Prevalence of the Prefoldin Subunit 5 Gene Deletion in Canine Mammary Tumors
2015 | journal article. A publication with affiliation to the University of Göttingen.
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Prevalence of the Prefoldin Subunit 5 Gene Deletion in Canine Mammary Tumors
Hennecke, S.; Beck, J.; Bornemann-Kolatzki, K.; Neumann, S.; Escobar, H. M.; Nolte, I. & Hammer, S. C. et al. (2015)
PLoS ONE, 10(7) art. e0131280. DOI: https://doi.org/10.1371/journal.pone.0131280
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Details
- Authors
- Hennecke, Silvia; Beck, Julia; Bornemann-Kolatzki, Kirsten; Neumann, Stephan; Escobar, Hugo Murua; Nolte, Ingo; Hammer, Susanne Conradine; Hewicker-Trautwein, Marion; Junginger, Johannes; Kaup, Franz-Josef; Brenig, Bertram; Schuetz, Ekkehard
- Abstract
- Background A somatic deletion at the proximal end of canine chromosome 27 (CFA27) was recently reported in 50% of malignant mammary tumors. This region harbours the tumor suppressor gene prefoldin subunit 5 (PFDN5) and the deletion correlated with a higher Ki-67 score. PFDN5 has been described to repress c-MYC and is, therefore, a candidate tumor-suppressor and cancer-driver gene in canine mammary cancer. Aim of this study was to confirm the recurrent deletion in a larger number of tumors. Methods Droplet digital PCR for PFDN5 was performed in DNA from 102 malignant, 40 benign mammary tumors/dysplasias, 11 non-neoplastic mammary tissues and each corresponding genomic DNA from leukocytes. The copy number of PFDN5 was normalized to a reference amplicon on canine chromosome 32 (CFA32). Z-scores were calculated, based on Gaussian distributed normalized PFDN5 copy numbers of the leukocyte DNA. Z-scores <= -3.0 in tissue were considered as being indicative of the PFDN5 deletion and called as such. The Ki-67 proliferation index was assessed in a subset of 79 tissue samples by immunohistochemistry. Results The deletion was confirmed in 24% of all malignant tumors, detected in only 7.5% of the benign tumors and was not present in any normal mammary tissue sample. The subgroup of solid carcinomas (n = 9) showed the highest frequency of the deletion (67%) and those malignomas without microscopical high fraction of benign tissue (n = 71) had a 32% frequency (p < 0.01 vs. benign samples). The Ki-67 score was found to be significantly higher (p<0.05) in the PFDN5-deleted group compared to malignant tumors without the deletion. Conclusions A somatic deletion of the PFDN5 gene is recurrently present in canine mammary cancer, supporting a potential role in carcinogenesis. The association of this deletion with higher Ki-67 indicates an increased proliferation rate and thus a link to tumor aggressiveness can be hypothesized. The confirmation of earlier results warrants further studies on PFDN5 as cancer-driver gene.
- Issue Date
- 2015
- Status
- published
- Publisher
- Public Library Science
- Journal
- PLoS ONE
- ISSN
- 1932-6203
- Sponsor
- Open-Access Publikationsfonds 2015
- Notes
- Silvia Hennecke (University of Göttingen) is the submitting author of this article.