@phdthesis{Gruendahl2020,
  author    = {Gr{\"u}ndahl, Marie},
  title     = {Inzidenz und assoziierte Letalit{\"a}t invasiver Mykosen bei Patienten mit akuter lymphatischer Leuk{\"a}mie},
  doi       = {10.25972/OPUS-20643},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-206434},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2020},
  abstract  = {Invasive Mykosen stellen bei Patienten mit h{\"a}matologischer Grunderkrankung eine lebensbedrohliche Komplikation dar. Im Rahmen dieser retrospektiven monozentrischen Studie wurde die Inzidenz und Letalit{\"a}t invasiver Mykosen bei erwachsenen Patienten mit einer neu diagnostizierten akuten lymphatischen Leuk{\"a}mie erfasst, sowie die Krankheitsverl{\"a}ufe und der Einfluss einer antimykotischen Prophylaxe analysiert. In der untersuchten Kohorte war eine erh{\"o}hte Inzidenz invasiver Mykosen feststellbar, ebenso wie eine negative Beeinflussung des Krankheitsverlaufs durch invasive Mykosen. Es konnte kein signifikanter Nutzen einer antimykotischen Prophylaxe verzeichnet werden. Eine diagnostisch gesteuerte Therapie der invasiven Mykosen ist anzustreben. Die Frage nach dem Nutzen einer antimykotischen Prophylaxe bleibt auch in dieser Arbeit nicht abschließend gekl{\"a}rt. Eine großangelegte prospektive Studie hierzu w{\"a}re w{\"u}nschenswert. Durch Risiken insbesondere hinsichtlich schwerwiegender Medikamenteninteraktionen scheinen aktuell jedoch retrospektive Daten mit individuell angesetzter Prophylaxe die einzige m{\"o}gliche N{\"a}herung an diese Fragestellung zu sein.},
  subject      = {Mykose},
  language  = {de}
}
@article{DeakPopZimtaetal.2019,
  author    = {Deak, Dalma and Pop, Cristina and Zimta, Alina-Andreea and Jurj, Ancuta and Ghiaur, Alexandra and Pasca, Sergiu and Teodorescu, Patric and Dascalescu, Angela and Antohe, Ion and Ionescu, Bogdan and Constantinescu, Catalin and Onaciu, Anca and Munteanu, Raluca and Berindan-Neagoe, Ioana and Petrushev, Bobe and Turcas, Cristina and Iluta, Sabina and Selicean, Cristina and Zdrenghea, Mihnea and Tanase, Alina and Danaila, Catalin and Colita, Anca and Colita, Andrei and Dima, Delia and Coriu, Daniel and Einsele, Hermann and Tomuleasa, Ciprian},
  title     = {Let's Talk About BiTEs and Other Drugs in the Real-Life Setting for B-Cell Acute Lymphoblastic Leukemia},
  series = {Frontiers in Immunology},
  volume    = {10},
  journal   = {Frontiers in Immunology},
  number    = {2856},
  issn      = {1664-3224},
  doi       = {10.3389/fimmu.2019.02856},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-193921},
  year      = {2019},
  abstract  = {Background: Therapy for acute lymphoblastic leukemia (ALL) are currently initially efficient, but even if a high percentage of patients have an initial complete remission (CR), most of them relapse. Recent data shows that immunotherapy with either bispecific T-cell engagers (BiTEs) of chimeric antigen receptor (CAR) T cells can eliminate residual chemotherapy-resistant B-ALL cells. Objective: The objective of the manuscript is to present improvements in the clinical outcome for chemotherapy-resistant ALL in the real-life setting, by describing Romania's experience with bispecific antibodies for B-cell ALL. Methods: We present the role of novel therapies for relapsed B-cell ALL, including the drugs under investigation in phase I-III clinical trials, as a potential bridge to transplant. Blinatumomab is presented in a critical review, presenting both the advantages of this drug, as well as its limitations. Results: Bispecific antibodies are discussed, describing the clinical trials that resulted in its approval by the FDA and EMA. The real-life setting for relapsed B-cell ALL is described and we present the patients treated with blinatumomab in Romania. Conclusion: In the current manuscript, we present blinatumomab as a therapeutic alternative in the bridge-to-transplant setting for refractory or relapsed ALL, to gain a better understanding of the available therapies and evidence-based data for these patients in 2019.},
  language  = {en}
}
@article{RouhigharabaeiFerreiroTousseynetal.2014,
  author    = {Rouhigharabaei, Leila and Ferreiro, Julio Finalet and Tousseyn, Thomas and van der Krogt, Jo-Anne and Put, Natalie and Haralambieva, Eugenia and Graux, Carlos and Maes, Brigitte and Vicente, Carmen and Vandenberghe, Peter and Cools, Jan and Wlodarska, Iwona},
  title     = {Non-IG Aberrations of FOXP1 in B-Cell Malignancies Lead to an Aberrant Expression of N-Truncated Isoforms of FOXP1},
  series = {PLOS ONE},
  volume    = {9},
  journal   = {PLOS ONE},
  number    = {1},
  issn      = {1932-6203},
  doi       = {10.1371/journal.pone.0085851},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-117679},
  pages     = {e85851},
  year      = {2014},
  abstract  = {The transcription factor FOXP1 is implicated in the pathogenesis of B-cell lymphomas through chromosomal translocations involving either immunoglobulin heavy chain (IGH) locus or non-IG sequences. The former translocation, t(3; 14)(p13; q32), results in dysregulated expression of FOXP1 juxtaposed with strong regulatory elements of IGH. Thus far, molecular consequences of rare non-IG aberrations of FOXP1 remain undetermined. Here, using molecular cytogenetics and molecular biology studies, we comprehensively analyzed four lymphoma cases with non-IG rearrangements of FOXP1 and compared these with cases harboring t(3; 14)(p13; q32)/IGH-FOXP1 and FOXP1-expressing lymphomas with no apparent structural aberrations of the gene. Our study revealed that non-IG rearrangements of FOXP1 are usually acquired during clinical course of various lymphoma subtypes, including diffuse large B cell lymphoma, marginal zone lymphoma and chronic lymphocytic leukemia, and correlate with a poor prognosis. Importantly, these aberrations constantly target the coding region of FOXP1, promiscuously fusing with coding and non-coding gene sequences at various reciprocal breakpoints (2q36, 10q24 and 3q11). The non-IG rearrangements of FOXP1, however, do not generate functional chimeric genes but commonly disrupt the full-length FOXP1 transcript leading to an aberrant expression of N-truncated FOXP1 isoforms (FOXP1NT), as shown by QRT-PCR and Western blot analysis. In contrast, t(3; 14)(p13; q32)/IGH-FOXP1 affects the 59 untranslated region of FOXP1 and results in overexpress the full-length FOXP1 protein (FOXP1FL). RNA-sequencing of a few lymphoma cases expressing FOXP1NT and FOXP1FL detected neither FOXP1-related fusions nor FOXP1 mutations. Further bioinformatic analysis of RNA-sequencing data retrieved a set of genes, which may comprise direct or non-direct targets of FOXP1NT, potentially implicated in disease progression. In summary, our findings point to a dual mechanism through which FOXP1 is implicated in B-cell lymphomagenesis. We hypothesize that the primary t(3; 14)(p13; q32)/IGH-FOXP1 activates expression of the FOXP1FL protein with potent oncogenic activity, whereas the secondary non-IG rearrangements of FOXP1 promote expression of the FOXP1NT proteins, likely driving progression of disease.},
  language  = {en}
}