@article{RuizHerediaSanchezVegaOnechaetal.2018,
  author    = {Ruiz-Heredia, Yanira and S{\´a}nchez-Vega, Beatriz and Onecha, Esther and Barrio, Santiago and Alonso, Rafael and Carlos Mart{\´i}nez-Avila, Jose and Cuenca, Isabel and Agirre, Xabier and Braggio, Esteban and Hern{\´a}ndez, Miguel-T. and Mart{\´i}nez, Rafael and Rosi{\~n}ol, Laura and Gutierrez, Norma and Martin-Ramos, Marisa and Ocio, Enrique M. and Echeveste, Mar{\´i}a-Asunci{\´o}n and P{\´e}rez de Oteyza, Jaime and Oriol, Albert and Bargay, Joan and Gironella, Mercedes and Ayala, Rosa and Blad{\´e}, Joan and Mateos, Mar{\´i}a-Victoria and Kortum, Klaus M. and Stewart, Keith and Garc{\´i}a-Sanz, Ram{\´o}n and San Miguel, Jes{\´u}s and Jos{\´e} Lahuerta, Juan and Martinez-Lopez, Joaqu{\´i}n},
  title     = {Mutational screening of newly diagnosed multiple myeloma patients by deep targeted sequencing},
  series = {Haematologica},
  volume    = {103},
  journal   = {Haematologica},
  number    = {11},
  doi       = {10.3324/haematol.2018.188839},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-227151},
  pages     = {e544-e548},
  year      = {2018},
  abstract  = {no abstract available},
  language  = {en}
}
@article{HaertleBuenacheCuestaHernandezetal.2023,
  author    = {Haertle, Larissa and Buenache, Natalia and Cuesta Hern{\´a}ndez, Hip{\´o}lito Nicol{\´a}s and Simicek, Michal and Snaurova, Renata and Rapado, Inmaculada and Martinez, Nerea and L{\´o}pez-Mu{\~n}oz, Nieves and S{\´a}nchez-Pina, Jos{\´e} Mar{\´i}a and Munawar, Umair and Han, Seungbin and Ruiz-Heredia, Yanira and Colmenares, Rafael and Gallardo, Miguel and Sanchez-Beato, Margarita and Piris, Miguel Angel and Samur, Mehmet Kemal and Munshi, Nikhil C. and Ayala, Rosa and Kort{\"u}m, Klaus Martin and Barrio, Santiago and Mart{\´i}nez-L{\´o}pez, Joaqu{\´i}n},
  title     = {Genetic alterations in members of the proteasome 26S subunit, AAA-ATPase (PSMC) gene family in the light of proteasome inhibitor resistance in multiple myeloma},
  series = {Cancers},
  volume    = {15},
  journal   = {Cancers},
  number    = {2},
  issn      = {2072-6694},
  doi       = {10.3390/cancers15020532},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-305013},
  year      = {2023},
  abstract  = {For the treatment of Multiple Myeloma, proteasome inhibitors are highly efficient and widely used, but resistance is a major obstacle to successful therapy. Several underlying mechanisms have been proposed but were only reported for a minority of resistant patients. The proteasome is a large and complex machinery. Here, we focus on the AAA ATPases of the 19S proteasome regulator (PSMC1-6) and their implication in PI resistance. As an example of cancer evolution and the acquisition of resistance, we conducted an in-depth analysis of an index patient by applying FISH, WES, and immunoglobulin-rearrangement sequencing in serial samples, starting from MGUS to newly diagnosed Multiple Myeloma to a PI-resistant relapse. The WES analysis uncovered an acquired PSMC2 Y429S mutation at the relapse after intensive bortezomib-containing therapy, which was functionally confirmed to mediate PI resistance. A meta-analysis comprising 1499 newly diagnosed and 447 progressed patients revealed a total of 36 SNVs over all six PSMC genes that were structurally accumulated in regulatory sites for activity such as the ADP/ATP binding pocket. Other alterations impact the interaction between different PSMC subunits or the intrinsic conformation of an individual subunit, consequently affecting the folding and function of the complex. Interestingly, several mutations were clustered in the central channel of the ATPase ring, where the unfolded substrates enter the 20S core. Our results indicate that PSMC SNVs play a role in PI resistance in MM.},
  language  = {en}
}
@article{LupianezVillaescusaCarvalhoetal.2016,
  author    = {Lupia{\~n}ez, Carmen B. and Villaescusa, Maria T. and Carvalho, Agostinho and Springer, Jan and Lackner, Michaela and S{\´a}nchez-Maldonado, Jos{\´e} M. and Canet, Luz M. and Cunha, Cristina and Segura-Catena, Joana and Alcazar-Fuoli, Laura and Solano, Carlos and Fianchi, Luana and Pagano, Livio and Potenza, Leonardo and Aguado, Jos{\´e} M. and Luppi, Mario and Cuenca-Estrella, Manuel and Lass-Fl{\"o}rl, Cornelia and Einsele, Hermann and V{\´a}zquez, Lourdes and R{\´i}os-Tamayo, Rafael and Loeffler, J{\"u}rgen and Jurado, Manuel and Sainz, Juan},
  title     = {Common Genetic Polymorphisms within NF kappa B-Related Genes and the Risk of Developing Invasive Aspergillosis},
  series = {Frontiers in Microbiology},
  volume    = {7},
  journal   = {Frontiers in Microbiology},
  number    = {1243},
  doi       = {10.3389/fmicb.2016.01243},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165209},
  year      = {2016},
  abstract  = {Invasive Aspergillosis (IA) is an opportunistic infection caused by Aspergillus, a ubiquitously present airborne pathogenic mold. A growing number of studies suggest a major host genetic component in disease susceptibility. Here, we evaluated whether 14 single-nucleotide polymorphisms within NFκB1, NFκB2, RelA, RelB, Rel, and IRF4 genes influence the risk of IA in a population of 834 high-risk patients (157 IA and 677 non-IA) recruited through a collaborative effort involving the aspBIOmics consortium and four European clinical institutions. No significant overall associations between selected SNPs and the risk of IA were found in this large cohort. Although a hematopoietic stem cell transplantation (HSCT)-stratified analysis revealed that carriers of the IRF4rs12203592T/T genotype had a six-fold increased risk of developing the infection when compared with those carrying the C allele (ORREC = 6.24, 95\%CI 1.25-31.2, P = 0.026), the association of this variant with IA risk did not reach significance at experiment-wide significant threshold. In addition, we found an association of the IRF4AATC and IRF4GGTC haplotypes (not including the IRF4rs12203592T risk allele) with a decreased risk of IA but the magnitude of the association was similar to the one observed in the single-SNP analysis, which indicated that the haplotypic effect on IA risk was likely due to the IRF4rs12203592 SNP. Finally, no evidence of significant interactions among the genetic markers tested and the risk of IA was found. These results suggest that the SNPs on the studied genes do not have a clinically relevant impact on the risk of developing IA.},
  language  = {en}
}
@article{SanchezThierschmannMolenkamp2017,
  author    = {S{\´a}nchez, Rafael and Thierschmann, Holger and Molenkamp, Laurens W.},
  title     = {Single-electron thermal devices coupled to a mesoscopic gate},
  series = {New Journal of Physics},
  volume    = {19},
  journal   = {New Journal of Physics},
  doi       = {10.1088/1367-2630/aa8b94},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-172982},
  year      = {2017},
  abstract  = {We theoretically investigate the propagation of heat currents in a three-terminal quantum dot engine. Electron-electron interactions introduce state-dependent processes which can be resolved by energy-dependent tunneling rates. We identify the relevant transitions which define the operation of the system as a thermal transistor or a thermal diode. In the former case, thermal-induced charge fluctuations in the gate dot modify the thermal currents in the conductor with suppressed heat injection, resulting in huge amplification factors and the possible gating with arbitrarily low energy cost. In the latter case, enhanced correlations of the state-selective tunneling transitions redistribute heat flows giving high rectification coefficients and the unexpected cooling of one conductor terminal by heating the other one. We propose quantum dot arrays as a possible way to achieve the extreme tunneling asymmetries required for the different operations.},
  language  = {en}
}
@article{BousquetAntoBachertetal.2021,
  author    = {Bousquet, Jean and Anto, Josep M. and Bachert, Claus and Haahtela, Tari and Zuberbier, Torsten and Czarlewski, Wienczyslawa and Bedbrook, Anna and Bosnic-Anticevich, Sinthia and Walter Canonica, G. and Cardona, Victoria and Costa, Elisio and Cruz, Alvaro A. and Erhola, Marina and Fokkens, Wytske J. and Fonseca, Joao A. and Illario, Maddalena and Ivancevich, Juan-Carlos and Jutel, Marek and Klimek, Ludger and Kuna, Piotr and Kvedariene, Violeta and Le, LTT and Larenas-Linnemann, D{\´e}sir{\´e}e E. and Laune, Daniel and Louren{\c{c}}o, Olga M. and Mel{\´e}n, Erik and Mullol, Joaquim and Niedoszytko, Marek and Odemyr, Mika{\"e}la and Okamoto, Yoshitaka and Papadopoulos, Nikos G. and Patella, Vincenzo and Pfaar, Oliver and Pham-Thi, Nh{\^a}n and Rolland, Christine and Samolinski, Boleslaw and Sheikh, Aziz and Sofiev, Mikhail and Suppli Ulrik, Charlotte and Todo-Bom, Ana and Tomazic, Peter-Valentin and Toppila-Salmi, Sanna and Tsiligianni, Ioanna and Valiulis, Arunas and Valovirta, Erkka and Ventura, Maria-Teresa and Walker, Samantha and Williams, Sian and Yorgancioglu, Arzu and Agache, Ioana and Akdis, Cezmi A. and Almeida, Rute and Ansotegui, Ignacio J. and Annesi-Maesano, Isabella and Arnavielhe, Sylvie and Basaga{\~n}a, Xavier and D. Bateman, Eric and B{\´e}dard, Annabelle and Bedolla-Barajas, Martin and Becker, Sven and Bennoor, Kazi S. and Benveniste, Samuel and Bergmann, Karl C. and Bewick, Michael and Bialek, Slawomir and E. Billo, Nils and Bindslev-Jensen, Carsten and Bjermer, Leif and Blain, Hubert and Bonini, Matteo and Bonniaud, Philippe and Bosse, Isabelle and Bouchard, Jacques and Boulet, Louis-Philippe and Bourret, Rodolphe and Boussery, Koen and Braido, Fluvio and Briedis, Vitalis and Briggs, Andrew and Brightling, Christopher E. and Brozek, Jan and Brusselle, Guy and Brussino, Luisa and Buhl, Roland and Buonaiuto, Roland and Calderon, Moises A. and Camargos, Paulo and Camuzat, Thierry and Caraballo, Luis and Carriazo, Ana-Maria and Carr, Warner and Cartier, Christine and Casale, Thomas and Cecchi, Lorenzo and Cepeda Sarabia, Alfonso M. and H. Chavannes, Niels and Chkhartishvili, Ekaterine and Chu, Derek K. and Cingi, Cemal and Correia de Sousa, Jaime and Costa, David J. and Courbis, Anne-Lise and Custovic, Adnan and Cvetkosvki, Biljana and D'Amato, Gennaro and da Silva, Jane and Dantas, Carina and Dokic, Dejan and Dauvilliers, Yves and De Feo, Giulia and De Vries, Govert and Devillier, Philippe and Di Capua, Stefania and Dray, Gerard and Dubakiene, Ruta and Durham, Stephen R. and Dykewicz, Mark and Ebisawa, Motohiro and Gaga, Mina and El-Gamal, Yehia and Heffler, Enrico and Emuzyte, Regina and Farrell, John and Fauquert, Jean-Luc and Fiocchi, Alessandro and Fink-Wagner, Antje and Fontaine, Jean-Fran{\c{c}}ois and Fuentes Perez, Jos{\´e} M. and Gemicioğlu, Bilun and Gamkrelidze, Amiran and Garcia-Aymerich, Judith and Gevaert, Philippe and Gomez, Ren{\´e} Maximiliano and Gonz{\´a}lez Diaz, Sandra and Gotua, Maia and Guldemond, Nick A. and Guzm{\´a}n, Maria-Antonieta and Hajjam, Jawad and Huerta Villalobos, Yunuen R. and Humbert, Marc and Iaccarino, Guido and Ierodiakonou, Despo and Iinuma, Tomohisa and Jassem, Ewa and Joos, Guy and Jung, Ki-Suck and Kaidashev, Igor and Kalayci, Omer and Kardas, Przemyslaw and Keil, Thomas and Khaitov, Musa and Khaltaev, Nikolai and Kleine-Tebbe, Jorg and Kouznetsov, Rostislav and Kowalski, Marek L. and Kritikos, Vicky and Kull, Inger and La Grutta, Stefania and Leonardini, Lisa and Ljungberg, Henrik and Lieberman, Philip and Lipworth, Brian and Lodrup Carlsen, Karin C. and Lopes-Pereira, Catarina and Loureiro, Claudia C. and Louis, Renaud and Mair, Alpana and Mahboub, Bassam and Makris, Micha{\"e}l and Malva, Joao and Manning, Patrick and Marshall, Gailen D. and Masjedi, Mohamed R. and Maspero, Jorge F. and Carreiro-Martins, Pedro and Makela, Mika and Mathieu-Dupas, Eve and Maurer, Marcus and De Manuel Keenoy, Esteban and Melo-Gomes, Elisabete and Meltzer, Eli O. and Menditto, Enrica and Mercier, Jacques and Micheli, Yann and Miculinic, Neven and Mihaltan, Florin and Milenkovic, Branislava and Mitsias, Dimitirios I. and Moda, Giuliana and Mogica-Martinez, Maria-Dolores and Mohammad, Yousser and Montefort, Steve and Monti, Ricardo and Morais-Almeida, Mario and M{\"o}sges, Ralph and M{\"u}nter, Lars and Muraro, Antonella and Murray, Ruth and Naclerio, Robert and Napoli, Luigi and Namazova-Baranova, Leyla and Neffen, Hugo and Nekam, Kristoff and Neou, Angelo and Nordlund, Bj{\"o}rn and Novellino, Ettore and Nyembue, Dieudonn{\´e} and O'Hehir, Robyn and Ohta, Ken and Okubo, Kimi and Onorato, Gabrielle L. and Orlando, Valentina and Ouedraogo, Solange and Palamarchuk, Julia and Pali-Sch{\"o}ll, Isabella and Panzner, Peter and Park, Hae-Sim and Passalacqua, Gianni and P{\´e}pin, Jean-Louis and Paulino, Ema and Pawankar, Ruby and Phillips, Jim and Picard, Robert and Pinnock, Hilary and Plavec, Davor and Popov, Todor A. and Portejoie, Fabienne and Price, David and Prokopakis, Emmanuel P. and Psarros, Fotis and Pugin, Benoit and Puggioni, Francesca and Quinones-Delgado, Pablo and Raciborski, Filip and Rajabian-S{\"o}derlund, Rojin and Regateiro, Frederico S. and Reitsma, Sietze and Rivero-Yeverino, Daniela and Roberts, Graham and Roche, Nicolas and Rodriguez-Zagal, Erendira and Rolland, Christine and Roller-Wirnsberger, Regina E. and Rosario, Nelson and Romano, Antonino and Rottem, Menachem and Ryan, Dermot and Salim{\"a}ki, Johanna and Sanchez-Borges, Mario M. and Sastre, Joaquin and Scadding, Glenis K. and Scheire, Sophie and Schmid-Grendelmeier, Peter and Sch{\"u}nemann, Holger J. and Sarquis Serpa, Faradiba and Shamji, Mohamed and Sisul, Juan-Carlos and Sofiev, Mikhail and Sol{\´e}, Dirceu and Somekh, David and Sooronbaev, Talant and Sova, Milan and Spertini, Fran{\c{c}}ois and Spranger, Otto and Stellato, Cristiana and Stelmach, Rafael and Thibaudon, Michel and To, Teresa and Toumi, Mondher and Usmani, Omar and Valero, Antonio A. and Valenta, Rudolph and Valentin-Rostan, Marylin and Pereira, Marilyn Urrutia and van der Kleij, Rianne and Van Eerd, Michiel and Vandenplas, Olivier and Vasankari, Tuula and Vaz Carneiro, Antonio and Vezzani, Giorgio and Viart, Fr{\´e}d{\´e}ric and Viegi, Giovanni and Wallace, Dana and Wagenmann, Martin and Wang, De Yun and Waserman, Susan and Wickman, Magnus and Williams, Dennis M. and Wong, Gary and Wroczynski, Piotr and Yiallouros, Panayiotis K. and Yusuf, Osman M. and Zar, Heather J. and Zeng, St{\´e}phane and Zernotti, Mario E. and Zhang, Luo and Shan Zhong, Nan and Zidarn, Mihaela},
  title     = {ARIA digital anamorphosis: Digital transformation of health and care in airway diseases from research to practice},
  series = {Allergy},
  volume    = {76},
  journal   = {Allergy},
  number    = {1},
  doi       = {10.1111/all.14422},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-228339},
  pages     = {168 -- 190},
  year      = {2021},
  abstract  = {Digital anamorphosis is used to define a distorted image of health and care that may be viewed correctly using digital tools and strategies. MASK digital anamorphosis represents the process used by MASK to develop the digital transformation of health and care in rhinitis. It strengthens the ARIA change management strategy in the prevention and management of airway disease. The MASK strategy is based on validated digital tools. Using the MASK digital tool and the CARAT online enhanced clinical framework, solutions for practical steps of digital enhancement of care are proposed.},
  language  = {en}
}
@article{SierraSanchezGutierrezetal.2019,
  author    = {Sierra, Miguel A. and S{\´a}nchez, David and Gutierrez, Rafael and Cuniberti, Gianaurelio and Dom{\´i}nguez-Adame, Francisco and D{\´i}az, Elena},
  title     = {Spin-polarized electron transmission in DNA-like systems},
  series = {Biomolecules},
  volume    = {10},
  journal   = {Biomolecules},
  number    = {1},
  issn      = {2218-273X},
  doi       = {10.3390/biom10010049},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-193813},
  year      = {2019},
  abstract  = {The helical distribution of the electronic density in chiral molecules, such as DNA and bacteriorhodopsin, has been suggested to induce a spin-orbit coupling interaction that may lead to the so-called chirality-induced spin selectivity (CISS) effect. Key ingredients for the theoretical modelling are, in this context, the helically shaped potential of the molecule and, concomitantly, a Rashba-like spin-orbit coupling due to the appearance of a magnetic field in the electron reference frame. Symmetries of these models clearly play a crucial role in explaining the observed effect, but a thorough analysis has been largely ignored in the literature. In this work, we present a study of these symmetries and how they can be exploited to enhance chiral-induced spin selectivity in helical molecular systems.},
  language  = {en}
}
@article{MorisVandenBroeckToscoetal.2016,
  author    = {Moris, Lisa and Van den Broeck, Thomas and Tosco, Lorenzo and Van Baelen, Anthony and Gontero, Paolo and Karnes, Robert Jeffrey and Everaerts, Wouter and Albersen, Maarten and Bastian, Patrick J. and Chlosta, Piotr and Claessens, Frank and Chun, Felix K. and Graefen, Markus and Gratzke, Christian and Kneitz, Burkhard and Marchioro, Giansilvio and Salas, Rafael Sanchez and Tombal, Bertrand and Van Der Poel, Henk and Walz, Jochen Christoph and De Meerleer, Gert and Bossi, Alberto and Haustermans, Karin and Montorsi, Francesco and Van Poppel, Hendrik and Spahn, Martin and Briganti, Alberto and Joniau, Steven},
  title     = {Impact of lymph node burden on survival of high-risk prostate cancer patients following radical prostatectomy and pelvic lymph node dissection},
  series = {Frontiers in Surgery},
  volume    = {3},
  journal   = {Frontiers in Surgery},
  organization    = {European Multicenter Prostate Cancer Clinical and Translational Research Group (EMPaCT)},
  issn      = {2296-875X},
  doi       = {10.3389/fsurg.2016.00065},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-195721},
  year      = {2016},
  abstract  = {Aim To determine the impact of the extent of lymph node invasion (LNI) on long-term oncological outcomes after radical prostatectomy (RP). Material and methods In this retrospective study, we examined the data of 1,249 high-risk, non-metastatic PCa patients treated with RP and pelvic lymph node dissection (PLND) between 1989 and 2011 at eight different tertiary institutions. We fitted univariate and multivariate Cox models to assess independent predictors of cancer-specific survival (CSS) and overall survival (OS). The number of positive lymph node (LN) was dichotomized according to the most informative cutoff predicting CSS. Kaplan-Meier curves assessed CSS and OS rates. Only patients with at least 10 LNs removed at PLND were included. This cutoff was chosen as a surrogate for a well performed PNLD. Results Mean age was 65 years (median: 66, IQR 60-70). Positive surgical margins were present in 53.7\% (n = 671). Final Gleason score (GS) was 2-6 in 12.7\% (n = 158), 7 in 52\% (n = 649), and 8-10 in 35.4\% (n = 442). The median number of LNs removed during PLND was 15 (IQR 12-17). Of all patients, 1,128 (90.3\%) had 0-3 positive LNs, while 126 (9.7\%) had ≥4 positive LNs. Patients with 0-3 positive LNs had significantly better CSS outcome at 10-year follow-up compared to patients with ≥4 positive LNs (87 vs. 50\%; p < 0.0001). Similar results were obtained for OS, with a 72 vs. 37\% (p < 0.0001) survival at 10 years for patients with 0-3 vs. ≥4 positive LNs, respectively. At multivariate analysis, final GS of 8-10, salvage ADT therapy, and ≥4 (vs. <4) positive LNs were predictors of worse CSS and OS. Pathological stage pT4 was an additional predictor of worse CSS. Conclusion Four or more positive LNs, pathological stage pT4, and final GS of 8-10 represent independent predictors for worse CSS in patients with high-risk PCa. Primary tumor biology remains a strong driver of tumor progression and patients having ≥4 positive LNs could be considered an enriched patient group in which novel treatment strategies should be studied.},
  language  = {en}
}