Publikationsdatenbank

Immuno-oncological characterization of canine cutaneous histiocytoma by gene expression profiling utilizing NanoString nCounter® RNA hybridization technique (2024)

Art

Poster

Autoren

Langenhagen, A. K. (WE 12)

Haake, A. F. H. (WE 12)

Gruber, A. D. (WE 12)

Kongress

European Congress of Veterinary Pathology and Clinical Pathology (ESVP/ECVP/ESVCP/ECVCP)

Lisbon, 30.08. – 02.09.2023

Quelle

Journal of comparative pathology

Bandzählung: 210

Seiten: 64 – 65

ISSN: 0021-9975

Sprache

Englisch

Verweise

URL (Volltext): https://www.sciencedirect.com/science/article/pii/S0021997524000811?via%3Dihub

DOI: 10.1016/j.jcpa.2024.03.052

Kontakt

Institut für Tierpathologie

Robert-von-Ostertag-Str. 15
14163 Berlin
+49 30 838 62450
pathologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

Introduction: The stereotypic regression of canine cutaneous histiocytoma (CCH) is a unique phenomenon of broader oncomechanistic interest. However, its mechanisms have only partially been investigated. In this study, we asked which specific immuno-oncological dynamics may underlie regression of CCH at mRNA level. In addition to general pathways such as apoptosis, proliferation and hypoxia, spatiotemporal dynamics of expression of co-stimulatory CD80 and CD86 molecules were investigated.

Materials and methods: HE-stained FFPE sections from 35 CCHs were staged and RNA isolated for nCounter®️ Analysis System, an RNA hybridisation assay which allows 800 genes to be analysed. Forty-six immuno-oncologically relevant pathways were compared between stages 1, 2 and 3. Expression of CD80 and CD86 was measured by in-situ hybridization followed by quantitation of positive tumour cells, and finally compared to three canine histiocytic sarcoma (HS) samples.

Results: Surprisingly, no significant differences were found for any of the pathways tested between the three stages. Over time, CD80 displayed an increase in expression from bottom to top, while CD86 remained unchanged (average: 95.1% expressing tumour cells). Overall, expression of CD80 in CCH (73.3%) was similar to HS (62.1%), while CD86 was significantly less expressed in HS (57.6%) compared to CCH.

Conclusions: Our data reveal that major immuno-oncological pathways are seemingly not regulated at mRNA level during the course of CCH. We speculate that key processes leading to tumour regression may occur at an earlier time point than examined here. Our data further support a role of co-stimulatory molecules in CCH regression involving cytotoxic lymphocytes.