Arndt-Jovin, Donna J.

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Valley, Christopher C."],["dc.contributor.author","Arndt-Jovin, Donna J."],["dc.contributor.author","Jovin, Thomas M."],["dc.contributor.author","Steinkamp, Mara P."],["dc.contributor.author","Chizhik, Alexey I."],["dc.contributor.author","Karedla, Narain V. R."],["dc.contributor.author","Hlavacek, William S."],["dc.contributor.author","Wilson, Bridget S."],["dc.contributor.author","Lidke, Keith A."],["dc.contributor.author","Lidke, Diane S."],["dc.date.accessioned","2018-11-07T10:01:57Z"],["dc.date.available","2018-11-07T10:01:57Z"],["dc.date.issued","2015"],["dc.format.extent","351A"],["dc.identifier.isi","000362849400177"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38135"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.publisher.place","Cambridge"],["dc.relation.conference","59th Annual Meeting of the Biophysical-Society"],["dc.relation.eventlocation","Baltimore, MD"],["dc.relation.issn","1542-0086"],["dc.relation.issn","0006-3495"],["dc.title","Inside-Out Signaling of Oncogenic EGFR Mutants Promotes Ligand-Independent Dimerization"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E4971"],["dc.bibliographiccitation.issue","25"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","E4977"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Turriani, Elisa"],["dc.contributor.author","Lázaro, Diana F."],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Schön, Margarete"],["dc.contributor.author","Schön, Michael P."],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Outeiro, Tiago F."],["dc.contributor.author","Arndt-Jovin, Donna J."],["dc.contributor.author","Becker, Dorothea"],["dc.date.accessioned","2018-04-23T11:47:36Z"],["dc.date.available","2018-04-23T11:47:36Z"],["dc.date.issued","2017"],["dc.description.abstract","Recent epidemiological and clinical studies have reported a significantly increased risk for melanoma in people with Parkinson’s disease. Because no evidence could be obtained that genetic factors are the reason for the association between these two diseases, we hypothesized that of the three major Parkinson’s disease-related proteins—α-synuclein, LRRK2, and Parkin—α-synuclein might be a major link. Our data, presented here, demonstrate that α-synuclein promotes the survival of primary and metastatic melanoma cells, which is the exact opposite of the effect that α-synuclein has on dopaminergic neurons, where its accumulation causes neuronal dysfunction and death. Because this detrimental effect of α-synuclein on neurons can be rescued by the small molecule anle138b, we explored its effect on melanoma cells. We found that treatment with anle138b leads to massive melanoma cell death due to a major dysregulation of autophagy, suggesting that α-synuclein is highly beneficial to advanced melanoma because it ensures that autophagy is maintained at a homeostatic level that promotes and ensures the cell’s survival."],["dc.identifier.doi","10.1073/pnas.1700200114"],["dc.identifier.gro","3142238"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13362"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0027-8424"],["dc.title","Treatment with diphenyl–pyrazole compound anle138b/c reveals that α-synuclein protects melanoma cells from autophagic cell death"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1994"],["dc.bibliographiccitation.journal","Cell Death and Disease"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Oliveira, Luis M. A."],["dc.contributor.author","Falomir-Lockhart, Lisandro J."],["dc.contributor.author","Botelho, Michelle Gralle"],["dc.contributor.author","Lin, K-H"],["dc.contributor.author","Wales, Pauline"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Gerhardt, Ellen"],["dc.contributor.author","Taschenberger, Holger"],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Schuele, B."],["dc.contributor.author","Arndt-Jovin, Donna J."],["dc.contributor.author","Jovin, Thomas M."],["dc.date.accessioned","2018-11-07T09:49:15Z"],["dc.date.available","2018-11-07T09:49:15Z"],["dc.date.issued","2015"],["dc.description.abstract","We have assessed the impact of alpha-synuclein overexpression on the differentiation potential and phenotypic signatures of two neural-committed induced pluripotent stem cell lines derived from a Parkinson's disease patient with a triplication of the human SNCA genomic locus. In parallel, comparative studies were performed on two control lines derived from healthy individuals and lines generated from the patient iPS-derived neuroprogenitor lines infected with a lentivirus incorporating a small hairpin RNA to knock down the SNCA mRNA. The SNCA triplication lines exhibited a reduced capacity to differentiate into dopaminergic or GABAergic neurons and decreased neurite outgrowth and lower neuronal activity compared with control cultures. This delayed maturation phenotype was confirmed by gene expression profiling, which revealed a significant reduction in mRNA for genes implicated in neuronal differentiation such as delta-like homolog 1 (DLK1), gamma-aminobutyric acid type B receptor subunit 2 (GABABR2), nuclear receptor related 1 protein (NURR1), G-protein-regulated inward-rectifier potassium channel 2 (GIRK-2) and tyrosine hydroxylase (TH). The differentiated patient cells also demonstrated increased autophagic flux when stressed with chloroquine. We conclude that a two-fold overexpression of alpha-synuclein caused by a triplication of the SNCA gene is sufficient to impair the differentiation of neuronal progenitor cells, a finding with implications for adult neurogenesis and Parkinson's disease progression, particularly in the context of bioenergetic dysfunction."],["dc.identifier.doi","10.1038/cddis.2015.318"],["dc.identifier.isi","000367155300027"],["dc.identifier.pmid","26610207"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12755"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35470"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2041-4889"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Elevated alpha-synuclein caused by SNCA gene triplication impairs neuronal differentiation and maturation in Parkinson's patient-derived induced pluripotent stem cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","794"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cytometry Part A"],["dc.bibliographiccitation.lastpage","805"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Ziomkiewicz, Iwona"],["dc.contributor.author","Loman, Anastasia"],["dc.contributor.author","Klement, Reinhard"],["dc.contributor.author","Fritsch, Cornelia"],["dc.contributor.author","Klymchenko, Andrey S."],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Jovin, Thomas M."],["dc.contributor.author","Arndt-Jovin, Donna J."],["dc.date.accessioned","2018-11-07T09:20:45Z"],["dc.date.available","2018-11-07T09:20:45Z"],["dc.date.issued","2013"],["dc.description.abstract","We have revealed a reorientation of ectodomain I of the epidermal growth factor receptor (EGFR; ErbB1; Her1) in living CHO cells expressing the receptor, upon binding of the native ligand EGF. The state of the unliganded, nonactivated EGFR was compared to that exhibited after ligand addition in the presence of a kinase inhibitor that prevents endocytosis but does not interfere with binding or the ensuing conformational rearrangements. To perform these experiments, we constructed a transgene EGFR with an acyl carrier protein sequence between the signal peptide and the EGFR mature protein sequence. This protein, which behaves similarly to wild-type EGFR with respect to EGF binding, activation, and internalization, can be labeled at a specific serine in the acyl carrier tag with a fluorophore incorporated into a 4-phosphopantetheine (P-pant) conjugate transferred enzymatically from the corresponding CoA derivative. By measuring Forster resonance energy transfer between a molecule of Atto390 covalently attached to EGFR in this manner and a novel lipid probe NR12S distributed exclusively in the outer leaflet of the plasma membrane, we determined the apparent relative separation of ectodomain I from the membrane under nonactivating and activating conditions. The data indicate that the unliganded domain I of the EGFR receptor is situated much closer to the membrane before EGF addition, supporting the model of a self-inhibited configuration of the inactive receptor in quiescent cells. (c) 2013 International Society for Advancement of Cytometry"],["dc.identifier.doi","10.1002/cyto.a.22311"],["dc.identifier.isi","000323480200005"],["dc.identifier.pmid","23839800"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28950"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1552-4922"],["dc.title","Dynamic conformational transitions of the EGF receptor in living mammalian cells determined by FRET and fluorescence lifetime imaging microscopy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","619"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","626"],["dc.bibliographiccitation.volume","170"],["dc.contributor.author","Lidke, Diane S."],["dc.contributor.author","Lidke, Keith A."],["dc.contributor.author","Rieger, Bernd"],["dc.contributor.author","Jovin, Thomas M."],["dc.contributor.author","Arndt-Jovin, Donna J."],["dc.date.accessioned","2021-06-01T10:51:14Z"],["dc.date.available","2021-06-01T10:51:14Z"],["dc.date.issued","2005"],["dc.description.abstract","ErbB1 receptors situated on cellular filopodia undergo systematic retrograde transport after binding of the epidermal growth factor (EGF) and activation of the receptor tyrosine kinase. Specific inhibitors of the erbB1 receptor tyrosine kinase as well as cytochalasin D, a disruptor of the actin cytoskeleton, abolish transport but not free diffusion of the receptor–ligand complex. Diffusion constants and transport rates were determined with single molecule sensitivity by tracking receptors labeled with EGF conjugated to fluorescent quantum dots. Retrograde transport precedes receptor endocytosis, which occurs at the base of the filopodia. Initiation of transport requires the interaction and concerted activation of at least two liganded receptors and proceeds at a constant rate mediated by association with actin. These findings suggest a mechanism by which filopodia detect the presence and concentration of effector molecules far from the cell body and mediate cellular responses via directed transport of activated receptors."],["dc.identifier.doi","10.1083/jcb.200503140"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86938"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1540-8140"],["dc.relation.issn","0021-9525"],["dc.title","Reaching out for signals"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4087"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Molecular Biology of the Cell"],["dc.bibliographiccitation.lastpage","4099"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Valley, Christopher C."],["dc.contributor.author","Arndt-Jovin, Donna J."],["dc.contributor.author","Karedla, Narain V. R."],["dc.contributor.author","Steinkamp, Mara P."],["dc.contributor.author","Chizhik, Alexey I."],["dc.contributor.author","Hlavacek, William S."],["dc.contributor.author","Wilson, Bridget S."],["dc.contributor.author","Lidke, Keith A."],["dc.contributor.author","Lidke, Diane S."],["dc.date.accessioned","2018-11-07T09:49:02Z"],["dc.date.available","2018-11-07T09:49:02Z"],["dc.date.issued","2015"],["dc.description.abstract","Mutations within the epidermal growth factor receptor (EGFR/erbB1/Her1) are often associated with tumorigenesis. In particular, a number of EGFR mutants that demonstrate ligand-independent signaling are common in non-small cell lung cancer (NSCLC), including kinase domain mutations L858R (also called L834R) and exon 19 deletions (e.g., Delta L747-P753insS), which collectively make up nearly 90% of mutations in NSCLC. The molecular mechanisms by which these mutations confer constitutive activity remain unresolved. Using multiple subdiffraction-limit imaging modalities, we reveal the altered receptor structure and interaction kinetics of NSCLC-associated EGFR mutants. We applied two-color single quantum dot tracking to quantify receptor dimerization kinetics on living cells and show that, in contrast to wild-type EGFR, mutants are capable of forming stable, ligand-independent dimers. Two-color superresolution localization microscopy confirmed ligand-independent aggregation of EGFR mutants. Live-cell Forster resonance energy transfer measurements revealed that the L858R kinase mutation alters ectodomain structure such that unliganded mutant EGFR adopts an extended, dimerization-competent conformation. Finally, mutation of the putative dimerization arm confirmed a critical role for ectodomain engagement in ligand-independent signaling. These data support a model in which dysregulated activity of NSCLC-associated kinase mutants is driven by coordinated interactions involving both the kinase and extracellular domains that lead to enhanced dimerization."],["dc.identifier.doi","10.1091/mbc.E15-05-0269"],["dc.identifier.isi","000366324900022"],["dc.identifier.pmid","26337388"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35430"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Cell Biology"],["dc.relation.issn","1939-4586"],["dc.relation.issn","1059-1524"],["dc.title","Enhanced dimerization drives ligand-independent activity of mutant epidermal growth factor receptor in lung cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Arndt-Jovin, Donna J."],["dc.contributor.author","Lidke, Diane S."],["dc.contributor.author","Chizhik, Alexey I."],["dc.contributor.author","Karedla, Narain V. R."],["dc.contributor.author","Jovin, Thomas M."],["dc.date.accessioned","2018-11-07T09:44:57Z"],["dc.date.available","2018-11-07T09:44:57Z"],["dc.date.issued","2014"],["dc.format.extent","237A"],["dc.identifier.isi","000337000401317"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34509"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.publisher.place","Cambridge"],["dc.relation.conference","58th Annual Meeting of the Biophysical-Society"],["dc.relation.eventlocation","San Francisco, CA"],["dc.relation.issn","1542-0086"],["dc.relation.issn","0006-3495"],["dc.title","Flim-FRET, a Structural Tool for ErbB Receptor Studies in the Living Cell"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e11323"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Kantelhardt, Sven Rainer"],["dc.contributor.author","Caarls, Wouter"],["dc.contributor.author","de Vries, Anthony H. B."],["dc.contributor.author","Hagen, Guy M."],["dc.contributor.author","Jovin, Thomas M."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Giese, Alf"],["dc.contributor.author","Arndt-Jovin, Donna J."],["dc.date.accessioned","2018-11-07T08:42:07Z"],["dc.date.available","2018-11-07T08:42:07Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: The current therapy of malignant gliomas is based on surgical resection, radio-chemotherapy and chemotherapy. Recent retrospective case-series have highlighted the significance of the extent of resection as a prognostic factor predicting the course of the disease. Complete resection in low-grade gliomas that show no MRI-enhanced images are especially difficult. The aim in this study was to develop a robust, specific, new fluorescent probe for glioma cells that is easy to apply to live tumor biopsies and could identify tumor cells from normal brain cells at all levels of magnification. Methodology/Principal Findings: In this investigation we employed brightly fluorescent, photostable quantum dots (QDs) to specifically target epidermal growth factor receptor (EGFR) that is upregulated in many gliomas. Living glioma and normal cells or tissue biopsies were incubated with QDs coupled to EGF and/or monoclonal antibodies against EGFR for 30 minutes, washed and imaged. The data include results from cell-culture, animal model and ex vivo human tumor biopsies of both low-grade and high-grade gliomas and show high probe specificity. Tumor cells could be visualized from the macroscopic to single cell level with contrast ratios as high as 1000: 1 compared to normal brain tissue. Conclusions/Significance: The ability of the targeted probes to clearly distinguish tumor cells in low-grade tumor biopsies, where no enhanced MRI image was obtained, demonstrates the great potential of the method. We propose that future application of specifically targeted fluorescent particles during surgery could allow intraoperative guidance for the removal of residual tumor cells from the resection cavity and thus increase patient survival."],["dc.identifier.doi","10.1371/journal.pone.0011323"],["dc.identifier.isi","000279370000006"],["dc.identifier.pmid","20614029"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6912"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19633"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Specific Visualization of Glioma Cells in Living Low-Grade Tumor Tissue"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1238"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Optics Letters"],["dc.bibliographiccitation.lastpage","1240"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Hell, Stefan"],["dc.contributor.author","Booth, Martin J."],["dc.contributor.author","Wilms, S"],["dc.contributor.author","Schnetter, C. M."],["dc.contributor.author","Kirsch, A. K."],["dc.contributor.author","Arndt-Jovin, D. J."],["dc.contributor.author","Jovin, Thomas M."],["dc.date.accessioned","2017-09-07T11:48:08Z"],["dc.date.available","2017-09-07T11:48:08Z"],["dc.date.issued","1998"],["dc.description.abstract","We report on scanning far- and near-field two-photon microscopy of cell nuclei stained with DAPI and bisbenzimidazole Hoechst 33342 (BBI-342) with the 647-nm laser line of a cw ArKr mixed-gas laser. Two-photon-excited fluorescence images are obtained for 50-200 mW of average power at the sample. A nearly quadratic dependence of fluorescence intensity on laser power confirmed the two-photon effect. The nonlinearity was further supported by evidence of three-dimensional sectioning in a scanning farfield microscope. We find that the cw two-photon irradiation sufficient for imaging within typically 5 s does not significantly impair cell cycling of BBI-342-labeled live cells. Finally, high-resolution imaging in scanning near-field microscopy with good contrast is demonstrated. (C) 1998 Optical Society of America."],["dc.identifier.doi","10.1364/OL.23.001238"],["dc.identifier.gro","3144533"],["dc.identifier.isi","000075024400031"],["dc.identifier.pmid","18087486"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2168"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0146-9592"],["dc.title","Two-photon near- and far-field fluorescence microscopy with continuous-wave excitation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","65"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","IEEE Transactions on NanoBioscience"],["dc.bibliographiccitation.lastpage","71"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Arndt-Jovin, Donna J."],["dc.contributor.author","Kantelhardt, Sven Rainer"],["dc.contributor.author","Caarls, Wouter"],["dc.contributor.author","de Vries, Anthony H. B."],["dc.contributor.author","Giese, Alf"],["dc.contributor.author","Jovin, Thomas M."],["dc.date.accessioned","2018-11-07T08:32:11Z"],["dc.date.available","2018-11-07T08:32:11Z"],["dc.date.issued","2009"],["dc.description.abstract","Despite surgical advances and recent progress in adjuvant therapies, the prognosis for patients with malignant brain tumors such as glioblastoma multiforme has remained poor, and the neurological deterioration suffered by most patients as a consequence of tumor progression is dramatic and severe. In addition, malignant brain tumors have > 95% recurrence close to the primary site of initial resection. Unfortunately, standard imaging techniques do not permit the intraoperative identification of individual or small clusters of residual tumor cells, precluding their selective removal while sparing the surrounding normal brain tissue. In this report, we show that quantum dots (QDs) coupled to epidermal growth factor (EGF) or anti-EGF receptor receptor (EGFR, Her1) specifically and sensitively label glial tumor cells in cell culture, glioma mouse models, and human brain-tumor biopsies. A clear demarcation between brain and tumor tissue at the macroscopic as well as the cellular level is provided by the fluorescence emission of the QDs."],["dc.identifier.doi","10.1109/TNB.2009.2016548"],["dc.identifier.isi","000268040200009"],["dc.identifier.pmid","19304503"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17278"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ieee-inst Electrical Electronics Engineers Inc"],["dc.relation.issn","1536-1241"],["dc.title","Tumor-Targeted Quantum Dots Can Help Surgeons Find Tumor Boundaries"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]