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Institute
- Pathologisches Institut (320) (remove)
Schriftenreihe
Sonstige beteiligte Institutionen
- Center for Interdisciplinary Clinical Research, Würzburg University, Würzburg, Germany (1)
- Department of Paediatric Radiology, Institute of Diagnostic and Interventional Radiology, Josef-Schneider-Straße 2, Wuerzburg 97080, Germany (1)
- IZKF Nachwuchsgruppe Geweberegeneration für muskuloskelettale Erkrankungen (1)
- Lehrstuhl für Regeneration Muskuloskelettaler Gewebe (1)
- Muskuloskelettales Centrum Würzburg (MCW) (1)
„Black esophagus“ oder „akute Ösophagusnekrose“ (AÖN) ist eine seltene Erkrankung, die sich makroskopisch durch eine zirkumferente Schwarzverfärbung der Ösophagusmukosa mit abruptem Ende am gastroösophagealen Übergang auszeichnet. Die genaue Pathogenese ist unbekannt; es werden multifaktorielle Einflüsse wie z. B. Säurereflux, Ischämie und verringerte Schutzmechanismen der Mukosa als mögliche Ursachen diskutiert.
Vorgestellt werden 2 Obduktionsfälle, die typische Befunde einer AÖN aufwiesen. Zusätzlich hatten Fall 1 eine Candida-Infektion und Fall 2 eine Appendizitis, sodass eine infektiöse Genese in beiden Fällen eine Rolle gespielt haben könnte.
Über die Rolle der Neuroinflammation bei Entstehung und Progression der Demenz vom Alzheimer-Typ
(2022)
Die vorliegende Studie bringt neue Erkenntnisse bezüglich der Rolle und Ver-teilung der Mikroglia und der eingewanderten Monozyten im Verlauf der Alz-heimer Erkrankung in postmortem Gehirnen. Im Gegensatz zu Studien an Tiermodellen konnten wir in unserer Kohorte eine nur sehr geringe Beteili-gung myeloischer Monozyten an der AD Pathologie beobachten, so dass man annehmen kann, dass bei Menschen die Immunantwort des Gehirns haupt-sächlich von den hirneigenen Mikrogliazellen getragen wird. Dies wurde an humanem postmortem Hirngewebe bis zu diesem Zeitpunkt noch nicht unter-sucht.
Zudem konnte gezeigt werden, dass die vulnerablen, früh von Tangles und Plaques betroffenen Hirnregionen auch eine frühe Mikrogliareaktion aufwei-sen und insbesondere von proinflammatorischen Zellen besiedelt werden und dass die Reaktion in manchen Regionen im Verlauf zunimmt, während in an-deren eine Abflachung oder sogar Abnahme beobachtet wird.
Zielsetzung dieser Arbeit war die Untersuchung von Gehirngewebe in der asymptomatischen Phase der SIV-Infektion zur Erfassung immunologischer Vorgänge bei der Entstehung einer SIV-Enzephalitis am Beispiel der gewebeständigen Lymphozyten und Makrophagen. Wir benutzten das etablierte SIV-AIDS Modell mit Makakenaffen. Untersucht wurden 24 Versuchstiere im Zeitraum von bis zu 20 Wochen, die zuvor mit einem der beiden Virusstämme (SIVmac251/ 32H oder SIVmac251/ MPBMC) infiziert worden waren, vier der Versuchstiere entwickelten eine SIV-Enzephalitis, eines dieser Tiere war mit Selegilin behandelt worden. Fünf weitere infektfreie Makaken dienten als Kontrollen. Nach definierten Zeiträumen wurden die Versuchstiere getötet, die Gehirne präpariert und mittels Immunhistochemie Lymphozyten und Makrophagen angefärbt. Im weiteren führten wir eine lichtmikroskopische Morphometrie, getrennt nach einzelnen Kompartimenten des Gehirns, wie Cortex, subcorticalem weißem Mark und perivaskulärem Raum, durch. Die Ergebnisse unserer Arbeit — die infizierte, asymptomatische Tiere mit den Kontrolltieren vergleicht — zeigen eine ausgeprägte lymphozytäre Reaktion speziell im Cortex, zum Teil auch im subcorticalen Mark. Die Makrophagen zeigen eine Zunahme der Zelldichte perivaskulär und im Cortex, welche quantitativ deutlich unter der der Lymphoyzten bleibt. Die Tiere mit Enzephalitis zeigen allesamt eine corticale, wie auch subcorticale Zunahme der lymphozytären Zelldichte, bei den Makrophagen zeigt sich eine überwiegend generelle Stimulierung in allen drei Kompartimenten. Die Ergebnisse unserer Arbeit — die sich durch die Untersuchung asymptomatischer Versuchstiere sehr gut an die Verhältnisse bei der HIV-Infektion annähert — lassen vermuten, daß es dem Immunsystem mit Hilfe der gewebeständigen Lymphozyten im Cortex und subcorticalen Mark für eine ganze Weile gelingt, den Ausbruch einer Enzephalitis und damit der AIDS Erkrankung zu verzögern.
Background
Wilms’ tumor 1-associating protein (WTAP) is a nuclear protein, which is ubiquitously expressed in many tissues. Furthermore, in various types of malignancies WTAP is overexpressed and plays a role as an oncogene. The function of WTAP in diffuse large B-cell lymphoma (DLBCL), however, remains unclear.
Methods
Immunohistochemistry was applied to evaluate the levels of WTAP expression in DLBCL tissues and normal lymphoid tissues. Overexpression and knock-down of WTAP in DLBCL cell lines, verified on mRNA and protein level served to analyze cell proliferation and apoptosis in DLBCL cell lines by flow cytometry. Finally, co-immunoprecipitation (Co-IP), IP, and GST-pull down assessed the interaction of WTAP with Heat shock protein 90 (Hsp90) and B-cell lymphoma 6 (BCL6) as well as determined the extend of its ubiquitinylation.
Results
WTAP protein levels were consistently upregulated in DLBCL tissues. WTAP promoted DLBCL cell proliferation and improved the ability to confront apoptosis, while knockdown of WTAP in DLBCL cell lines allowed a significant higher apoptosis rate after treatment with Etoposide, an anti-tumor drug. The stable expression of WTAP was depended on Hsp90. In line, we demonstrated that WTAP could form a complex with BCL6 via Hsp90 in vivo and in vitro.
Conclusion
WTAP is highly expressed in DLBCL, promoting growth and anti-apoptosis in DLBCL cell lines. WTAP is a client protein of Hsp90 and can appear in a complex with BCL6 and Hsp90 in DLBCL. Down-regulation of WTAP could improve the chemotherapeutic treatments in DLBCL.
Despite improved survival in the Rituximab (R) era, a considerable number of patients with diffuse large B-cell lymphoma (DLBCL) ultimately die from the disease. Functional imaging using [18F]fluorodeoxyglucose-PET is suggested for assessment of residual viable tumor very early during treatment but is compromised by non-specific tracer retention in inflammatory lesions. The PET tracer [18F]fluorodeoxythymidine (FLT) as surrogate marker of tumor proliferation may overcome this limitation. We present results of a prospective clinical study testing FLT-PET as superior and early predictor of response to chemotherapy and outcome in DLBCL. 54 patients underwent FLT-PET prior to and one week after the start of R-CHOP chemotherapy. Repetitive FLT-PET imaging was readily implemented into the diagnostic work-up. Our data demonstrate that the reduction of FLT standard uptake valuemean (SUVmean) and SUVmax one week after chemotherapy was significantly higher in patients achieving complete response (CR, n=48; non-CR, n=6; p<0.006). Martingale-residual and Cox proportional hazard analyses showed a significant monotonous decrease of mortality risk with increasing change in SUV. Consistent with these results, early FLT-PET response showed relevant discriminative ability in predicting CR. In conclusion, very early FLT-PET in the course of R-CHOP chemotherapy is feasible and enables identification of patients at risk for treatment failure.
Background:
During the last years, (19)F-MRI and perfluorocarbon nanoemulsion (PFC) emerged as a powerful contrast agent methodology to track cells and to visualize inflammation. We applied this new modality to visualize deep tissue abscesses during acute and chronic phase of inflammation caused by Staphylococcus aureus infection.
Methodology and Principal Findings:
In this study, a murine thigh infection model was used to induce abscess formation and PFC or CLIO (cross linked ironoxides) was administered during acute or chronic phase of inflammation. 24 h after inoculation, the contrast agent accumulation was imaged at the site of infection by MRI. Measurements revealed a strong accumulation of PFC at the abscess rim at acute and chronic phase of infection. The pattern was similar to CLIO accumulation at chronic phase and formed a hollow sphere around the edema area. Histology revealed strong influx of neutrophils at the site of infection and to a smaller extend macrophages during acute phase and strong influx of macrophages at chronic phase of inflammation.
Conclusion and Significance:
We introduce (19)F-MRI in combination with PFC nanoemulsions as a new platform to visualize abscess formation in a murine thigh infection model of S. aureus. The possibility to track immune cells in vivo by this modality offers new opportunities to investigate host immune response, the efficacy of antibacterial therapies and the influence of virulence factors for pathogenesis.
Personalized oncology is a rapidly evolving area and offers cancer patients therapy options that are more specific than ever. However, there is still a lack of understanding regarding transcriptomic similarities or differences of metastases and corresponding primary sites. Applying two unsupervised dimension reduction methods (t-Distributed Stochastic Neighbor Embedding (t-SNE) and Uniform Manifold Approximation and Projection (UMAP)) on three datasets of metastases (n = 682 samples) with three different data transformations (unprocessed, log10 as well as log10 + 1 transformed values), we visualized potential underlying clusters. Additionally, we analyzed two datasets (n = 616 samples) containing metastases and primary tumors of one entity, to point out potential familiarities. Using these methods, no tight link between the site of resection and cluster formation outcome could be demonstrated, or for datasets consisting of solely metastasis or mixed datasets. Instead, dimension reduction methods and data transformation significantly impacted visual clustering results. Our findings strongly suggest data transformation to be considered as another key element in the interpretation of visual clustering approaches along with initialization and different parameters. Furthermore, the results highlight the need for a more thorough examination of parameters used in the analysis of clusters.
Follikuläre Lymphome (FL) machen etwa 25-40% der Non-Hodgkin-Lymphome aus und sind in der Regel bereits bei Diagnosestellung nicht mehr auf den Lymphknoten beschränkt, sondern systemische Erkrankungen. In jüngeren Untersuchungen konnte gezeigt werden, dass die selten diagnostizierten limitierten Stadien (Ann Arbor I und II) der Erkrankung häufig einen nur partiellen Befall der betroffenen Lymphknoten durch das Lymphom zeigen. In diesen frühen Stadien kolonisieren follikuläre Lymphome präexistente Follikel (in situ- Lymphom) und breiten sich dann offenbar auf die übrigen Follikel des Lymphknotens aus, bevor ein systemischer Befall des gesamten Organismus feststellbar ist. Ziel der vorliegenden Arbeit war es zunächst zu untersuchen, auf welchem Weg die Zellen eines Tumorklons im follikulären Lymphom die Keimzentren eines Lymphknotens kolonisieren. Dazu wurde die genetische Verwandtschaft der einzelnen Tumorsubklone untereinander anhand ihrer individuellen Mutationsmuster bestimmt. Mit Hilfe von daraus berechneten phylogenetischen Stammbäumen konnte die Ausbreitung der Subklone auf die vorbestehenden Keimzentren nachvollzogen werden. Zweitens sollte in dieser Studie der Frage nachgegangen werden, ob die Tumorsubklone auch unter dem Einfluss der Keimzentrumsumgebung stehen, die in der physiologischen B-Zell-Reifung für die enorme Vielfalt der Antikörperspezifität sorgt (Hypermutation). Anhaltende Mutationen (ongoing mutations) innerhalb eines Tumorklons würden auf einen solchen erhaltenen Einfluss der Hypermutationsmaschinerie hinweisen. Schließlich sollte untersucht werden, ob es auch in follikulären Lymphomen eine antigenabhängige B-Zell-Reifung gibt, wie sie bei der physiologischen „Optimierung“ von Antikörpern auf die korrespondierenden Antigene zu finden ist. Material und Methode: Sieben Fälle von follikulären Lymphomen von vier Patienten (davon einer mit einem und einer mit zwei Rezidiven ihrer Lymphomerkrankung) wurden morphologisch und immunhistochemisch reevaluiert. Pro Fall wurden bis zu zehn Follikel mikrodisseziert und pro Follikel die VH-Gene von bis zu zehn Subklonen sequenziert. Computerunterstützt wurden sowohl die genetische Verwandtschaft der Tumorsubklone untereinander und ihre Verteilung auf die einzelnen Follikel, als auch das Verhältnis von R- zu S- Mutationen in den verschiedenen Abschnitten des BCR-Gens und damit ein möglicher Antigen-Einfluss auf die Hypermutation analysiert. Ergebnisse: Ein FL Grad I zeigte ein deutliches Clustering von genetisch miteinander verwandten Tumorsubklonen im selben Follikel. Dennoch fand sich ein moderater interfollikulärer Austausch der Subklone. Bei morphologisch höhergradigen FL (Grad II und IIIa) nahm das Clustering deutlich ab und der interfollikuläre Austausch zu, bis im zweiten Rezidiv eines Patienten ein weitgehend diffuses Wachstum resultierte. Als Ausdruck des erhaltenen Einflusses des Keimzentrums zeigten alle Primärtumoren (FL Grad I und II) noch ongoing mutations, während bei FL in Progression keine ongoing mutations mehr feststellbar waren. Eine Häufung von R-Mutationen in den antigenbindenden Domänen des B-Zell-Rezeptors (CDR) und S-Mutationen in den strukturellen Domänen (FR) als Hinweis auf eine antigen-gesteuerte Hypermutation in den Tumorsubklonen fand sich nur in einem FL Grad I. Aus den genetischen Analysen ergaben sich aber Hinweise auf eine erhaltene Funktionalität des B-Zell-Rezeptors in allen sieben Fällen.
In der vorliegenden Arbeit wurden die Expressionshäufigkeiten von MAGE-A-Antigenen, E -Cadherin, Laminin-5-gamma-2, MMP2 und MMP9 in Plattenepithelkarzinomen im Kopf- und Halsbereich untersuchen. Hierbei findet der Vergleich zwischen Primärtumoren und korrespondierenden Lymphknotenmetastasen besondere Beachtung. Um die Hypothese zu verifizieren, dass die o.g. Parameter einen signifikanten Einfluss auf die Progression und Metastasierung haben, wird der Zusammenhang zwischen den in der vorliegenden Arbeit gewonnenen Ergebnissen und diversen klinischen Parametern mittels Korrelationsanalyse untersucht.
Zur Entscheidungshilfe in der Therapiefindung des Mammakarzinoms haben sich bezüglich der Indikation zur Chemotherapie neben den klinischen und histopathologischen Kriterien in den letzten Jahren vorrangig Multigentests etabliert. In der vorliegenden Arbeit wurden Zusammenhänge zwischen dem Oncotyp DX® und 18 immunhistochemischen Markern aus der Tumorbiologie für 78 Fälle hormonrezeptorpositiver, Her2/neu negativer Mammafrühkarzinome mit niedrigem Lymphknotenstatus untersucht. Es erfolgten immunhistochemische Färbungen an Microtissue-Arrays der Tumorproben. Für die Marker AMACR, Cyclin D1, p53, MDM2 und PDL1 ergab sich eine klare statistisch signifikante Korrelation zum Recurrence-Score®des Oncotyp DX® und mit Einschränkungen auch für CDK4. Die Marker p27, Bcl2 und Glut 1 erreichten ein etwas niedrigeres Signifikanzniveau in der statistischen Analyse. Der immunhistochemische Routinemarker Ki67% zeigte eine hochsignifikante Korrelation mit dem Recurrence-Score®. Hierdurch ergeben sich neue Perspektiven zur Risikostratifizierung des Mammakarzinoms, wie beispielsweise die konsekutive Entwicklung eines immunhistochemischen Scores mit prädiktivem Wert für den Recurrence-Score® mit klinischer Anwendung als Prätest oder als eigenständiges Stratifizierungstool bei Brustkrebs.