@article{GeyerChalmersMacKintoshetal.2013,
  author    = {Geyer, Kathrin K. and Chalmers, Iain W. and MacKintosh, Neil and Hirst, Julie E. and Geoghegan, Rory and Badets, Mathieu and Brophy, Peter M. and Brehm, Klaus and Hoffmann, Karl F.},
  title     = {Cytosine methylation is a conserved epigenetic feature found throughout the phylum Platyhelminthes},
  series = {BMC Genomics},
  volume    = {14},
  journal   = {BMC Genomics},
  number    = {462},
  issn      = {1471-2164},
  doi       = {10.1186/1471-2164-14-462},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-121892},
  year      = {2013},
  abstract  = {Background: The phylum Platyhelminthes (flatworms) contains an important group of bilaterian organisms responsible for many debilitating and chronic infectious diseases of human and animal populations inhabiting the planet today. In addition to their biomedical and veterinary relevance, some platyhelminths are also frequently used models for understanding tissue regeneration and stem cell biology. Therefore, the molecular (genetic and epigenetic) characteristics that underlie trophic specialism, pathogenicity or developmental maturation are likely to be pivotal in our continued studies of this important metazoan group. Indeed, in contrast to earlier studies that failed to detect evidence of cytosine or adenine methylation in parasitic flatworm taxa, our laboratory has recently defined a critical role for cytosine methylation in Schistosoma mansoni oviposition, egg maturation and ovarian development. Thus, in order to identify whether this epigenetic modification features in other platyhelminth species or is a novelty of S. mansoni, we conducted a study simultaneously surveying for DNA methylation machinery components and DNA methylation marks throughout the phylum using both parasitic and non-parasitic representatives. Results: Firstly, using both S. mansoni DNA methyltransferase 2 (SmDNMT2) and methyl-CpG binding domain protein (SmMBD) as query sequences, we illustrate that essential DNA methylation machinery components are well conserved throughout the phylum. Secondly, using both molecular (methylation specific amplification polymorphism, MSAP) and immunological (enzyme-linked immunoabsorbent assay, ELISA) methodologies, we demonstrate that representative species (Echinococcus multilocularis, Protopolystoma xenopodis, Schistosoma haematobium, Schistosoma japonicum, Fasciola hepatica and Polycelis nigra) within all four platyhelminth classes (Cestoda, Monogenea, Trematoda and 'Turbellaria') contain methylated cytosines within their genome compartments. Conclusions: Collectively, these findings provide the first direct evidence for a functionally conserved and enzymatically active DNA methylation system throughout the Platyhelminthes. Defining how this epigenetic feature shapes phenotypic diversity and development within the phylum represents an exciting new area of metazoan biology.},
  language  = {en}
}
@article{RickmanLachAbhyankaretal.2015,
  author    = {Rickman, Kimberly A. and Lach, Francis P. and Abhyankar, Avinash and Donovan, Frank X. and Sanborn, Erica M. and Kennedy, Jennifer A. and Sougnez, Carrie and Gabriel, Stacey B. and Elemento, Olivier and Chandrasekharappa, Settara C. and Schindler, Detlev and Auerbach, Arleen D. and Smogorzewska, Agata},
  title     = {Deficiency of UBE2T, the E2 Ubiquitin Ligase Necessary for FANCD2 and FANCI Ubiquitination, Causes FA-T Subtype of Fanconi Anemia},
  series = {Cell Reports},
  volume    = {12},
  journal   = {Cell Reports},
  doi       = {10.1016/j.celrep.2015.06.014},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-151525},
  pages     = {35 -- 41},
  year      = {2015},
  abstract  = {Fanconi anemia (FA) is a rare bone marrow failure and cancer predisposition syndrome resulting from pathogenic mutations in genes encoding proteins participating in the repair of DNA interstrand crosslinks (ICLs). Mutations in 17 genes (FANCA-FANCS) have been identified in FA patients, defining 17 complementation groups. Here, we describe an individual presenting with typical FA features who is deficient for the ubiquitin-conjugating enzyme (E2), UBE2T. UBE2T is known to interact with FANCL, the E3 ubiquitin-ligase component of the multiprotein FA core complex, and is necessary for the monoubiquitination of FANCD2 and FANCI. Proband fibroblasts do not display FANCD2 and FANCI monoubiquitination, do not form FANCD2 foci following treatment with mitomycin C, and are hypersensitive to crosslinking agents. These cellular defects are complemented by expression of wild-type UBE2T, demonstrating that deficiency of the protein UBE2T can lead to Fanconi anemia. UBE2T gene gains an alias of FANCT.},
  language  = {en}
}
@article{LitovkinVanEyndeJoniauetal.2015,
  author    = {Litovkin, Kirill and Van Eynde, Aleyde and Joniau, Steven and Lerut, Evelyne and Laenen, Annouschka and Gevaert, Thomas and Gevaert, Olivier and Spahn, Martin and Kneitz, Burkhard and Gramme, Pierre and Helleputte, Thibault and Isebaert, Sofie and Haustermans, Karin and Bollen, Mathieu},
  title     = {DNA Methylation-Guided Prediction of Clinical Failure in High-Risk Prostate Cancer},
  series = {PLoS ONE},
  volume    = {10},
  journal   = {PLoS ONE},
  number    = {6},
  doi       = {10.1371/journal.pone.0130651},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-151705},
  pages     = {e0130651},
  year      = {2015},
  abstract  = {Background Prostate cancer (PCa) is a very heterogeneous disease with respect to clinical outcome. This study explored differential DNA methylation in a priori selected genes to diagnose PCa and predict clinical failure (CF) in high-risk patients. Methods A quantitative multiplex, methylation-specific PCR assay was developed to assess promoter methylation of the APC, CCND2, GSTP1, PTGS2 and RARB genes in formalin-fixed, paraffin-embedded tissue samples from 42 patients with benign prostatic hyperplasia and radical prostatectomy specimens of patients with high-risk PCa, encompassing training and validation cohorts of 147 and 71 patients, respectively. Log-rank tests, univariate and multivariate Cox models were used to investigate the prognostic value of the DNA methylation. Results Hypermethylation of APC, CCND2, GSTP1, PTGS2 and RARB was highly cancer-specific. However, only GSTP1 methylation was significantly associated with CF in both independent high-risk PCa cohorts. Importantly, trichotomization into low, moderate and high GSTP1 methylation level subgroups was highly predictive for CF. Patients with either a low or high GSTP1 methylation level, as compared to the moderate methylation groups, were at a higher risk for CF in both the training (Hazard ratio [HR], 3.65; 95\% CI, 1.65 to 8.07) and validation sets (HR, 4.27; 95\% CI, 1.03 to 17.72) as well as in the combined cohort ( HR, 2.74; 95\% CI, 1.42 to 5.27) in multivariate analysis. Conclusions Classification of primary high-risk tumors into three subtypes based on DNA methylation can be combined with clinico-pathological parameters for a more informative risk-stratification of these PCa patients.},
  language  = {en}
}
@article{CerezoEchevarriaKehlBeitzingeretal.2023,
  author    = {Cerezo-Echevarria, Argi{\~n}e and Kehl, Alexandra and Beitzinger, Christoph and M{\"u}ller, Tobias and Klopfleisch, Robert and Aupperle-Lellbach, Heike},
  title     = {Evaluating the histologic grade of digital squamous cell carcinomas in dogs and copy number variation of KIT Ligand — a correlation study},
  series = {Veterinary Sciences},
  volume    = {10},
  journal   = {Veterinary Sciences},
  number    = {2},
  issn      = {2306-7381},
  doi       = {10.3390/vetsci10020088},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-304824},
  year      = {2023},
  abstract  = {Dark-haired dogs are predisposed to the development of digital squamous cell carcinoma (DSCC). This may potentially suggest an underlying genetic predisposition not yet completely elucidated. Some authors have suggested a potential correlation between the number of copies KIT Ligand (KITLG) and the predisposition of dogs to DSCC, containing a higher number of copies in those affected by the neoplasm. In this study, the aim was to evaluate a potential correlation between the number of copies of the KITLG and the histological grade of malignancy in dogs with DSCC. For this, 72 paraffin-embedded DSCCs with paired whole blood samples of 70 different dogs were included and grouped according to their haircoat color as follow: Group 0/unknown haircoat color (n = 11); Group 1.a/black non-Schnauzers (n = 15); group 1.b/black Schnauzers (n = 33); group 1.c/black and tan dogs (n = 7); group 2/tan animals (n = 4). The DSCCs were histologically graded. Additionally, KITLG Copy Number Variation (CNV) was determined by ddPCR. A significant correlation was observed between KITLG copy number and the histological grade and score value. This finding may suggest a possible factor for the development of canine DSCC, thus potentially having an impact on personalized veterinary oncological strategies and breeding programs.},
  language  = {en}
}
@article{HaarmannNehenDeissetal.2015,
  author    = {Haarmann, Axel and Nehen, Mathias and Deiß, Annika and Buttmann, Mathias},
  title     = {Fumaric acid esters do not reduce inflammatory NF-\(\kappa\)B/p65 nuclear translocation, ICAM-1 expression and T-cell adhesiveness of human brain microvascular endothelial cells},
  series = {International Journal of Molecular Sciences},
  volume    = {16},
  journal   = {International Journal of Molecular Sciences},
  doi       = {10.3390/ijms160819086},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-148295},
  pages     = {19086-19095},
  year      = {2015},
  abstract  = {Dimethyl fumarate (DMF) is approved for disease-modifying treatment of patients with relapsing-remitting multiple sclerosis. Animal experiments suggested that part of its therapeutic effect is due to a reduction of T-cell infiltration of the central nervous system (CNS) by uncertain mechanisms. Here we evaluated whether DMF and its primary metabolite monomethyl fumarate (MMF) modulate pro-inflammatory intracellular signaling and T-cell adhesiveness of nonimmortalized single donor human brain microvascular endothelial cells at low passages. Neither DMF nor MMF at concentrations of 10 or 50 \(\mu\)M blocked the IL-1\(\beta\)-induced nuclear translocation of NF-\(\kappa\)B/p65, whereas the higher concentration of DMF inhibited the nuclear entry of p65 in human umbilical vein endothelium cultured in parallel. DMF and MMF also did not alter the IL-1\(\beta\)-stimulated activation of p38 MAPK in brain endothelium. Furthermore, neither DMF nor MMF reduced the basal or IL-1\(\beta\)-inducible expression of ICAM-1. In accordance, both fumaric acid esters did not reduce the adhesion of activated Jurkat T cells to brain endothelium under basal or inflammatory conditions. Therefore, brain endothelial cells probably do not directly mediate a potential blocking effect of fumaric acid esters on the inflammatory infiltration of the CNS by T cells.},
  language  = {en}
}
@phdthesis{Cremer2012,
  author    = {Cremer, Nicole},
  title     = {Genexpression bei der Alzheimer Demenz und dem Morbus Parkinson},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76748},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2012},
  abstract  = {Die Alzheimer Demenz und der Morbus Parkinson als h{\"a}ufigste neurodegenerative Erkrankungen f{\"u}hren zu schwerer Behinderung, zu Pflegebed{\"u}rftigkeit und meist {\"u}ber Komplikationen zum Tod. Ihr langer Verlauf stellt f{\"u}r Betroffene, Angeh{\"o}rige sowie f{\"u}r das Gesundheitssystem eine enorme Belastung dar. Da die {\"A}tiologie der Alzheimer Demenz und des Morbus Parkinson sowie der meisten neurodegenerativen Krankheiten im Einzelnen nicht bekannt sind und ph{\"a}notypische {\"U}berschneidungen auftreten, sind die M{\"o}glichkeiten der eindeutigen Diagnosestellung h{\"a}ufig eingeschr{\"a}nkt oder erst postmortal m{\"o}glich. Um eine Therapie bei Auftreten der ersten klinischen Symptome zu beginnen oder eine Voraussage der Erkrankungen zu erm{\"o}glichen, ist eine sensitive und validierte Fr{\"u}hdiagnostik n{\"o}tig. Ziel der vorliegenden Arbeit war deshalb, auf der Genebene potentielle pathogenetische Verbindungen, m{\"o}gliche diagnostische Markerproteine sowie Zusammenh{\"a}nge zum zeitlichen Verlauf beider Krankheiten zu identifizieren. Daf{\"u}r wurde mit der Real-Time Polymerasekettenreaktion die Expression von 44 Genen anhand von post mortem Gehirngewebe von Patienten mit Alzheimer Demenz, Morbus Parkionson im Vergleich zu Gesunden aus den vier Hirnregionen Hippocampus, Gyrus frontalis medialis, Gyrus temporalis medialis und Kleinhirn untersucht. Im Resultat zeigen die Gene mit einer statistisch signifikant ver{\"a}nderten Expression, z. B. Glutamattransporter, olfaktorische Rezeptoren oder vakuol{\"a}re Sortierungsproteine, bei beiden Erkrankungen geh{\"a}uft gleichsinnige {\"A}nderungen. Anhand dieser Ergebnisse ist eine kausale Verkn{\"u}pfung des ver{\"a}nderten Genmetabolismus mit der ablaufenden Neurodegeneration zu vermuten. Zus{\"a}tzlich wird die Hypothese gemeinsamer pathogenetischer Mechanismen beider Erkrankungen untermauert. Zusammenh{\"a}nge der Genexpression zum zeitlichen Verlauf der Erkrankungen werden nur vereinzelt belegt, bekr{\"a}ftigten dann aber die Annahme einer Assoziation zu den degenerativen Prozessen. Die Identifizierung eines spezifischen Biomarkers f{\"u}r eine der beiden Erkrankungen war ein Ziel der vorliegenden Arbeit. Aufgrund seiner Expressions{\"a}nderung im Hippocampus bei Patienten mit Alzheimer Demenz k{\"o}nnte das BACE1-Gen (Beta site APP cleaving enzyme 1), das dort eine signifikante Expressionsabnahme zeigt, als solcher f{\"u}r dieses Patientenkollektiv diskutiert werden. Die h{\"a}ufig in dieser Arbeit im Hippocampus detektierten, signifikanten Expressions{\"a}nderungen, weisen zudem auf eine besondere Affektion dieser Hirnregion bei der Alzheimer Demenz als auch beim Morbus Parkinson hin. Des Weiteren werden in der vorliegenden Arbeit im Kleinhirn, einer Hirnregion, in der bei beiden Erkrankungen scheinbar kaum oder keine pathologischen Prozesse ablaufen, geh{\"a}uft und dann {\"a}hnliche {\"A}nderungen der Genexpression gemessen, die f{\"u}r eine Beteiligung des Kleinhirns bei beiden Krankheiten sprechen, deren Bedeutung bislang unklar ist.},
  subject      = {Alzheimer},
  language  = {de}
}
@article{PaligeLindeMartinetal.2013,
  author    = {Palige, Katja and Linde, J{\"o}rg and Martin, Ronny and B{\"o}ttcher, Bettina and Citiulo, Francesco and Sullivan, Derek J. and Weber, Johann and Staib, Claudia and Rupp, Steffen and Hube, Bernhard and Morschh{\"a}user, Joachim and Staib, Peter},
  title     = {Global Transcriptome Sequencing Identifies Chlamydospore Specific Markers in Candida albicans and Candida dubliniensis},
  series = {PLoS ONE},
  volume    = {8},
  journal   = {PLoS ONE},
  number    = {4},
  doi       = {10.1371/journal.pone.0061940},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-131007},
  pages     = {e61940},
  year      = {2013},
  abstract  = {Candida albicans and Candida dubliniensis are pathogenic fungi that are highly related but differ in virulence and in some phenotypic traits. During in vitro growth on certain nutrient-poor media, C. albicans and C. dubliniensis are the only yeast species which are able to produce chlamydospores, large thick-walled cells of unknown function. Interestingly, only C. dubliniensis forms pseudohyphae with abundant chlamydospores when grown on Staib medium, while C. albicans grows exclusively as a budding yeast. In order to further our understanding of chlamydospore development and assembly, we compared the global transcriptional profile of both species during growth in liquid Staib medium by RNA sequencing. We also included a C. albicans mutant in our study which lacks the morphogenetic transcriptional repressor Nrg1. This strain, which is characterized by its constitutive pseudohyphal growth, specifically produces masses of chlamydospores in Staib medium, similar to C. dubliniensis. This comparative approach identified a set of putatively chlamydospore-related genes. Two of the homologous C. albicans and C. dubliniensis genes (CSP1 and CSP2) which were most strongly upregulated during chlamydospore development were analysed in more detail. By use of the green fluorescent protein as a reporter, the encoded putative cell wall related proteins were found to exclusively localize to C. albicans and C. dubliniensis chlamydospores. Our findings uncover the first chlamydospore specific markers in Candida species and provide novel insights in the complex morphogenetic development of these important fungal pathogens.},
  language  = {en}
}
@phdthesis{Putz2008,
  author    = {Putz, Evelyn},
  title     = {Haplotypenbasierte Assoziationsanalyse der COMT-Gen-Region bei schizophrenen Psychosen in einem polydiagnostischen Ansatz},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-28691},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2008},
  abstract  = {In den vergangenen Jahren wurde vermehrt das Gen, welches f{\"u}r Catechol-O-Methyltransferase codiert, als starker Kandidat f{\"u}r ein erh{\"o}htes Schizophrenierisiko diskutiert. Grund daf{\"u}r ist die zentrale Rolle der Catechol-O-Methyltransferase beim Katecholaminabbau im menschlichen pr{\"a}frontalen Cortex. Aufgrund der zunehmend akzeptierten Tatsache, daß die singul{\"a}re Betrachtung einzelner Marker bei der komplexen genetischen Textur von Kandidatengenen nur wenig zur Erhellung komplexer Erkrankungen beizutragen vermag (Licinio, 2003), untersuchten wir neben dem Val108/158Met-Polymorphismus (rs4680) vier weitere, die COMT-Gen-Region umspannende SNPs (rs2097603, rs740603, rs4818, rs165599) an einer Stichprobe von 459 Schizophrenen und 150 Kontrollpersonen. Zwar ergab sich f{\"u}r den Marker rs740603 auf Intron 1 eine signifikante Allel- (p = 0.0060) und Genotypassoziation (p = 0.019), der funktionelle Val108/158Met-Polymorphismus (rs4680) zeigte aber keinen signifikanten Zusammenhang mit der Erkrankung. Zudem fand sich in unserer Haplotypanalyse keine Markerkombination, die in {\"u}berdurchschnittlichem Zusammenhang mit schizophrenen Psychosen stand. F{\"u}r die Untergruppe der zykloiden Psychosen ließ sich bei einem p-Wert von 0.031 eine 4-Marker-Kombination ermitteln, die die SNPs rs740603, rs4818, rs4680 und rs165599 einschliesst und die Region von Intron 1 bis 3´-UTR umspannt. Zus{\"a}tzlich ergab sich in der Subgruppe der zykloiden Psychosen ein geschlechtsspezifischer Effekt im Sinne eines signifikanten 3-Marker-Haplotypen (rs4818-rs4680-rs165599) (p = .0044) in der Gruppe der Frauen (n = 27) mit rs165599 als st{\"a}rkstem Einzelmarker. Aufgrund des komplexen genetischen Zusammenhangs zwischen den untersuchten Markern und der Erkrankung sollte auch in der zuk{\"u}nftigen Forschung eine differenzierte Betrachtung der verschiedenen schizophrenen Zustandsbilder angestrebt werden, wie dies die Klassifikation nach Leonhard erm{\"o}glicht. Neben gewebsspezifischen Transkriptionsfaktoren k{\"o}nnten auch epigenetische Faktoren, wie die Cytosinmethylierung von CpG-Stellen in promotorregulierenden Regionen, einen Erkl{\"a}rungsansatz f{\"u}r die Entstehung schizophrener St{\"o}rungsbilder darstellen.},
  subject      = {Catecholmethyltransferase <Catechol-0-Methyltransferase>},
  language  = {de}
}
@article{VieiraJonesDanonetal.2012,
  author    = {Vieira, Jacqueline and Jones, Alex R. and Danon, Antoine and Sakuma, Michiyo and Hoang, Nathalie and Robles, David and Tait, Shirley and Heyes, Derren J. and Picot, Marie and Yoshii, Taishi and Helfrich-F{\"o}rster, Charlotte and Soubigou, Guillaume and Coppee, Jean-Yves and Klarsfeld, Andr{\´e} and Rouyer, Francois and Scrutton, Nigel S. and Ahmad, Margaret},
  title     = {Human Cryptochrome-1 Confers Light Independent Biological Activity in Transgenic Drosophila Correlated with Flavin Radical Stability},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {3},
  doi       = {10.1371/journal.pone.0031867},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134513},
  pages     = {e31867},
  year      = {2012},
  abstract  = {Cryptochromes are conserved flavoprotein receptors found throughout the biological kingdom with diversified roles in plant development and entrainment of the circadian clock in animals. Light perception is proposed to occur through flavin radical formation that correlates with biological activity in vivo in both plants and Drosophila. By contrast, mammalian (Type II) cryptochromes regulate the circadian clock independently of light, raising the fundamental question of whether mammalian cryptochromes have evolved entirely distinct signaling mechanisms. Here we show by developmental and transcriptome analysis that Homo sapiens cryptochrome - 1 (HsCRY1) confers biological activity in transgenic expressing Drosophila in darkness, that can in some cases be further stimulated by light. In contrast to all other cryptochromes, purified recombinant HsCRY1 protein was stably isolated in the anionic radical flavin state, containing only a small proportion of oxidized flavin which could be reduced by illumination. We conclude that animal Type I and Type II cryptochromes may both have signaling mechanisms involving formation of a flavin radical signaling state, and that light independent activity of Type II cryptochromes is a consequence of dark accumulation of this redox form in vivo rather than of a fundamental difference in signaling mechanism.},
  language  = {en}
}
@article{KellerLeidingerVogeletal.2014,
  author    = {Keller, Andreas and Leidinger, Petra and Vogel, Britta and Backes, Christina and ElSharawy, Abdou and Galata, Valentina and Mueller, Sabine C. and Marquart, Sabine and Schrauder, Michael G. and Strick, Reiner and Bauer, Andrea and Wischhusen, J{\"o}rg and Beier, Markus and Kohlhaas, Jochen and Katus, Hugo A. and Hoheisel, J{\"o}rg and Franke, Andre and Meder, Benjamin and Meese, Eckart},
  title     = {miRNAs can be generally associated with human pathologies as exemplified for miR-144*},
  series = {BMC MEDICINE},
  volume    = {12},
  journal   = {BMC MEDICINE},
  issn      = {1741-7015},
  doi       = {10.1186/s12916-014-0224-0},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-114349},
  pages     = {224},
  year      = {2014},
  abstract  = {Background: miRNA profiles are promising biomarker candidates for a manifold of human pathologies, opening new avenues for diagnosis and prognosis. Beyond studies that describe miRNAs frequently as markers for specific traits, we asked whether a general pattern for miRNAs across many diseases exists. Methods: We evaluated genome-wide circulating profiles of 1,049 patients suffering from 19 different cancer and non-cancer diseases as well as unaffected controls. The results were validated on 319 individuals using qRT-PCR. Results: We discovered 34 miRNAs with strong disease association. Among those, we found substantially decreased levels of hsa-miR-144* and hsa-miR-20b with AUC of 0.751 ( 95\% CI: 0.703-0.799), respectively. We also discovered a set of miRNAs, including hsa-miR-155*, as rather stable markers, offering reasonable control miRNAs for future studies. The strong downregulation of hsa-miR-144* and the less variable pattern of hsa-miR-155* has been validated in a cohort of 319 samples in three different centers. Here, breast cancer as an additional disease phenotype not included in the screening phase has been included as the 20th trait. Conclusions: Our study on 1,368 patients including 1,049 genome-wide miRNA profiles and 319 qRT-PCR validations further underscores the high potential of specific blood-borne miRNA patterns as molecular biomarkers. Importantly, we highlight 34 miRNAs that are generally dysregulated in human pathologies. Although these markers are not specific to certain diseases they may add to the diagnosis in combination with other markers, building a specific signature. Besides these dysregulated miRNAs, we propose a set of constant miRNAs that may be used as control markers.},
  language  = {en}
}