Perske, Christina

[["dc.bibliographiccitation.firstpage","599"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Translational oncology"],["dc.bibliographiccitation.lastpage","603"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Wienbeck, Susanne"],["dc.contributor.author","Fischer, Uwe"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Wienke, Andreas"],["dc.contributor.author","Meyer, Hans Jonas"],["dc.contributor.author","Lotz, Joachim"],["dc.contributor.author","Surov, Alexey"],["dc.date.accessioned","2019-07-09T11:43:26Z"],["dc.date.available","2019-07-09T11:43:26Z"],["dc.date.issued","2017-06-27"],["dc.description.abstract","PURPOSE: Recently, cone-beam breast computed tomography (CBCT) is established for the breast investigation. The purpose of the present study was to investigate possible associations between CBCT findings and histopathological features in breast cancer. METHODS: Overall, 59 female patients, mean age of 64.6 years with histological proven breast cancer were included into the study. In all cases, non-contrast CBCT examination was done. The diagnosis of the identified lesions was confirmed histologically by biopsy. Immunohistochemical staining against estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and Ki-67 was performed for every lesion. Collected data were evaluated by means of descriptive statistics. Spearman's correlation coefficient was used to analyze the association between CT density and Ki-67 values. P values <0.05 were taken to indicate statistical significance in all instances. RESULTS: The size of the lesion varied from 2.7 to 90.0, mean size, 15.88±13.0 mm. The mean value of CT density of the lesions was 63.95±38.18 HU. The density tended to be higher in tubular carcinoma. Correlation analysis identified no significant correlations between CT density and Ki-67 level (r=-0.031, P=.784). There were no statistically significant differences of CT density between tumors with different receptor status. CONCLUSIONS: No significant associations between CT density and receptor status in breast cancer. Tubular carcinoma tended to have higher CT density in comparison to other subtypes of breast carcinomas."],["dc.identifier.doi","10.1016/j.tranon.2017.05.004"],["dc.identifier.pmid","28666188"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14534"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58889"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1936-5233"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Cone-beam Breast Computed Tomography: CT Density Does Not Reflect Proliferation Potential and Receptor Expression of Breast Carcinoma."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","904"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Translational oncology"],["dc.bibliographiccitation.lastpage","910"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Uhlig, Johannes"],["dc.contributor.author","Fischer, Uwe"],["dc.contributor.author","von Fintel, Eva"],["dc.contributor.author","Stahnke, Vera"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Lotz, Joachim"],["dc.contributor.author","Wienbeck, Susanne"],["dc.date.accessioned","2019-07-09T11:44:45Z"],["dc.date.available","2019-07-09T11:44:45Z"],["dc.date.issued","2017-12"],["dc.description.abstract","PURPOSE: To evaluate whether contrast enhancement on cone-beam breast-CT (CBBCT) could aid in discrimination of breast cancer subtypes and receptor status. METHODS: This study included female patients age >40 years with malignant breast lesions identified on contrast-enhanced CBBCT. Contrast enhancement of malignant breast lesions was standardized to breast fat tissue contrast enhancement. All breast lesions were approved via image-guided biopsy or surgery. Immunohistochemical staining was conducted for expression of estrogen (ER), progesterone (PR), human epidermal growth factor receptor-2 (HER2) and Ki-67 index. Contrast enhancement of breast lesions was correlated with immunohistochemical breast cancer subtypes (Luminal A, Luminal B, HER2 positive, triple negative), receptor status and Ki-67 expression. RESULTS: Highest contrast enhancement was seen for Luminal A lesions (93.6 HU) compared to Luminal B lesions (47.6 HU, P=.002), HER2 positive lesions (83.5 HU, P=.359) and triple negative lesions (45.3 HU, P=.005). Contrast enhancement of HER2 positive lesions was higher than Luminal B lesions (P=.044) and triple negative lesions (P=.039). No significant difference was evident between Luminal B and triple negative lesions (P=.439). Lesions with high Ki-67 index showed lower contrast enhancement than those with low Ki-67 index (P=.0043). ER, PR and HER2 positive lesions demonstrated higher contrast enhancement than their receptor negative counterparts, although differences did not reach statistical significance (P=.1714; P=.3603; P=.2166). CONCLUSIONS: Contrast enhancement of malignant breast lesions on CBBCT correlates with immunohistochemical subtype and proliferative potential. Thereby, CBBCT might aid in selecting individualized treatment strategies for breast cancer patients based on pre-operative imaging."],["dc.identifier.doi","10.1016/j.tranon.2017.08.010"],["dc.identifier.pmid","28946110"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14887"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59085"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1936-5233"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","Contrast Enhancement on Cone-Beam Breast-CT for Discrimination of Breast Cancer Immunohistochemical Subtypes."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2046"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The American journal of pathology"],["dc.bibliographiccitation.lastpage","2054"],["dc.bibliographiccitation.volume","177"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Lahat, Nitza"],["dc.contributor.author","Sheffy Levin, Sharon"],["dc.contributor.author","Bitterman, Haim"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Rahat, Michal Amit"],["dc.date.accessioned","2019-07-09T11:53:00Z"],["dc.date.available","2019-07-09T11:53:00Z"],["dc.date.issued","2010"],["dc.description.abstract","Tumor-associated macrophages can potentially kill tumor cells via the high concentrations of nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS); however, tumor-associated macrophages actually support tumor growth, as they are skewed toward M2 activation, which is characterized by low amounts of NO production and is proangiogenic. We show that the mouse renal cell carcinoma cell line, RENCA, which, on stimulation, expresses high levels of iNOS mRNA, loses its ability to express the iNOS protein. This effect is mediated by the microRNA miR-146a, as inhibition of RENCA cells with anti-miR- 146a restores iNOS expression and NO production (4.8 ± 0.4 versus 0.3 ± 0.1 μmol/L in uninhibited cells, P < 0.001). In vivo, RENCA tumor cells do not stain for iNOS, while infiltrating tumor-associated macrophages showed intense staining, and both cell types expressed iNOS mRNA. Restoring iNOS protein expression in RENCA cells using anti-miR-146a increases macrophage-induced death of RENCA cells by 73% (P < 0.01) in vitro and prevents tumor growth in vivo. These results suggest that, in addition to NO production by macrophages, tumor cells must produce NO to induce their own deaths, and some tumor cells may use miR-146a to reduce or abolish endogenous NO production to escape macrophage-mediated cell death. Thus, inhibiting miR-146a may render these tumor cells susceptible to therapeutic strategies, such as adoptive transfer of M1-activated macrophages."],["dc.identifier.doi","10.2353/ajpath.2010.091111"],["dc.identifier.fs","576544"],["dc.identifier.pmid","20709800"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6304"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60317"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1525-2191"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Apoptosis"],["dc.subject.mesh","Blotting, Western"],["dc.subject.mesh","Carcinoma, Renal Cell"],["dc.subject.mesh","Cell Movement"],["dc.subject.mesh","Cell Proliferation"],["dc.subject.mesh","Female"],["dc.subject.mesh","In Situ Hybridization"],["dc.subject.mesh","Kidney Neoplasms"],["dc.subject.mesh","Macrophages"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Inbred BALB C"],["dc.subject.mesh","MicroRNAs"],["dc.subject.mesh","Neovascularization, Pathologic"],["dc.subject.mesh","Nitric Oxide"],["dc.subject.mesh","Nitric Oxide Synthase Type II"],["dc.subject.mesh","Protein Biosynthesis"],["dc.subject.mesh","RNA, Messenger"],["dc.subject.mesh","Reverse Transcriptase Polymerase Chain Reaction"],["dc.title","Loss of inducible nitric oxide synthase expression in the mouse renal cell carcinoma cell line RENCA is mediated by microRNA miR-146a."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]