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11. Combined Heart-Lung Transplantation: A Single-Center Experience of 50 Patients over 30 Years

Author

Verlinden, H., primary, Brouckaert, J., additional, Guler, I., additional, Vos, R., additional, Verleden, G., additional, Delcroix, M., additional, Van Aelst, L., additional, Van Cleemput, J., additional, Ceulemans, L., additional, Van Raemdonck, D., additional, Neyrinck, A., additional, Rex, S., additional, Vlasselaers, D., additional, Jacobs, B., additional, De Troy, E., additional, Dauwe, D., additional, Meyns, B., additional, Rega, F., additional, and Verbelen, T., additional

Published
2022
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14. The novel proteomic signature for the detection of cardiac allograft vasculopathy

Author

Wei, D M, primary, Trenson, T, additional, Van Keer, J M, additional, Melgarejo, J, additional, Thijs, L, additional, He, T L, additional, Latosinska, A, additional, Vanassche, T, additional, Van Aelst, L, additional, Janssens, S, additional, Van Cleemput, J, additional, Mischak, H, additional, Staessen, J A, additional, Verhamme, P, additional, and Zhang, Z Y, additional

Published
2021
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15. IBRUTINIB AND ATRIAL FIBRILLATION: A BELGIAN EXPERT CONSENSUS PAPER

Author

UCL - SSS/IREC/MONT - Pôle Mont Godinne, UCL - (MGD) Service d'hématologie, Vandenbriele, C, Van der Linden, L, Van Aelst, L, Schwagten, P, Van Heuverswyn, F, Meers, S, Galle, V, Van Nieuwenhuyse, T, Wu, K, André, Marc, Hermans, C, Janssens, A, UCL - SSS/IREC/MONT - Pôle Mont Godinne, UCL - (MGD) Service d'hématologie, Vandenbriele, C, Van der Linden, L, Van Aelst, L, Schwagten, P, Van Heuverswyn, F, Meers, S, Galle, V, Van Nieuwenhuyse, T, Wu, K, André, Marc, Hermans, C, and Janssens, A

Abstract

Over the last decade, the oral Bruton’s tyrosine kinase (BTK) inhibitor ibrutinib induced a paradigm shift in the treatment of patients with chronic lymphocytic leukaemia (CLL), mantle cell lymphoma (MCL), and Waldenströms macroglobulinemia (WM). In clinical trials and in real-world studies, ibrutinib proved to be an effective agent with an overall favourable safety and tolerability profile. However, compared with standard chemo-immunotherapy (CIT), ibrutinib was associated with a higher incidence of atrial fibrillation (AF). The patho-physiological mechanisms underlying this increased AF incidence are not completely understood, but it is thought to be related to off-target inhibitory effects of ibrutinib on the Tec protein tyrosine kinase (TEC) in cardiac cells. The prevalence of AF in patients treated with ibrutinib is highest during the first three months of therapy, which warrants an increased vigilance during this treatment phase. However, AF in patients treated with ibrutinib is generally well manageable without ibrutinib discontinuation. Prior to the start of ibrutinib treatment, identification and addressing modifiable risk factors for AF is a first important step. The threshold for haematologists to consult a cardiologist or a cardio-oncologist should be low and a close collaboration between both specialties is warranted. Unnecessary ibrutinib interruptions should be avoided, and uncomplicated AF is not a valid reason to discontinue or interrupt ibrutinib. If anticoagulation is required, direct oral anticoagulants are preferred. In this paper, a panel of haematology and cardiology specialists have provided practical guidance on how to evaluate patients prior to ibrutinib treatment and monitor during ibrutinib therapy. Furthermore, they have provided practical guidance on how to manage AF in ibrutinib-treated patients.

Published
2021

22. P879Myocardial proteomic signatures in end-stage dilated and ischemic cardiomyopathy compared with normal human hearts

Author

Zhang, Z Y, primary, Trenson, S, additional, Yang, W Y, additional, Zoidakis, J, additional, Nkuipou-Kenfack, E, additional, Van Keer, J, additional, Schanstra, J P, additional, Van Aelst, L, additional, Vanhaecke, J, additional, Janssens, S, additional, Verhamme, P, additional, Van Cleemput, J, additional, Mischak, H, additional, Vlahou, A, additional, and Staessen, J A, additional

Published
2018
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23. Biomarkers and Donor Selection in Heart Transplantation

Author

Vorlat, A., primary, Dehous, N., additional, Vervaecke, A., additional, Van Hoof, V., additional, Rodrigus, I., additional, Vermeulen, T., additional, Van Craenenbroeck, E., additional, Heidbuchel, H., additional, Van Aelst, L., additional, Ancion, A., additional, and Claeys, M., additional

Published
2018
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27. Rapid Fire Abstract session: new insights in cardiomyopthies434The role of 4D echocardiography and cardiac biomarkers for early detection of chemotherapy induced cardiotoxicity in nonHodgkin lymphoma patients435Identification of proto-oncogenes and genes responsible for myocardial fibrosis and diastolic dysfunction after anticancer treatment under experimental conditions436Wild type transthyretin cardiac amyloidosis: clinical characteristics, echocardiographic findings, and predictors of outcome437A novel echocardiographic index for detection of cardiac amyloidosis.438Left ventricular outflow obstruction is a treatable feature rather than a risk marker in patients with hypertrophic cardiomyopathy439The international stress echo registry in hypertrophic cardiomyopathy440Value of left atrial size and function to risk stratify for new onset atrial fibrillation in hypertrophic cardiomyopathy441Right ventricle ejection fraction by cardiac resonance imaging is superior in discrimination between early phase ARVC and right ventricular outflow tract ventricular tachycardia

Author

Mihalcea, D, primary, Bergler-Klein, J, primary, Grogan, M, primary, Pagourelias, E, primary, Faber, L, primary, Ciampi, Q, primary, Debonnaire, P, primary, Saberniak, J, primary, Florescu, M, additional, Vladareanu, AM, additional, Mihaila, S, additional, Vinereanu, D, additional, Spannbauer, A, additional, Zlabinger, K, additional, Macejovska, D, additional, Maurer, G, additional, Gyongyosi, M, additional, Scott, C, additional, Lin, G, additional, Klarich, K, additional, Miller, W, additional, Dispenzieri, A, additional, Mirea, OC, additional, Duchenne, J, additional, Vovas, G, additional, Van Aelst, L, additional, Claus, P, additional, Van Cleemput, J, additional, Delforge, M, additional, Bogaert, J, additional, Voigt, JU, additional, Burghardt, A, additional, Seggewiss, H, additional, Van Buuren, F, additional, Horstkotte, D, additional, Olivotto, I, additional, Gardini, C, additional, Monserrat, L, additional, Peteiro, J, additional, Lopes, L, additional, Cotrim, C, additional, Losi, MA, additional, Lazzeroni, DE, additional, Picano, E, additional, Joyce, E, additional, Van Den Brink, OVW, additional, Bax, JJ, additional, Delgado, V, additional, Ajmone Marsan, N, additional, Leren, IS, additional, Haland, TF, additional, Hopp, E, additional, Edvardsen, T, additional, and Haugaa, KH, additional

Published
2015
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28. Rapid Fire Abstract session: assessment of systolic function: clinical perspectives and future directions782How the echocardiographic parameters of left ventricular function change during the first year after myocardial infarction when the ejection fraction remains normal?783Blunted increase in LV longitudinal deformation during exercise contributes to the transition from an asymptomatic stage to clinically overt HFpEF784A septal flash induced by right ventricular pacing is associated with left ventricular dysfunction and remodeling785Assessment of right ventricular systolic function in patients with significant functional tricuspid regurgitation: longitudinal parameters increase accuracy and predict cardiovascular outcomes786Effect of left ventricular augmentation with alginate biopolymer on right heart function787Left ventricular mechanics: novel tools to evaluate function and dyssynchrony in controls and cardiac resynchronization therapy candidates788How does regional wall thickness influence strain measurements?789TAPSE-estimated right ventricular systolic dysfunction predicts mortality among acute decompensated heart failure with preserved ejection fraction patients: a prospective study in a secondary center

Author

Baron, T, primary, Kosmala, W, primary, Sarvari, S I, primary, Garcia Martin, A, primary, Dumitrescu, S I, primary, Galli, E, primary, Pagourelias, E, primary, Martinez Santos, P, primary, Christersson, C, additional, Hedin, EM, additional, Johansson, K, additional, Flachskampf, FA, additional, Rojek, A, additional, Przewlocka-Kosmala, M, additional, Karolko, B, additional, Mysiak, A, additional, Marwick, TH, additional, Sitges, M, additional, Sanz, M, additional, Tolosana Viu, JM, additional, Edvardsen, T, additional, Stokke, TM, additional, Mont, L, additional, Bijnens, B, additional, Moya-Mur, JL, additional, Carbonell-San Roman, S-A, additional, Rodriguez-Munoz, D, additional, Garcia-Lledo, A, additional, Jimenez-Nacher, JJ, additional, Segura-De La Cal, T, additional, Fernandez-Golfin, C, additional, Zamorano-Gomez, JL, additional, Droc, I, additional, Neagoe, G, additional, Mocanu, I, additional, Murgu, V, additional, Savoiu, D, additional, Crisan, I, additional, Dragomir, D, additional, Stamate, S C, additional, Cristian, G, additional, Fournet, M, additional, Samset, E, additional, Leclercq, C, additional, Donal, E, additional, Vovas, G, additional, Duchenne, J, additional, Mirea, OC, additional, Van Aelst, L, additional, Claus, P, additional, Delforge, M, additional, Van Cleemput, J, additional, Bogaert, J, additional, Voigt, JU, additional, Batlle Lopez, E, additional, Vilacosta, I, additional, De La Rosa Riestra, A, additional, Sanchez Sauce, B, additional, Jimenez Valtierra, J, additional, Espana Barrio, E, additional, Campuzano Ruiz, R, additional, Alonso Bello, J, additional, and Perez Gonzalez, F, additional

Published
2015
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32. CED-12/ELMO, a novel member of the CrkII/Dock180/Rac pathway, is required for phagocytosis and cell migration

Author

Gumienny, T L, Brugnera, E, Tosello-Trampont, A C, Kinchen, J M, Haney, L B, Nishiwaki, K, Walk, S F, Nemergut, M E, Macara, I G, Francis, R, Schedl, T, Qin, Y, Van Aelst, L, Hengartner, M O, Ravichandran, K S, University of Zurich, and Hengartner, M O

Subjects
1300 General Biochemistry, Genetics and Molecular Biology, 570 Life sciences, biology, 10124 Institute of Molecular Life Sciences
Published
2001

33. Ras and rap 1 interaction with af-6 effector target

Author

Van Aelst L, Herrmann C, and Benjamin Boettner

Subjects
chemistry.chemical_compound, chemistry, Guanine, Effector, G protein, Rap1, GTPase, Phosphatidylinositol, Biology, Ras superfamily, PI3K/AKT/mTOR pathway, Cell biology
Abstract

Publisher Summary This chapter describes the Ras and Rap I interaction with AF-6 effector target. The chapter presents a spectrum of investigative approaches that served to demonstrate specific protein interactions among the Ras/Rapl GTPases and their potential effector molecule AF-6 in vivo and in vitro . The Rap types of small GTPases are members of the Ras superfamily and are the molecules that show the most identity with the oncogenic Ras proteins. Whereas the interaction of activated Ras proteins with their downstream effectors Raf, Ral guanine nucleotide dissociation stimulator (RalGDS), and phosphatidylinositol 3-kinase (PI3K) leads to a fairly defined picture, the role of Rapl is as yet poorly understood. The two-hybrid analysis and the investigation of the kinetic and thermodynamic properties of Ras-AF-6 and Rapl-AF-6 complexes leads to the same overall outcome—namely, Rap1 appears to form the tightest complex with AF-6-RBD1. The chapter concludes with a discussion on methods to quantitate Ras/Rapl and AF-6 interactions.

Published
2001
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35. Rac regulation of transformation, gene expression, and actin organization by multiple, PAK-independent pathways

Author

Van Aelst, L, Westwick, J K, Der, C J, Pestell, R G, Clark, G J, Symons, M, and Lambert, Q T

Subjects
macromolecular substances
Abstract

Rac1 and RhoA are members of the Rho family of Ras-related proteins and function as regulators of actin cytoskeletal organization, gene expression, and cell cycle progression. Constitutive activation of Rac1 and RhoA causes tumorigenic transformation of NIH 3T3 cells, and their functions may be required for full Ras transformation. The effectors by which Rac1 and RhoA mediate these diverse activities, as well as the interrelationship between these events, remain poorly understood. Rac1 is distinct from RhoA in its ability to bind and activate the p65 PAK serine/threonine kinase, to induce lamellipodia and membrane ruffling, and to activate the c-Jun NH2-terminal kinase (JNK). To assess the role of PAK in Rac1 function, we identified effector domain mutants of Rac1 and Rac1-RhoA chimeric proteins that no longer bound PAK. Surprisingly, PAK binding was dispensable for Rac1-induced transformation and lamellipodium formation, as well as activation of JNK, p38, and serum response factor (SRF). However, the ability of Rac1 to bind to and activate PAK correlated with its ability to stimulate transcription from the cyclin D1 promoter. Furthermore, Rac1 activation of JNK or SRF, or induction of lamellipodia, was neither necessary nor sufficient for Rac1 transforming activity. Finally, the signaling pathways that mediate Rac1 activation of SRF or JNK were distinct from those that mediate Rac1 induction of lamellipodia. Taken together, these observations suggest that Rac1 regulates at least four distinct effector-mediated functions and that multiple pathways may contribute to Rac1-induced cellular transformation.

Published
1997
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41. Glucose-induced hyperaccumulation of cAMP and absence of glucose repression in yeast strains with induced activity of cAMP-dependent protein kinase

Author

Mbonyi, K., van Aelst, L., Arguelles, J.C., Jans, A.W.H., and Thevelein, J.M.

Subjects
Biofysica, Biophysics, Life Science
Abstract

Addition of glucose or related fermentable sugars to derepressed cells of the yeast Saccharomyces cerevisiae triggers a RAS-mediated cyclic AMP (cAMP) signal that induces a protein phosphorylation cascade. In yeast mutants (tpk1w1, tpk2w1, and tpk3w1) containing reduced activity of cAMP-dependent protein kinase, fermentable sugars, as opposed to nonfermentable carbon sources, induced a permanent hyperaccumulation of cAMP. This finding confirms previous conclusions that fermentable sugars are specific stimulators of cAMP synthesis in yeast cells. Despite the huge cAMP levels present in these mutants, deletion of the gene (BCY1) coding for the regulatory subunit of cAMP-dependent protein kinase severely reduced hyperaccumulation of cAMP. Glucose-induced hyperaccumulation of cAMP was also observed in exponential-phase glucose-grown cells of the tpklw1 and tpk2w1 strains but not the tpk3w1 strain even though addition of glucose to glucose-repressed wild-type cells did not induce a cAMP signal. Investigation of mitochondrial respiration by in vivo 31P nuclear magnetic resonance spectroscopy showed the tpk1w1 and tpk2w1 strains, to be defective in glucose repression. These results are consistent with the idea that the signal transmission pathway from glucose to adenyl cyclase contains a glucose-repressible protein. They also show that a certain level of cAMP-dependent protein phosphorylation is required for glucose repression. Investigation of the glucose-induced cAMP signal and glucose-induced activation of trehalase in derepressed cells of strains containing only one of the wild-type TPK genes indicates that the transient nature of the cAMP signal is due to feedback inhibition by cAMP-dependent protein kinase.

Published
1990

44. Ras Partners

Author

Van Aelst, L., primary, White, M.A., additional, and Wigler, M.H., additional

Published
1994
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48. Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling.

Author

Lin, A W, Barradas, M, Stone, J C, van Aelst, L, Serrano, M, and Lowe, S W

Abstract

Oncogenic Ras transforms immortal rodent cells to a tumorigenic state, in part, by constitutively transmitting mitogenic signals through the mitogen-activated protein kinase (MAPK) cascade. In primary cells, Ras is initially mitogenic but eventually induces premature senescence involving the p53 and p16(INK4a) tumor suppressors. Constitutive activation of MEK (a component of the MAPK cascade) induces both p53 and p16, and is required for Ras-induced senescence of normal human fibroblasts. Furthermore, activated MEK permanently arrests primary murine fibroblasts but forces uncontrolled mitogenesis and transformation in cells lacking either p53 or INK4a. The precisely opposite response of normal and immortalized cells to constitutive activation of the MAPK cascade implies that premature senescence acts as a fail-safe mechanism to limit the transforming potential of excessive Ras mitogenic signaling. Consequently, constitutive MAPK signaling activates p53 and p16 as tumor suppressors.

Published
1998

49. Oncogenic Ras activation of Raf/mitogen-activated protein kinase-independent pathways is sufficient to cause tumorigenic transformation

Author

Khosravi-Far, R, White, M A, Westwick, J K, Solski, P A, Chrzanowska-Wodnicka, M, Van Aelst, L, Wigler, M H, and Der, C J

Abstract

Substantial evidence supports a critical role for the activation of the Raf-1/MEK/mitogen-activated protein kinase pathway in oncogenic Ras-mediated transformation. For example, dominant negative mutants of Raf-1, MEK, and mitogen-activated protein kinase all inhibit Ras transformation. Furthermore, the observation that plasma membrane-localized Raf-1 exhibits the same transforming potency as oncogenic Ras suggests that Raf-1 activation alone is sufficient to mediate full Ras transforming activity. However, the recent identification of other candidate Ras effectors (e.g., RalGDS and phosphatidylinositol-3 kinase) suggests that activation of other downstream effector-mediated signaling pathways may also mediate Ras transforming activity. In support of this, two H-Ras effector domain mutants, H-Ras(12V, 37G) and H-Ras(12V, 40C), which are defective for Raf binding and activation, induced potent tumorigenic transformation of some strains of NIH 3T3 fibroblasts. These Raf-binding defective mutants of H-Ras induced a transformed morphology that was indistinguishable from that induced by activated members of Rho family proteins. Furthermore, the transforming activities of both of these mutants were synergistically enhanced by activated Raf-1 and inhibited by the dominant negative RhoA(19N) mutant, indicating that Ras may cause transformation that occurs via coordinate activation of Raf-dependent and -independent pathways that involves Rho family proteins. Finally, cotransfection of H-Ras(12V, 37G) and H-Ras(12V, 40C) resulted in synergistic cooperation of their focus-forming activities, indicating that Ras activates at least two Raf-independent, Ras effector-mediated signaling events.

Published
1996
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