Publikationsserver der Universitätsbibliothek Marburg
Titel:CD34+ Fibrozyten im Stroma benigner und maligner Tumoren der Glandula parotidea
Autor:Langguth, Tobias
Weitere Beteiligte: Barth, Peter Josef (Prof. Dr.med.)
Veröffentlicht:2014
URI:https://archiv.ub.uni-marburg.de/diss/z2014/0755
URN: urn:nbn:de:hebis:04-z2014-07552
DOI: https://doi.org/10.17192/z2014.0755
ISBN: 978-3-8359-6230-9
DDC: Medizin
Titel (trans.):CD34+ fibrocytes in the stroma of benign and malignant parotid gland tumors.
Publikationsdatum:2014-12-16
Lizenz:https://rightsstatements.org/vocab/InC-NC/1.0/

Dokument

Schlagwörter:
stroma, Glandula parotidea, CD34+ Fibrozyten, α-SMA+ myofibroblasts, Glandula parotis, CD34+ fibrocytes, glandula parotidea, Stroma, α-SMA+ Myofibroblasten, Tumor, tumor

Zusammenfassung:
Hintergrund: Zur Verteilung und zum Vorkommen CD34+ Fibrozyten im Stroma der Glandula parotidea ist wenig bekannt. In der vorliegenden Studie sollte deshalb die Frage geklärt werden, ob CD34+ Fibrozyten und α-SMA+ Myofibroblasten einen integralen Bestandteil sowohl des Stromas der gesunden Parotis als auch neoplastischer Tumorerkrankungen der Glandula parotidea darstellen. Methode: In der vorliegenden Studie wurden eine Studienpopulation aus insgesamt 122 Fällen - bestehend aus 8 Fällen normalen Parotisgewebes, 68 benignen und 46 malignen Neoplasien der Glandula parotidea - aus einem monozentrischen Registeram Institut für Pathologie des Universitätsklinikums Marburg aus den Jahren 2000- 2009 retrospektiv immunhistochemisch analysiert. Neben einer semiquantitativen Analyse nach einem definierten Auswertemodus und nachfolgender deskriptiver Statistik erfolgte eine explorative Analyse, wobei die gewonnenen Daten der 3 Subgruppen sowohl global als auch durch Einzelgruppenvergleiche mit Hilfe des Exakten Tests nach Fisher ausgewertet wurden. Ergebnisse: Im Stroma der normalen Parotis kam ein lockeres, retikuläres Maschenwerk CD34+ Fibrozyten zur Darstellung. Das Stroma der normalen Parotis beherbergt keine α-SMA+ Myofibroblasten. Das Stroma von pleomorphen Adenomen, Warthin-Tumoren, nicht-membranösen Basalzelladenomen und nicht-sklerosierten Onkozytomen zeigt keine CD34+ Fibrozyten. In der Gruppe der benignen Tumoren nimmt sowohl das membranöse Basalzelladenom als auch das sklerosierte Onkozytom eine Sonderstellung ein, da sie ein gleichmäßig verteiltes Stromanetzwerk aus CD34+ Fibrozyten besitzen. Mit Ausnahme weniger Warthin-Tumoren konnten im Stroma benigner Parotisneoplasien keine zusätzlichen α-SMA+ Myofibroblasten dargestellt werden. Das konstante Auftreten von CD34+ Fibrozyten in der Kapsel benigner Parotistumoren kann als pathognostisches Merkmal dienen, während das Fehlen CD34+ Fibrozyten im Stroma benigner Parotistumoren nicht als Malignitätskriterium gewertet werden darf. In fast allen untersuchten Fällen zeigte das Stroma primärer und sekundärer Parotiskarzinome einen kompletten, stereotypen Verlust CD34+ Fibrozyten, während das umgebende tumorfreie Parotisstroma ein normales Netzwerk residenter CD34+ Fibrozyten aufwies. Gleichzeitig konnte für die Mehrzahl der Karzinome ein Zugewinn stromaler α-SMA+ SPARC+ Myofibroblasten nachgewiesen werden. Dieser Wandel der Stromazellen vom CD34+ α-SMA- SPARC- hin zum CD34- α-SMA+ SPARC+ Phänotyp scheint sich in einer präexistenten Zellpopulation ortsständiger CD34+ Fibrozyten abzuspielen. Der Verlust CD34+ Fibrozyten und der komplementäre Zugewinn α-SMA+ Myofibroblasten kann in der histopathologischen Diagnostik als ergänzendes Hilfsmittel zur Abgrenzung benigner und maligner Parotisneoplasien Anwendung finden, darf jedoch niemals als ausschließliches Dignitätskriterium zu Rate gezogen werden. Hinsichtlich der Phänotypisierung des Parotisstromas konnte global gezeigt werden, dass es deutliche Verteilungsunterschiede CD34+ Fibrozyten und α-SMA+ Myofibroblasten zwischen der gesunden Parotis und benignen als auch malignen Parotistumoren gibt. Somit ist eine immunphänotypische Charakterisierung des jeweiligen Stromas möglich. Das adenoidzystische Karzinome stellt einen diagnostischen Pitfall dar, da der Phänotypwandel der Stromazellen ausblieb. Das Stroma zeigte einen variablen Erhalt der CD34+ Fibrozyten, während α-SMA+ Myofibroblasten nicht nachweisbar waren. Dieser Befund impliziert, dass diese hochaggressive Karzinomentität ein alternatives biologisches Verhalten besitzt. Im Gegensatz zu den anderen untersuchten Parotiskarzinomen könnte die Präsenz CD34+ Fibrozyten im Stroma adenoidzystischer Karzinome ein Malignitätskriterium darstellen. Zusammenfassung: Diese Studie an 114 Tumoren der Glandula parotidea zeigt erstmalig vergleichende Daten bezüglich der Verteilungsunterschiede CD34+ Fibrozyten bei Patienten mit Tumorerkrankungen der Glandula parotidea. Der stromale Phänotypwandel invasiver Parotiskarzinome ist mit Ausnahme des adenoidzystischen Karzinoms durch einen Verlust CD34+ Fibrozyten und einem simultanen Zugewinn α-SMA+ SPARC+ Myofibroblasten gekennzeichnet. Das zelluläre Biomarkersystem aus CD34+ Fibrozyten und α-SMA+ Myofibroblasten könnte Einzug in die Differentialdiagnostik benigner und maligner Parotistumoren halten. Das alleinige Fehlen CD34+ Fibrozyten im Stroma von Parotistumoren darf jedoch nie als alleiniges Dignitätskriterium gewertet werden. Die SPARC-Expression durch α-SMA+ Myofibroblasten könnte als Progressionsmarker für maligne Speicheldrüsentumoren Anwendung finden. Die vorliegende explorative Studie könnte zur Planung einer prospektiven, multizentrischen Studie dienlich sein.

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