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  • 1
    Keywords: CELLS ; EXPRESSION ; carcinoma ; ACTIVATION ; CARCINOGENESIS ; METASTASIS ; BETA ; POOR-PROGNOSIS ; TUMORIGENESIS ; EPITHELIAL-MESENCHYMAL TRANSITION
    Abstract: Epithelial-to-mesenchymal transition (EMT) contributes significantly to tumor progression and metastasis. The assessment of EMT-associated transcription factors could be a promising approach to identify biomarkers and potential therapeutic targets in colorectal cancer. In our study, we focused on the transcription factor Sine oculis homeobox (SIX) 1, which is a member of the superfamily of the homeobox genes and has been described to promote EMT in different types of tumors. Immunohistochemistry against SIX1 was performed on colorectal mucosa, adenomas, carcinomas-in situ and primary adenocarcinomas. An expression score was developed and subsequently assessed for its prognostic value in two independent cohorts. Cohort 1 consisted of 128 patients with stage I-III colorectal cancer; cohort 2 included 817 patients with stage I-III colorectal cancer who had participated in the DACHS study. HCT-116 cells were transfected with SIX1 plasmids and subjected to migration and colony formation assays. The expression of SIX1 increases gradually from mucosa to colorectal adenocarcinomas (p〉0.0001). Univariate and multivariate analyses reveal that high expression of SIX1 is associated with decreased overall survival (cohort 1: HR: 4.01, CI: 1.20-14.07, p=0.025; cohort 2: HR: 1.43, CI: 1.014-2.02, p=0.047). Overexpression of SIX1 induces a more mesenchymal-like phenotype in HCT-116 cells and enhances tumor migration. High expression of SIX1 is an independent prognostic marker in colorectal cancer. It might be a promising biomarker to stratify patients into different risk groups. Moreover, targeting SIX1 might be a novel therapeutic approach in patients with colorectal cancer. What's new? Gains in stem cell-like properties by tumor cells may be linked to the epithelial-to-mesenchymal transition (EMT), suggesting that changes in the expression of EMT-associated transcription factors are predictive of tumor progression. This study shows that progression of colorectal mucosa from normal to adenomatous to cancerous is accompanied by gradually increasing expression of sine oculis homeobox 1 (SIX1), a transcription factor known to regulate EMT-related mechanisms. In two separate colorectal patient cohorts, elevated SIX1 expression was found to be associated with decreased overall survival. The results indicate that SIX1 is of prognostic value in colorectal cancer.
    Type of Publication: Journal article published
    PubMed ID: 25951369
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  • 2
    Keywords: carcinoma ; CLASSIFICATION ; MORTALITY ; TUMORS ; TRENDS ; EUROPE ; PERIOD ANALYSIS ; ENGLAND ; WALES ; EUROCARE-4
    Abstract: Introduction: The aim of this study was to provide detailed age-specific (5-year age groups) and histology-specific (histologic subtypes of seminoma and nonseminoma) relative survival estimates of testicular germ cell cancer patients in Germany and the United States (U.S.) for the years 2002-2006 and to compare these estimates between countries. Methods: We pooled data from 11 cancer registries of Germany and used data from the U.S. (SEER-13 database) including 11,508 and 10,774 newly diagnosed cases (1997-2006) in Germany and the U.S., respectively. We estimated 5-year relative survival (5-year-RS) by histology and age based on period analysis. Results: 5-year-RS for testicular germ cell tumors was 96.7% and 96.3% in Germany and the U.S., respectively. 5-Year-RS for spermatocytic seminoma was close to 100% in both countries. 5-Year-RS for nonseminoma was lower than for classical seminoma in Germany (93.3% versus 97.6%) and the U.S. (91.0% versus 98.2%). Among nonseminomas, choriocarcinomas provided the lowest 5-year-RS in both countries (Germany 80.1%, U.S. 79.6%). Age-specific 5-year-RS for seminoma showed only little variation by age. 5-Year-RS for nonseminomas tended to be lower at higher ages, especially for malignant teratoma. Discussion: This is the first study that provides up-to-date survival estimates for testicular cancer by histology and age in Germany and the U.S. Survival after a diagnosis of testicular cancer is very comparable between Germany and the U.S. 5-Year-RS for spermatocytic seminoma was close to 100% and the lowest 5-year-RS occurred among choriocarcinoma. Higher age at diagnosis is associated with a poorer prognosis among nonseminoma patients.
    Type of Publication: Journal article published
    PubMed ID: 23623488
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  • 3
    Keywords: CANCER ; EXPRESSION ; IN-VITRO ; proliferation ; tumor ; carcinoma ; human ; IN-VIVO ; MODEL ; VITRO ; EXPOSURE ; GENE ; GENES ; PROTEIN ; PROTEINS ; TUMORS ; LINES ; MICE ; CARCINOGENESIS ; CONTRAST ; KERATINOCYTES ; SKIN ; cell cycle ; CELL-CYCLE ; CYCLE ; E7 ; papillomavirus ; SUSCEPTIBILITY ; TRANSGENIC MICE ; PROGRESSION ; PROMOTER ; LINE ; human papillomavirus ; LIFE-SPAN ; E6 ; HUMAN KERATINOCYTES ; keratin ; SQUAMOUS-CELL CARCINOMA ; CARCINOMAS ; REPLICATION ; squamous cell carcinoma ; HUMAN-PAPILLOMAVIRUS TYPE-16 ; SQUAMOUS-CELL CARCINOMAS ; epidermis ; immunosuppression ; RE ; immortalization ; keratinocyte ; CARCINOGEN ; ONCOGENESIS ; CHECKPOINT ; EPIDERMODYSPLASIA-VERRUCIFORMIS ; LIFE ; HYPERPLASIA ; LEVEL ; EVENTS ; BOVINE ; chemical carcinogenesis ; CYCLE ARREST ; DYSPLASIA
    Abstract: The oncoproteins E6 and E7 of human papillomavirus type 38 (HPV38) display several transforming activities in vitro, including immortalization of primary human keratinocytes. To evaluate the oncogenic activities of the viral proteins in an in vivo model, we generated transgenic mice expressing HPV38 E6 and E7 under the control of the bovine homologue of the human keratin 10 (K10) promoter. Two distinct lines of HPV38 E6/E7-expressing transgenic mice that express the viral genes at different levels were obtained. In both lines, HPV38 E6 and E7 induced cellular proliferation, hyperplasia, and dysplasia, in the epidermis. The rate of occurrence of these events was proportional to the levels of HPV38 E6 and E7 expression in the two transgenic lines. Exposure of the epidermis of nontransgenic mice to UV led to p21(WAF1) accumulation and cell cycle arrest. In contrast, keratinocytes from transgenic mice continued to proliferate and were not positive for p21(WAF1), indicating that cell cycle checkpoints are altered in keratinocytes expressing the viral genes. Although the HPV38 E6/E7-expressing transgenic mice did not develop spontaneous tumors during their life span, two-stage carcinogen treatment led to a high incidence of papillomas, keratoacanthomas, and squamous-cell carcinomas in HPV38 mice compared with nontransgenic animals. Together, these data show that HPV38 E6 and E7 display transforming properties in vivo, providing further support for the role of HPV38 in carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 16282489
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  • 4
    Keywords: PEPTIDE ; RECEPTOR ; CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; Germany ; human ; VITRO ; MOLECULES ; TISSUE ; ACCUMULATION ; LINES ; ACTIVATION ; LIGAND ; CONTRAST ; T-CELLS ; CELL-LINES ; DOWN-REGULATION ; MOLECULE ; TARGET ; IN-SITU ; NEOPLASIA ; PROGRESSION ; NUMBER ; cervical cancer ; cervical intraepithelial neoplasia ; CERVICAL-CANCER ; CELL-LINE ; LYMPHOCYTES ; PEPTIDES ; LIGANDS ; CLASS-I ; HUMAN-PAPILLOMAVIRUS ; NATURAL-KILLER-CELLS ; NK cells ; EPITHELIAL-CELLS ; CERVICAL-CARCINOMA ; CARCINOMAS ; PROGNOSTIC-SIGNIFICANCE ; IMMUNOTHERAPY ; intraepithelial neoplasia ; T-LYMPHOCYTES ; T lymphocyte ; BIOPSY ; T lymphocytes ; ONCOLOGY ; RE ; USA ; LOSSES ; NKG2D RECEPTOR ; viral ; NOV ; NK-CELLS ; NKG2D ligands ; DNAM-1 ligands ; I-RELATED CHAIN ; PARTICLE VACCINE ; QUADRIVALENT VACCINE
    Abstract: Human papillomavirus-induced cervical carcinomas often show impaired expression of MHC class I molecules resulting in the inability of tumor cells to directly present viral peptides to cytotoxic T lymphocytes. Loss of MHC class I expression combined with the expression of activating NK cell receptor ligands renders tumor cells potentially susceptible to NK cell attack. Thus, in this study, we analyzed the expression of activating NK cell receptor ligands, NK cell accumulation and activation status in situ in normal ectocervical tissue (NCT), cervical intraepithelial neoplasia (CIN) and squamous cervical carcinoma (CxCa). We observed that expression of the DNAM-I ligand CD155 was frequently upregulated in CxCa, but not in CIN. The NKG2D ligand MICA was upregulated in fewer CxCa biopsies. In contrast, another NKG2D ligand ULBP2 was preferentially expressed in differentiated epithelial cells of NCT. Increased numbers of NK cells were detected in CIN as compared to NCT and CxCa. Expression of activating NK cell receptor ligands combined with loss of MHC class I was not correlated with enhanced NK cell accumulation or activation status. Furthermore, we demonstrate that cervical cancer cell lines are killed by the NK cell line, NKL, in a NKG2D- and DNAM-1-dependent manner in vitro. Since a significant number of CxCa biopsies showed low MHC class I expression combined with high expression of one or more of the tested activating NK cell receptor ligands, we conclude that CxCa might be a promising target for NK cell-based adoptive immunotherapy. (C) 2008 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 18712710
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  • 5
    Keywords: carcinoma ; POPULATION ; EXPERIENCE ; QUALITY-CONTROL ; UNITED-STATES ; TRENDS ; EUROPE ; PERIOD ANALYSIS ; UP-TO-DATE ; 21ST-CENTURY
    Abstract: The purpose of the present study was to describe the survival of patients diagnosed with oral cavity cancer in Germany. The analyses relied on data from eleven population-based cancer registries in Germany covering a population of 33 million inhabitants. Patients with a diagnosis of oral cavity cancer (ICD-10: C00-06) between 1997 and 2006 are included. Period analysis for 2002-2006 was applied to estimate five-year age-standardized relative survival, taking into account patients' sex as well as grade and tumor stage. Overall five-year relative survival for oral cavity cancer patients was 54.6%. According to tumor localization, five-year survival was 86.5% for lip cancer, 48.1% for tongue cancer and 51.7% for other regions of the oral cavity. Differences in survival were identified with respect to age, sex, tumor grade and stage. The present study is the first to provide a comprehensive overview on survival of oral cavity cancer patients in Germany.
    Type of Publication: Journal article published
    PubMed ID: 23349710
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  • 6
    Keywords: PROTECTION ; carcinoma ; RISK ; ADENOMAS ; RECURRENCE ; SURVEILLANCE ; UPDATE ; SOCIETY ; POLYPECTOMY ; SERRATED POLYPS
    Abstract: Colonoscopy with detection and removal of neoplasms strongly reduces risk of colorectal cancer (CRC). Nevertheless, CRCs occur after colonoscopic polypectomy. We assessed agreement beyond chance of location of polyps detected at colonoscopy and of subsequent CRCs to estimate the share of cancers that might be due to field effects or neoplasm recrudescence. In a population-based case-control study conducted in Germany (3,148 cases), detailed history and results of colonoscopies conducted within 10 years before cancer diagnosis were obtained by interview and from medical records. We determined the observed proportion of cancers for which a polyp had been detected at the same colorectal subsite at the preceding colonoscopy and compared it to the proportion expected by chance. A total of 155 cases with physician validated polyp detection at the preceding colonoscopy were identified. Among 148 cases with cancer restricted to a single subsite, 43 (29.1%) had a polyp detected in the same colorectal subsite at the preceding colonoscopy. Agreement of location of cancer occurrence and preceding polyp detection would have been expected by chance for 27 cases, and agreement beyond chance was estimated to account for 16 cases (10.8%, 95% confidence interval 2.7%-19.3%). Our study suggests that less than one of nine CRCs occurring within 10 years after colonoscopy with polyp detection may be due to field effects or polyp recrudescence.
    Type of Publication: Journal article published
    PubMed ID: 23526227
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