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  • 1
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    Abstract 5839: Novel stroma-derived prostate cancer subtypes are associated with risk of clinical progression
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7_Supplement ( 2023-04-04), p. 5839-5839
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 5839-5839
    Abstract: The tumor microenvironment influences prostate cancer aggressiveness, and by focusing on how different changes to the microenvironment can affect the cancer, we aimed to identify novel stromal subtypes in localized prostate cancer (LPC), characterize these subtypes, and utilize subtypes to increase accuracy in prostate cancer risk stratification. Subtype identification was conducted using non-negative matrix factorization with consensus clustering on a stroma-specific expression signature in RNA sequencing data. A discovery cohort (127 LPC patients) and two independent validation cohorts (406 LPC & 126 LPC patients) were used for subtype identification. All three cohorts were subsequently used for subtype characterization and prognostic evaluation. Identified subtypes were characterized by evaluation of clinical characteristics, by gene set enrichment analysis, and by cell-type deconvolution analysis. Survival differences between subtypes were assessed using Kaplan-Meier and univariate Cox regression analyses with biochemical recurrence (BCR) as endpoint. Lastly, a high-risk stromal subtype was investigated for its ability to improve risk stratification for intermediate risk prostate cancer using hazard ratio changes from univariate Cox regression analysis. We identified three stromal subtypes (S1-S3) in prostate cancer. Of these, subtype S3 showed characteristics of a highly reactive stromal environment with significantly (adj. p & lt; 0.05) decreased cell polarity and stroma related functions, significantly (adj. p & lt; 0.05) reduced fibroblast infiltration, and a significantly (adj. p & lt; 0.05) increased immune cells infiltration compared to the other subtypes. Survival analysis also revealed significant (p & lt; 0.05) association of S3 with BCR in all three cohorts (HR = 3.2, 2.1, and 3.4 in cohorts 1, 2 and 3 respectively). Lastly, S3 significantly (p & lt; 0.05) improved the risk prediction for patients with intermediate recurrence risk according to the clinical nomogram CAPRA-S (cohort 1, delta HR = 1.4; cohort 2, delta HR = 2.3; cohort 3, delta HR = 4.2). In conclusion, by focusing on the stromal alteration in prostate cancer, this study sheds new light on the influence of tumor microenvironment on LPC aggressiveness. A stromal subtype characterized by dysregulated stromal functions and changes in stroma and immune cells infiltration predicted adverse outcome in patients with a high prognostic ambiguity. This utilization of stromal information to improve risk assessment for clinically intermediate risk PC indicates a potential use in future evaluation of PC aggressiveness. Citation Format: Martin Rasmussen, Jacob Fredsøe, Paul V. Salachan, Marcus P. Blanke, Benedicte P. Ulhøi, Michael Borre, Karina D. Sørensen. Novel stroma-derived prostate cancer subtypes are associated with risk of clinical progression. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5839.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-5839
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 2
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    GENE-33. INTEGRATED GLIOMA DIAGNOSTICS USING TARGETED NEXT-GENERATION SEQUENCING
    Oxford University Press (OUP) ; 2019
    In:  Neuro-Oncology Vol. 21, No. Supplement_6 ( 2019-11-11), p. vi104-vi104
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 21, No. Supplement_6 ( 2019-11-11), p. vi104-vi104
    Abstract: Targeted next-generation sequencing (NGS) offers promising diagnostic perspectives by making it possible to detect genetic alterations with high accuracy in multiple genes as part of the daily diagnostic work-up. The importance of genetic alterations is reflected in the 2016 WHO classification of CNS tumors, where specific alterations are incorporated in the definition of certain entities. The aim of this study was to assess the diagnostic potential of a customized targeted glioma-tailored 20-gene panel to identify molecular entities of gliomas and explore their distinct mutational profiles. Moreover, the prognostic impact of molecular diagnostics was explored. METHODS We used a setup with NGS, immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) on a series of 756 glioma from both a retro- and prospective cohort. NGS data were obtained for 347 gliomas (225 analyzed prospectively, 122 analyzed retrospectively). RESULTS Three major clusters were identified by unsupervised hierarchial cluster analysis: 1) isocitrate dehydrogenase gene (IDH) 1 or 2 mutant astrocytomas with frequent mutations in TP53 (83%) and ATRX (69%), 2) IDH-mutant and 1p/19q-codeleted oligodendrogliomas with frequent mutations in TERT (65%) and CIC (52%), and 3) IDH-wildtype astrocytic gliomas/glioblastomas with frequent mutations in TERT (32%), PTEN (28%) and TP53 (22%). Among the IHC IDH1-R132H negative gliomas, NGS detected other IDH mutations in 16% of the cases. Moreover, rare but diagnostically important mutations such as BRAF V600E and H3F3A K27M were detected. Survival analysis of the reclassified gliomas showed a clear difference in survival between patients with WHO 2007 and 2016 diagnoses. Successful prospective NGS analyses were obtained for 98% of the gliomas in daily diagnostics. CONCLUSION Application of NGS panel sequencing improves diagnostic accuracy and is feasible in daily diagnostics. NGS is ready to become part of standard diagnostics in the field of gliomas.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noz175.435
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
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  • 3
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    Delayed leukoencephalopathy from suspected polymer embolism after neuroendovascular procedures
    SAGE Publications ; 2021
    In:  The Neuroradiology Journal Vol. 34, No. 4 ( 2021-08), p. 373-378
    Details
    In: The Neuroradiology Journal, SAGE Publications, Vol. 34, No. 4 ( 2021-08), p. 373-378
    Abstract: As the neurointervention field grows, a new side effect emerges. Delayed leukoencephalopathy (DL) is believed to be an inflammatory or allergic reaction to polymer material that is shed from catheters during endovascular procedures. We present four cases of DL after aneurysm treatment in two patients, endovascular stroke treatment and diagnostic arteriography. We present our diagnostic process, including biopsy results in two patients, our anti-inflammatory treatment and outcomes together with a review of the literature. In our series, prognosis was variable with ongoing seizures in two patients. Our literature review reveals that asymptomatic shedding of polymer material is common, occurring in a third of endovascular stroke procedures, whereas symptomatic DL occurs in 〈 0.5% of therapeutic neuroendovascular procedures. Clinicians should be aware of this rare complication, and oral glucocorticoids seem to be a reasonable first-line treatment strategy.
    Type of Medium: Online Resource
    ISSN: 1971-4009 , 2385-1996
    URL: Article
    DOI: 10.1177/19714009211029172
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2021
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  • 4
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    Abstract 4182: Tissue microarray validation of Cathepsin E, Maspin, PLK-1, Survivin and TRIM29 expression as prognostic protein markers for stage pTa and pT1 urothelial carcinoma
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4182-4182
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4182-4182
    Abstract: The majority of patients with bladder cancer are initially diagnosed with noninvasive or superficially invasive urothelial tumors. These tumors form a heterogeneous group, spanning from benign low grade Ta tumors that rarely progress to high grade T1 tumors with concomitant CIS that progress in up to 60% of cases. No biomarkers have yet been accepted in clinical routine for predicting the individual disease courses of these patients. Previously, we have identified gene expression signatures for prediction disease outcome for patients with non-muscle invasive bladder cancer. The aim of the present study was to validate key candidate markers from these signatures on the protein level. Five proteins were selected for investigation: Cathepsin E, Maspin, PLK-1, Survivin and TRIM29. A total of 289 primary non-muscle invasive urothelial carcinomas (182 pTa, 101 pT1 and 6 CIS lesions) were chosen for tissue microarray (TMA) construction and protein expression was measured by immunohistochemistry (IHC). High resolution scans of the IHC stainings were scored dichotomized. The results were further validated using TMAs from Germany and Spain holding a total of 609 tumors from patients with stage pT1 bladder cancer. We found significant correlations to progression to muscle invasive bladder cancer for Survivin (p & lt;0.001), Maspin (p & lt;0.001), PLK-1 (p & lt;0.001) and Cathepsin E expression (p & lt;0.001). TRIM29 expression was significantly associated with overall survival (p & lt;0.04) but not with disease progression (p=0.16). Furthermore, multivariate Cox regression analysis showed that Cathepsin E (p=0.004), PLK-1 (p=0.021) and Survivin expression (p=0.001) were independent prognostic markers for progression to muscle invasive bladder cancer. We successfully validated Maspin as a prognostic marker for overall survival (p=0.045) in the Spanish patient cohort and PLK-1 as a marker for progression to muscle invasive disease (P=0.030) and overall survival (P=0.008) in the German patient cohort. In addition, both Maspin (p=0.022) and PLK-1 (p=0.002) were significantly associated with overall survival in multivariate Cox regression analysis when stratifying for other known risk factors for disease progression in these patient cohorts. We conclude that Survivin, Maspin, PLK-1 and Cathepsin E have been successfully validated as strong prognostic markers for progression to muscle invasive bladder cancer. In addition, Maspin and PLK-1 expression was significantly associated with outcome in large German and Spanish patient cohorts. All four proteins may be clinically relevant markers for guiding optimal treatment of patients with non-muscle invasive urothelial carcinoma. Additional future prospective studies are needed for further validation of the clinical relevance of the marker panel. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4182. doi:10.1158/1538-7445.AM2011-4182
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-4182
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 5
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    Abstract 4642: Risk stratification of bladder cancer patients using a panel of 5 prognostic protein markers
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 4642-4642
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 4642-4642
    Abstract: The majority of patients with bladder cancer are initially diagnosed with noninvasive or superficially invasive urothelial tumors. These tumors form a heterogeneous group, spanning from benign low grade Ta tumors that rarely progress to high grade T1 tumors with concomitant CIS that progress in up to 60% of cases. No biomarkers have yet been accepted in clinical routine for predicting the individual disease courses of these patients. Previously, we have identified gene expression signatures for prediction disease outcome for patients with non-muscle invasive bladder cancer. The aim of the present study was to validate key candidate markers from these signatures on the protein level. Five genes were selected for investigation: CTSE, BIRC5, TRIM29, PLK1 and SERPINB5. A total of 289 primary non-muscle invasive urothelial tumors (182 pTa, 101 pT1 and 6 CIS) were chosen for tissue microarray construction. 118 patients showed later disease progression to pT2-4 bladder cancer with a median time to progression of 22 months. None of the remaining 171 patients showed later disease progression within the follow-up period with a median follow-up of 93 months. Protein expression was investigated using immunohistochemistry. We found that high expression of BIRC5 and PLK1 identified patients with an increased risk of progression; (HR=2.47 (1.57-3.87), P & lt;0.001 and HR=1.52 (1.00-2.29), P=0.048 respectively). Whereas high expression of CTSE, SERPINB5 and TRIM29 identified patients with a reduced risk of progression; (HR=0.60 (0.39-0.93), P=0.02), (HR=0.58 (0.38-0.89), P=0.01) and (HR=0.38 (0.20-0.73), P=0.003 respectively). We found all five proteins to be independent prognostic variables for predicting disease progression to muscle invasive bladder cancer when stratifying for other known clinical and histopathological risk factors. Consequently, we successfully transferred key markers from the gene expression signatures to the protein level. This marker panel is currently being validated in a new series of pT1 bladder tumors and the results from this independent validation set will also be presented at the meeting. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4642.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-4642
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 6
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    Genomic Profiling of MicroRNAs in Bladder Cancer: miR-129 Is Associated with Poor Outcome and Promotes Cell Death In vitro
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Research Vol. 69, No. 11 ( 2009-06-01), p. 4851-4860
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 69, No. 11 ( 2009-06-01), p. 4851-4860
    Abstract: microRNAs (miRNA) are involved in cancer development and progression, acting as tumor suppressors or oncogenes. Here, we profiled the expression of 290 unique human miRNAs in 11 normal and 106 bladder tumor samples using spotted locked nucleic acid–based oligonucleotide microarrays. We identified several differentially expressed miRNAs between normal urothelium and cancer and between the different disease stages. miR-145 was found to be the most down-regulated in cancer compared with normal, and miR-21 was the most up-regulated in cancer. Furthermore, we identified miRNAs that significantly correlated to the presence of concomitant carcinoma in situ. We identified several miRNAs with prognostic potential for predicting disease progression (e.g., miR-129, miR-133b, and miR-518c*). We localized the expression of miR-145, miR-21, and miR-129 to urothelium by in situ hybridization. We then focused on miR-129 that exerted significant growth inhibition and induced cell death upon transfection with a miR-129 precursor in bladder carcinoma cell lines T24 and SW780 cells. Microarray analysis of T24 cells after transfection showed significant miR-129 target down-regulation (P = 0.0002) and pathway analysis indicated that targets were involved in cell death processes. By analyzing gene expression data from clinical tumor samples, we identified significant expression changes of target mRNA molecules related to the miRNA expression. Using luciferase assays, we documented a direct link between miR-129 and the two putative targets GALNT1 and SOX4. The findings reported here indicate that several miRNAs are differentially regulated in bladder cancer and may form a basis for clinical development of new biomarkers for bladder cancer. [Cancer Res 2009;69(11):4851–60]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-08-4043
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
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  • 7
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    Abstract 1354: Expression of macrophage scavenger receptor (CD163) by tumor-infiltrating macrophages and malignant cells in bladder cancer: association with disease severity and poor patient survival
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1354-1354
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1354-1354
    Abstract: Introduction: Infiltrating cells of the tumor microenvironment are important for the growth and spreading of cancer. CD163 is a macrophage-specific hemoglobin scavenger receptor. It is predominantly expressed by alternatively activated macrophages (M2), which is a cell subtype thought to have important tumor-supporting functions. We hypothesized that CD163 mRNA and protein expression may be significant markers of disease severity in bladder cancer. Furthermore, recent findings have indicated that malignant cells express molecular pathways normally only expressed in macrophages, which led us to investigate the possible tumor cell CD163 expression. Materials and Methods: CD163, IL-6, and IL-10 mRNA expression levels were measured using quantitative real-time polymerase chain reaction (RT-qPCR) in bladder cancer biopsy samples obtained from 87 patients followed for a median of 5.1 years (range, 0.07 to 12.9 years). The subcellular distribution of CD163-positive cells was investigated by immunohistochemistry in a subset of 46 bladder cancer biopsy samples. After co-culturing human monocyte-derived macrophages with T24 bladder cancer cells for 48 hours, the expression of the macrophage scavenger receptor CD163 was examined using flow cytometry. Results: CD163 mRNA was expressed in all 87 biopsies, and its expression was strongly correlated with overall (p=0.0028) and relapse-free survival (p=0.0003). Moreover, it was significantly increased in invasive (T2-T4) (p=0.017) and aggressive (grade III/IV) cancers (p=0.015). The expression strongly correlated with local expression of IL-6 (r=0.72, p & lt;0.0001) and IL-10 (r=0.75, p & lt;0.0001), mediators known to induce CD163 expression in vitro. An association between the density of CD163 immunohistochemical positive infiltrating cells and histologically advanced bladder cancer, confirmed the mRNA expression findings. Surprisingly, a large fraction of biopsies (39%) showed definite expression of CD163 by the tumor cells, which indicated the possibility of horizontal mRNA transfer or heterotypic cell fusion. RT-qPCR and flow cytometric analysis showed that human bladder cancer cell lines did not express CD163; however, co-culturing bladder cancer cells with macrophages induced significant tumor cell CD163-expression. Conclusion: In conclusion, we show a strong association between CD163 mRNA expression in bladder cancer biopsies and the severity of the disease, on the one hand, and poor survival on the other hand. CD163 expression was not confined to the infiltrating macrophages. It was also observed in a significant portion of the tumor cells. Our findings identify CD163 as a possible target for novel cancer therapy and underline the importance of the cellular interaction between tumor cells and immune cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1354.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-1354
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 8
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    Cathepsin E, Maspin, Plk1, and Survivin Are Promising Prognostic Protein Markers for Progression in Non-Muscle Invasive Bladder Cancer
    Elsevier BV ; 2012
    In:  The American Journal of Pathology Vol. 180, No. 5 ( 2012-05), p. 1824-1834
    Details
    In: The American Journal of Pathology, Elsevier BV, Vol. 180, No. 5 ( 2012-05), p. 1824-1834
    Type of Medium: Online Resource
    ISSN: 0002-9440
    URL: Article
    DOI: 10.1016/j.ajpath.2012.01.023
    RVK:
    XA 10000
    RVK:
    XA 19800
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2012
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  • 9
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    TLR3 deficiency renders astrocytes permissive to herpes simplex virus infection and facilitates establishment of CNS infection in mice
    American Society for Clinical Investigation ; 2012
    In:  Journal of Clinical Investigation Vol. 122, No. 4 ( 2012-4-2), p. 1368-1376
    Details
    In: Journal of Clinical Investigation, American Society for Clinical Investigation, Vol. 122, No. 4 ( 2012-4-2), p. 1368-1376
    Type of Medium: Online Resource
    ISSN: 0021-9738
    URL: Article
    URL: Article
    DOI: 10.1172/JCI60893
    DOI: 10.1172/JCI60893DS1
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 2012
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  • 10
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    The HTN3-MSANTD3 Fusion Gene Defines a Subset of Acinic Cell Carcinoma of the Salivary Gland
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  American Journal of Surgical Pathology Vol. 43, No. 4 ( 2019-04), p. 489-496
    Details
    In: American Journal of Surgical Pathology, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. 4 ( 2019-04), p. 489-496
    Abstract: The spectrum of tumors arising in the salivary glands is wide and has recently been shown to harbor a network of tumor-specific fusion genes. Acinic cell carcinoma (AciCC) is one of the more frequently encountered types of salivary gland carcinoma, but it has remained a genetic orphan until recently when a fusion between the HTN3 and MSANTD3 genes was described in one case. Neither of these 2 genes is known to be implicated in any other malignancy. This study was undertaken to investigate whether the HTN3 - MSANTD3 fusion is a recurrent genetic event in AciCC and whether it is a characteristic of one of its histological variants. Of the 273 AciCCs screened, 9 cases showed rearrangement of MSANTD3 by break-apart fluorescence in situ hybridization, 2 had 1 to 2 extra signals, and 1 had gain, giving a total of 4.4% with MSANTD3 aberrations. In 6 of 7 available cases with MSANTD3 rearrangement, the HTN3 - MSANTD3 fusion transcript was demonstrated with real-time polymerase chain reaction. Histologically, all fusion-positive cases were predominantly composed of serous tumor cells growing in solid sheets, with serous tumor cells expressing DOG-1 and the intercalated duct-like cell component being CK7 positive and S-100 positive in 6/9 cases. All but one case arose in the parotid gland, and none of the patients experienced a recurrence during follow-up. In contrast, the case with MSANTD3 gain metastasized to the cervical lymph nodes and lungs. In conclusion, we find the HTN3 - MSANTD3 gene fusion to be a recurrent event in AciCC with prominent serous differentiation and an indolent clinical course.
    Type of Medium: Online Resource
    ISSN: 0147-5185
    URL: Article
    DOI: 10.1097/PAS.0000000000001200
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
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