Classification of death causes after transplantation (CLASS):Evaluation of methodology and initial results

Correct classification of death causes is an important component of transplant trials.We aimed to develop and validate a system to classify causes of death in hematopoietic stem cell (HSCT) and solid organ (SOT) transplant recipients.Case record forms (CRF) of fatal cases were completed, including investigator-designated cause of death. Deaths occurring in 2010 to 2013 were used for derivation; and were validated by deaths occurring in 2013 to 2015. Underlying cause of death (referred to as recorded underlying cause) was determined through a central adjudication process involving 2 external reviewers, and subsequently compared with the Danish National Death Cause Registry.Three hundred eighty-eight recipients died 2010 to 2015 (196 [51%] SOT and 192 [49%] HSCT). The main recorded underlying causes of death among SOT and HSCT were classified as cancer (20%, 48%), graft rejection/failure/graft-versus-host-disease (35%, 28%), and infections (20%, 11%). Kappa between the investigator-designated and the recorded underlying cause of death was 0.74 (95% CI 0.69-0.80) in derivation and comparable in the validation cohort. Death causes were concordant with the Danish National Death Cause Registry in 37.2% (95% CI 31.5-42.9) and 38.4% (95% CI 28.8-48.0) in the derivation and validation cohorts, respectively.We developed and validated a method to systematically and reliably classify the underlying cause of death among transplant recipients. There was a high degree of discordance between this classification and that in the Danish National Death Cause Registry

Predictive value of galectin-1 in the development and progression of HIV-associated lymphoma

At AHIV-1 infection, the binding of the viral envelopeproteins to CD4þ is essential for viral transmission, andthis process is facilitated by interaction with the highlyconserved host lectin, galectin-1 (Gal-1) [1?3]. Withinthe tumor microenvironment, Gal-1 is expressed by bothtumor and stromal cells where it promotes tumorimmune escape and favors hypoxia-driven angiogenesis[4?6]. In sporadically occurring Hodgkin lymphoma,high Gal-1 expression at diagnosis is associated withpoorer treatment response [7], and high soluble Gal-1(sGal-1) correlates with adverse disease characteristics [8].Previous studies have shown that targeted inhibition ofGal-1 prevents tumor-induced immunosuppression[9,10] as well as inhibits tumor growth and metastasisin various tumor models [6,11?13].In conclusion, the results of our study indicate that Gal-1 is significantly associated with risk of lymphoma in HIV-infected individuals and may represent an attractive futuretarget for the management of HIV-associated lymphoma.Fil: Vase, MajaØlholm. University Aarhus; DinamarcaFil: Ludvigsen, Maja. University Aarhus; DinamarcaFil: Bendix, Knud. University Aarhus; DinamarcaFil: Dutoit, Stephen H.. University Aarhus; DinamarcaFil: Hjortebjerg, Rikke. University Aarhus; DinamarcaFil: Petruskevicius, Irma. University Aarhus; DinamarcaFil: Møller, Michael B.. Odense Universitetshospital; DinamarcaFil: Pedersen, Gitte. Aalborg Universitet; DinamarcaFil: Denton, Paul W.. University Aarhus; Dinamarca. Arhus Universitetshospital; DinamarcaFil: Honoré, Bent. University Aarhus; DinamarcaFil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Larsen, Carsten S.. Arhus Universitetshospital; DinamarcaFil: D'Amore, Francesco. Arhus Universitetshospital; Dinamarc