acidic tumor microenvironment"
Goode, Jamie A., et Derek J. Chadwick, dir. The Tumour Microenvironment : Causes and Consequences of Hypoxia and Acidity. Chichester, UK : John Wiley & Sons, Ltd, 2001. http://dx.doi.org/10.1002/0470868716.
Texte intégralJamie, Goode, Chadwick Derek, Novartis Foundation et Symposium on the Tumour Microenvironment : Causes and Consequences of Hypoxia and Acidity (2000 : London, England), dir. The tumour microenvironment : Causes and consequences of hypoxia and acidity. Chichester : Wiley, 2001.
Trouver le texte intégralGoode, Jamie A., Derek J. Chadwick et Novartis Foundation Symposium Staff. Tumour Microenvironment No. 240 : Causes and Consequences of Hypoxia and Acidity. Wiley & Sons, Incorporated, John, 2008.
Trouver le texte intégralBoyer, Michael Joseph. Tumor acidity and the influence of microenvironment on the regulation of intracellular pH : implications for therapy. 1993.
Trouver le texte intégralFoundation, Novartis. The Tumour Microenvironment - No. 240 : Causes and Consequences of Hypoxia and Acidity (Novartis Foundation Symposia). Wiley, 2001.
Trouver le texte intégralChapitres de livres sur le sujet "Acidic tumor microenvironment"
Ye, Zhizhou, et Donald E. Ayer. « Response to Acidity : The MondoA–TXNIP Checkpoint Couples the Acidic Tumor Microenvironment to Cell Metabolism ». Dans Molecular Genetics of Dysregulated pH Homeostasis, 69–100. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1683-2_5.
Texte intégralRiemann, Anne, M. Rauschner, M. Gießelmann, S. Reime et O. Thews. « The Acidic Tumor Microenvironment Affects Epithelial-Mesenchymal Transition Markers as Well as Adhesion of NCI-H358 Lung Cancer Cells ». Dans Advances in Experimental Medicine and Biology, 179–83. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-48238-1_28.
Texte intégralKhadge, Saraswoti, John Graham Sharp, Geoffrey M. Thiele, Timothy R. McGuire et James E. Talmadge. « Fatty Acid Mediators in the Tumor Microenvironment ». Dans Advances in Experimental Medicine and Biology, 125–53. Cham : Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43093-1_8.
Texte intégralBrix, Nikko, et Kirsten Lauber. « Immune Checkpoint Inhibition and Radiotherapy in Head and Neck Squamous Cell Carcinoma : Synergisms and Resistance Mechanisms ». Dans Critical Issues in Head and Neck Oncology, 11–21. Cham : Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23175-9_2.
Texte intégralJung, Jin G., et Anne Le. « Targeting Metabolic Cross Talk Between Cancer Cells and Cancer-Associated Fibroblasts ». Dans The Heterogeneity of Cancer Metabolism, 205–14. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_15.
Texte intégralDutta, Sarbajeet, et Shamik Sen. « Preparation and Characterization of Collagen–Hyaluronic Acid (Col–HA) Matrices : In Vitro Mimics of the Tumor Microenvironment ». Dans Methods in Molecular Biology, 131–39. New York, NY : Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3589-6_11.
Texte intégralJin, Cheng, You-Yi Liu et Bo-Shi Wang. « Mechanisms of Hepatocarcinogenesis Development in an Acidic Microenvironment ». Dans Liver Cancer - Genesis, Progression and Metastasis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108559.
Texte intégral« Fluorescence Nanoprobe Imaging Tumor by Sensing the Acidic Microenvironment ». Dans Nanomedicine and Cancer, 168–90. CRC Press, 2011. http://dx.doi.org/10.1201/b11516-11.
Texte intégralHermanus Johannes Sliepen, Sonny. « Bone Cancer Pain, Mechanism and Treatment ». Dans Recent Advances in Bone Tumours and Osteoarthritis. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95910.
Texte intégralTurk, Seyhan. « The Impact of Biochemical Alterations in the Tumor Microenvironment on Cancer Progression and Treatment ». Dans Current Researches in Health Sciences-II. Özgür Yayınları, 2023. http://dx.doi.org/10.58830/ozgur.pub128.c626.
Texte intégralActes de conférences sur le sujet "Acidic tumor microenvironment"
Lekić, Milica, Mohammad Zoofaghari, Mladen Veletić et Ilangko Balasingham. « Extracellular vesicle propagation in acidic tumor microenvironment ». Dans NANOCOM '22 : The Ninth Annual ACM International Conference on Nanoscale Computing and Communication. New York, NY, USA : ACM, 2022. http://dx.doi.org/10.1145/3558583.3558843.
Texte intégralLarijani, Nazanin Rohani, Traian Sulea, Mehdi Arbabi Ghahroudi, Beatrice Paul Roc, Mylene Gosselin, Joey Sheff, John C. Zwaagstra et Anne E. G. Lenferink. « Abstract PO-049 : Exploiting tumor acidic microenvironment for improved therapeutics ». Dans Abstracts : AACR Virtual Special Conference on Tumor Heterogeneity : From Single Cells to Clinical Impact ; September 17-18, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.tumhet2020-po-049.
Texte intégralParalkar, Vishwas, Robert J. Aiello, Dan Marshall, Johanna Csengery, Patricia Bourassa, Qing Zhang, Brett S. Robinson et al. « Abstract 2981 : Targeting solid tumor acidic microenvironment with an alphalex PARP inhibitor ». 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.am2019-2981.
Texte intégralDing, Xinliang, Jason Miller, Ashley Campbell, Jonathan Almazan, Stephen Gutowski et Tian Zhao. « Abstract 2867 : Delivery of immunomodulators to the acidic tumor microenvironment by ultra-pH sensitive nanoparticle technology ». Dans Proceedings : AACR Annual Meeting 2020 ; April 27-28, 2020 and June 22-24, 2020 ; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2867.
Texte intégralKrewson, Elizabeth A., Li V. Yang et Lixue Dong. « Abstract 1993 : Acidic tumor microenvironment stimulation of GPR4 alters cytoskeletal dynamics and migration of vascular endothelial cells ». Dans Proceedings : AACR Annual Meeting 2017 ; April 1-5, 2017 ; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1993.
Texte intégralSamykutty, Abhilash, Molly W. McNally, William E. Grizzle, Akiko Chiba, Alexandra Thomas et Lacey R. McNally. « Abstract 4122 : Acidic tumor microenvironment targeted wormhole-shaped mesoporous silica nanoparticles to detect ovarian cancer by multispectral optoacoustic tomography ». Dans Proceedings : AACR Annual Meeting 2018 ; April 14-18, 2018 ; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4122.
Texte intégralChen, Chong, Lipeng Bai, Fengqi Cao, shengnan wang, Yan Liu, Jian Guo, Qin Si, Rong Xiang et Yunping Luo. « Abstract 3546 : LIN28B/MYC loop regulates aerobic glycolysis and tumor acidic microenvironment to promote cancer stemness and cancer progression ». Dans Proceedings : AACR Annual Meeting 2017 ; April 1-5, 2017 ; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3546.
Texte intégralBrück, J., B. Klasen, N. Bausbacher, D. Kerner, D. Schauenburg, M. Schreckenberger et M. Miederer. « Strategies for PET Imaging in Acidic Tumor Microenvironments ». Dans 61. Jahrestagung der Deutschen Gesellschaft für Nuklearmedizin. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1766343.
Texte intégralWojtkowiak, Jonathan W., Natalie M. Barkey, Virendra Kumar, Mark C. Lloyd, Robert A. Gatenby et Robert J. Gillies. « Abstract 1254 : Altered lipid and glucose metabolism is a cellular adaptation to tumor acidic microenvironments ». Dans Proceedings : AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011 ; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1254.
Texte intégralSkill, Nicholas J., et Mary A. Maluccio. « Abstract 4941 : Lysophosphatidic acid receptor signaling and pancreatic adenocarcinoma tumor microenvironment ». Dans Proceedings : AACR Annual Meeting 2017 ; April 1-5, 2017 ; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4941.
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