Pardo, Luis A.

[["dc.bibliographiccitation.artnumber","1600253"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","BioEssays"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Pedersen, Stine F."],["dc.contributor.author","Novak, Ivana"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Schwab, Albrecht"],["dc.contributor.author","Pardo, Luis A."],["dc.date.accessioned","2018-10-10T13:25:55Z"],["dc.date.available","2018-10-10T13:25:55Z"],["dc.date.issued","2017"],["dc.description.abstract","We present here the hypothesis that the unique microenvironmental pH landscape of acid-base transporting epithelia is an important factor in development of epithelial cancers, by rendering the epithelial and stromal cells pre-adapted to the heterogeneous extracellular pH (pHe ) in the tumor microenvironment. Cells residing in organs with net acid-base transporting epithelia such as the pancreatic ductal and gastric epithelia are exposed to very different, temporally highly variable pHe values apically and basolaterally. This translates into spatially and temporally non-uniform intracellular pH (pHi ) patterns. Disturbed pHe - and pHi -homeostasis contributes to essentially all hallmarks of cancer. Our hypothesis, that the physiological pHe microenvironment in acid-base secreting epithelia shapes cancers arising in these tissues, can be tested using novel imaging tools. The acidic tumor pHe in turn might be exploited therapeutically. Pancreatic cancers are used as our prime example, but we propose that this concept is also relevant for other cancers of acid-base transporting epithelia."],["dc.fs.pkfprnr","66887"],["dc.identifier.doi","10.1002/bies.201600253"],["dc.identifier.fs","631974"],["dc.identifier.pmid","28440551"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15964"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1521-1878"],["dc.title","Alternating pH landscapes shape epithelial cancer initiation and progression: Focus on pancreatic cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Pharmacology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hartung, Franziska"],["dc.contributor.author","Krüwel, Thomas"],["dc.contributor.author","Shi, Xiaoyi"],["dc.contributor.author","Pfizenmaier, Klaus"],["dc.contributor.author","Kontermann, Roland"],["dc.contributor.author","Chames, Patrick"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Pardo, Luis A."],["dc.date.accessioned","2021-04-14T08:26:27Z"],["dc.date.available","2021-04-14T08:26:27Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3389/fphar.2020.00686"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81946"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1663-9812"],["dc.title","A Novel Anti-Kv10.1 Nanobody Fused to Single-Chain TRAIL Enhances Apoptosis Induction in Cancer Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","721"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Biophysics Journal"],["dc.bibliographiccitation.lastpage","733"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Napp, Joanna"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Hartung, Franziska"],["dc.contributor.author","Tietze, Lutz Friedjan"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Alves, Frauke"],["dc.date.accessioned","2018-11-07T10:07:59Z"],["dc.date.available","2018-11-07T10:07:59Z"],["dc.date.issued","2016"],["dc.description.abstract","The K(v)10.1 (Eag1) voltage-gated potassium channel represents a promising molecular target for novel cancer therapies or diagnostic purposes. Physiologically, it is only expressed in the brain, but it was found overexpressed in more than 70 % of tumours of diverse origin. Furthermore, as a plasma membrane protein, it is easily accessible to extracellular interventions. In this study we analysed the feasibility of the anti-K(v)10.1 monoclonal antibody mAb62 to target tumour cells in vitro and in vivo and to deliver therapeutics to the tumour. Using time-domain near infrared fluorescence (NIRF) imaging in a subcutaneous MDA-MB-435S tumour model in nude mice, we showed that mAb62-Cy5.5 specifically accumulates at the tumour for at least 1 week in vivo with a maximum intensity at 48 h. Blocking experiments with an excess of unlabelled mAb62 and application of the free Cy5.5 fluorophore demonstrate specific binding to the tumour. Ex vivo NIRF imaging of whole tumours as well as NIRF imaging and microscopy of tumour slices confirmed the accumulation of the mAb62-Cy5.5 in tumours but not in brain tissue. Moreover, mAb62 was conjugated to the prodrug-activating enzyme beta-D-galactosidase (beta-gal; mAb62-beta-gal). The beta-gal activity of the mAb62-beta-gal conjugate was analysed in vitro on K(v)10.1-expressing MDAMB-435S cells in comparison to control AsPC-1 cells. We show that the mAb62-beta-gal conjugate possesses high beta-gal activity when bound to K(v)10.1-expressing MDA-MB-435S cells. Moreover, using the beta-gal activatable NIRF probe DDAOG, we detected mAb62-beta-gal activity in vivo over the tumour area. In summary, we could show that the anti-K(v)10.1 antibody is a promising tool for the development of novel concepts of targeted cancer therapy."],["dc.identifier.doi","10.1007/s00249-016-1152-z"],["dc.identifier.isi","000384822200012"],["dc.identifier.pmid","27444284"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13779"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39387"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","1432-1017"],["dc.relation.issn","0175-7571"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","In vivo imaging of tumour xenografts with an antibody targeting the potassium channel K(v)10.1"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2850"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","FEBS Letters"],["dc.bibliographiccitation.lastpage","2852"],["dc.bibliographiccitation.volume","580"],["dc.contributor.author","Stuhmer, Walter"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Hartung, Franziska"],["dc.contributor.author","Zientkowska, M."],["dc.contributor.author","Pardo, L. A."],["dc.date.accessioned","2018-11-07T09:48:45Z"],["dc.date.available","2018-11-07T09:48:45Z"],["dc.date.issued","2006"],["dc.description.abstract","An increasing number of ion channels are being found to be causally involved in diseases, giving rise to the new field of \"channelopathies\". Cancer is no exception, and several ion channels have been linked to tumour progression. Among them is the potassium channel EAG (Ether-a-go-go). Over 75% of tumours have been tested positive using a monoclonal antibody specific for EAG, while inhibition of this channel decreased the proliferation of EAG expressing cells. The inhibition of EAG is accomplished using RNA interference, functional anti-EAG1 antibodies, or (unspecific) EAG channel blockers. Fluorescently labelled recombinant Fab fragments recognizing EAG allow the distribution of EAG to be visualized in an in vivo mouse tumour model. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.febslet.2006.03.062"],["dc.identifier.isi","000238167200009"],["dc.identifier.pmid","16783874"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35368"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0014-5793"],["dc.title","Potassium channels as tumour markers"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2247"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","2262"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Ufartes, Roser"],["dc.contributor.author","Schneider, Tomasz"],["dc.contributor.author","Mortensen, Lena Suenke"],["dc.contributor.author","de Juan Romero, Camino"],["dc.contributor.author","Hentrich, Klaus"],["dc.contributor.author","Knoetgen, Hendrik"],["dc.contributor.author","Beilinson, Vadim"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Tarabykin, Victor"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Rawlins, J. Nicholas P."],["dc.contributor.author","Stühmer, Walter"],["dc.date.accessioned","2018-11-07T09:24:20Z"],["dc.date.available","2018-11-07T09:24:20Z"],["dc.date.issued","2013"],["dc.description.abstract","K(v)10.1 (Eag1), member of the K(v)10 family of voltage-gated potassium channels, is preferentially expressed in adult brain. The aim of the present study was to unravel the functional role of K(v)10.1 in the brain by generating knockout mice, where the voltage sensor and pore region of K(v)10.1 were removed to render non-functional proteins through deletion of exon 7 of the KCNH1 gene using the '3 Lox P strategy'. K(v)10.1-deficient mice show no obvious alterations during embryogenesis and develop normally to adulthood; cortex, hippocampus and cerebellum appear anatomically normal. Other tests, including general health screen, sensorimotor functioning and gating, anxiety, social behaviour, learning and memory did not show any functional aberrations in K(v)10.1 null mice. K(v)10.1 null mice display mild hyperactivity and longer-lasting haloperidol-induced catalepsy, but there was no difference between genotypes in amphetamine sensitization and withdrawal, reactivity to apomorphine and haloperidol in the prepulse inhibition tests or to antidepressants in the haloperidol-induced catalepsy. Furthermore, electrical properties of K(v)10.1 in cerebellar Purkinje cells did not show any difference between genotypes. Bearing in mind that K(v)10.1 is overexpressed in over 70 of all human tumours and that its inhibition leads to a reduced tumour cell proliferation, the fact that deletion of K(v)10.1 does not show a marked phenotype is a prerequisite for utilizing K(v)10.1 blocking and/or reduction techniques, such as siRNA, to treat cancer."],["dc.description.sponsorship","Max Planck Society"],["dc.identifier.doi","10.1093/hmg/ddt076"],["dc.identifier.isi","000319432000011"],["dc.identifier.pmid","23424202"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29798"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0964-6906"],["dc.title","Behavioural and functional characterization of K(v)10.1 (Eag1) knockout mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Schwab, Albrecht"],["dc.contributor.author","Stock, C."],["dc.contributor.author","Swietach, P."],["dc.contributor.author","Hulikova, A."],["dc.contributor.author","Vaughan-Jones, R."],["dc.contributor.author","Pedersen, Stine Falsig"],["dc.contributor.author","Andersen, A. D."],["dc.contributor.author","Hoffmann, E."],["dc.contributor.author","Novak, I."],["dc.contributor.author","Reshkin, Stephan Joel"],["dc.contributor.author","Prevarskaya, N."],["dc.contributor.author","Lemonnier, L."],["dc.contributor.author","A-S, Borowiec"],["dc.contributor.author","Arcangeli, A."],["dc.contributor.author","Zanieri, F."],["dc.contributor.author","D'Amico, M."],["dc.contributor.author","Fraser, S. P."],["dc.contributor.author","Djamgoz, M. B."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Kalthoff, H."],["dc.contributor.author","Pardo, L."],["dc.contributor.author","Stühmer, Walter"],["dc.date.accessioned","2018-11-07T08:38:52Z"],["dc.date.available","2018-11-07T08:38:52Z"],["dc.date.issued","2010"],["dc.identifier.isi","000282988401317"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18859"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.title","Ion transport proteins control pancreatic ductal adenocarcinoma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","286"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Journal of Radiology"],["dc.bibliographiccitation.lastpage","293"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Napp, Joanna"],["dc.contributor.author","Missbach-Guentner, Jeannine"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Mathejczyk, Julia"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Tietze, Lutz Friedjan"],["dc.date.accessioned","2018-11-07T08:30:16Z"],["dc.date.available","2018-11-07T08:30:16Z"],["dc.date.issued","2009"],["dc.description.abstract","Conventional chemotherapy of cancer has its limitations, especially in advanced and disseminated disease and suffers from lack of specificity. This results in a poor therapeutic index and considerable toxicity to normal organs. Therefore, many efforts are made to develop novel therapeutic tools against cancer with the aim of selectively targeting the drug to the turnout site. Drug delivery strategies fundamentally rely on the identification of good-quality biomarkers, allowing unequivocal discrimination between cancer and healthy tissue. At present, antibodies or antibody fragments have clearly proven their value as carrier molecules specific for a tumour-associated molecular marker. This present review draws attention to the use of near-infrared fluorescence (NIRF) imaging to investigate binding specificity and kinetics of carrier molecules such as monoclonal antibodies. In addition, flat-panel volume computed tomography (fpVCT) will be presented to monitor anatomical structures in turnout mouse models over time in a non-invasive manner. Each imaging device sheds light on a different aspect; functional imaging is applied to optimise the dose schedule and the concept of selective tumour therapies, whereas anatomical imaging assesses preclinically the efficacy of novel turnout therapies. Both imaging techniques in combination allow the visualisation of functional information obtained by NIRF imaging within an adequate anatomic framework. (C) 2009 Elsevier Ireland Ltd. All rights reserved."],["dc.description.sponsorship","DFG [SFB 416, AL336/5-1]"],["dc.identifier.doi","10.1016/j.ejrad.2009.01.048"],["dc.identifier.isi","000266868900012"],["dc.identifier.pmid","19285818"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16849"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0720-048X"],["dc.title","Concept of a selective tumour therapy and its evaluation by near-infrared fluorescence imaging and flat-panel volume computed tomography in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]