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  • 1
    Abstract: BACKGROUND: The anti-programmed cell death-1 (PD-1) inhibitors pembrolizumab and nivolumab alone or in combination with ipilimumab have shown improved objective response rates and progression-free survival compared to ipilimumab only in advanced melanoma patients. Anti-PD-1 therapy demonstrated nearly equal clinical efficacy in patients who had progressed after ipilimumab or were treatment-naive. However, only limited evidence exists regarding the efficacy of ipilimumab alone or in combination with nivolumab after treatment failure to anti-PD-therapy. PATIENTS AND METHODS: A multicenter retrospective study in advanced melanoma patients who were treated with nivolumab (1 or 3 mg/kg) and ipilimumab (1 mg or 3 mg/kg) or ipilimumab (3 mg/kg) alone after treatment failure to anti-PD-1 therapy was performed. Patient, tumour, pre- and post-treatment characteristics were analysed. RESULTS: In total, 47 patients were treated with ipilimumab (ipi-group) and 37 patients with ipilimumab and nivolumab (combination-group) after treatment failure to anti-PD-1 therapy. Overall response rates for the ipi- and the combination-group were 16% and 21%, respectively. Disease control rate was 42% for the ipi-group and 33% for the combination-group. One-year overall survival rates for the ipi- and the combination-group were 54% and 55%, respectively. CONCLUSIONS: Ipilimumab should be considered as a viable treatment option for patients with failure to prior anti-PD-1 therapy, including those with progressive disease as best response to prior anti-PD-1. In contrast, the combination of ipilimumab and nivolumab appears significantly less effective in this setting compared to treatment-naive patients.
    Type of Publication: Journal article published
    PubMed ID: 28214657
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  • 2
    Abstract: AIM OF THE STUDY: A vast majority of human malignancies are associated with ageing, and age is a strong predictor of cancer risk. Recently, DNA methylation-based marker of ageing, known as 'epigenetic clock', has been linked with cancer risk factors. This study aimed to evaluate whether the epigenetic clock is associated with breast cancer risk susceptibility and to identify potential epigenetics-based biomarkers for risk stratification. METHODS: Here, we profiled DNA methylation changes in a nested case-control study embedded in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort (n = 960) using the Illumina HumanMethylation 450K BeadChip arrays and used the Horvath age estimation method to calculate epigenetic age for these samples. Intrinsic epigenetic age acceleration (IEAA) was estimated as the residuals by regressing epigenetic age on chronological age. RESULTS: We observed an association between IEAA and breast cancer risk (OR, 1.04; 95% CI, 1.007-1.076, P = 0.016). One unit increase in IEAA was associated with a 4% increased odds of developing breast cancer (OR, 1.04; 95% CI, 1.007-1.076). Stratified analysis based on menopausal status revealed that IEAA was associated with development of postmenopausal breast cancers (OR, 1.07; 95% CI, 1.020-1.11, P = 0.003). In addition, methylome-wide analyses revealed that a higher mean DNA methylation at cytosine-phosphate-guanine (CpG) islands was associated with increased risk of breast cancer development (OR per 1 SD = 1.20; 95 %CI: 1.03-1.40, P = 0.02) whereas mean methylation levels at non-island CpGs were indistinguishable between cancer cases and controls. CONCLUSION: Epigenetic age acceleration and CpG island methylation have a weak, but statistically significant, association with breast cancer susceptibility.
    Type of Publication: Journal article published
    PubMed ID: 28259012
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  • 3
    Abstract: BACKGROUND: The predictive value of microRNAs (miRNAs) in tumour cells and infiltrating immune cells for the efficacy of chemoradiation (CRTX) in locally advanced head and neck squamous cell carcinoma (HNSCC) was evaluated. METHODS: Formalin-fixed, paraffin-embedded tumour material was collected from patients with locally advanced HNSCC treated within the ARO-0401 phase III trial with radiotherapy in combination with either 5-fluorouracil/cisplatin (CDDP-CRTX) or 5-fluorouracil/mitomycin C (MMC-CRTX). MiRNA and immune profiles were established in a test cohort of 48 oropharyngeal carcinoma (OPSCC) cases by Affymetrix miRNA microarrays and the nanoString PanCancer Immune Panel, respectively. Expression of miRNA candidates was measured in 149 HNSCC patients by real-time PCR. Interference of miRNA profiles with CRTX efficacy was determined by Kaplan-Meier and Cox regression analysis. RESULTS: Expression levels of five miRNAs (miR-27b, -130b, -200b, -451 and -532-5p) were significantly associated with overall survival after MMC-CRTX. Six different miRNAs (miR-125b, -146a, -150, -155, -187 and -342-5p) were correlated with overall survival after CDDP-CRTX. Validation by real-time PCR confirmed the predictive value of miR-200b and miR-155 in OPSCC, which was absent in hypopharyngeal carcinomas. MiR-146a was revealed as a prognostic marker for both CRTX regimens. MiR-200b expression was mainly associated with distant metastasis, whereas miR-155 correlated with local recurrence. MiR-155 and miR-146a were identified as surrogate markers for tumour-infiltrating lymphocytes. CONCLUSIONS: MiR-200b and miR-155 were established as potential markers for personalised treatment selection of two standard regimens of CRTX. The predictive role of miR-155 deserves further investigation, especially within the framework of clinical trials of CRTX/immune checkpoint inhibitor combinations.
    Type of Publication: Journal article published
    PubMed ID: 28347920
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  • 4
    Keywords: CANCER ; neoplasms ; THERAPY ; DISEASE ; incidence ; RISK ; RISKS ; SITE ; SITES ; PATIENT ; primary ; SKIN ; LYMPHOMA ; MALIGNANCIES ; skin cancer ; MELANOMA ; SWEDEN ; DATABASE ; SQUAMOUS-CELL CARCINOMA ; SIR ; PRIMARY CANCERS ; FAMILY-CANCER DATABASE ; 2ND PRIMARY NEOPLASMS ; CANCER-THERAPY ; immunological factors ; immunosuppression ; LONG-TERM SURVIVORS ; MULTIPLE PRIMARY CANCERS ; non-hodgkin's lymphoma ; second cancer ; therapeutic effects
    Abstract: Successes in cancer therapy have led to increasing numbers of cancer survivors, who are at risk of developing second primary cancers. Therapy- or disease-induced suppression of the immune function may predispose cancer patients to a second malignancy. An excess of squamous cell skin cancers (SCC) and non-Hodgkin's lymphomas has been found in immunosuppressed patients. We used the nationwide Swedish Family-Cancer Database on 10.2 million individuals to calculate the risk of second primary skin cancers and non-Hodgkin's lymphomas following a previous malignancy. A total of 4301 second skin cancers and 1672 non- Hodgkin's lymphomas were identified. Standardised incidence ratios (SIR)s and 95% Confidence Intervals (CIs) were calculated and compared. Among 14 different sites for male or female first primary malignancies, 11 of these sites were followed by an increased risk of skin cancer (SIRs for males for risk of skin cancer as a second primary cancer: 14.1 for SCC; 9.7 for melanoma; 6.1 for leukaemia as the first site; SIRs for females for risk of skin cancer: 14.6 for SCC; 6.8 for larynx; 6.2 for upper aerodigestive tract (UADT) as the first site). The risk of non-Hodgkin's lymphoma was increased after 10 of 14 different male neoplasms and 12 of 17 different female neoplasms. (SIRs for males for risk of non-Hodgkin's lymphoma as a second primary cancer: 6.4 for non-Hodgkin's lymphoma; 3.2 for leukaemias; 3.1 for multiple myeloma as the first site; SIRs for females for risk of non-Hodgkin's lymphoma as a second primary cancer: 12.5 for leukaemias; 7.0 for Hodgkin's disease; 3.6 for UADT as the first site). The high, and after certain sites, very high risks of second skin cancer and non-Hodgkin's lymphoma suggest that immune suppression may be a contributory mechanism. (C) 2002 Elsevier Science Ltd. All rights reserved
    Type of Publication: Journal article published
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  • 5
    Keywords: CANCER ; MODEL ; FOLLOW-UP ; cohort studies ; MORTALITY ; RISK ; TUMORS ; tumour ; BREAST ; breast cancer ; BREAST-CANCER ; ovarian cancer ; OVARIAN-CANCER ; WOMEN ; smoking ; TOBACCO ; ALCOHOL ; HISTOLOGIC TYPE ; COFFEE ; menopause ; NORWEGIAN MEN ; ovarian neoplasms
    Abstract: Few cohort studies have examined the association between cigarette smoking and ovarian cancer risk, either overall, or by histological subtype. In relation to the latter, it has been suggested that mucinous ovarian tumours may be aetiologically unrelated to the other types of epithelial tumours and that their respective associations with cigarette smoking may differ. We examined the association between smoking and ovarian cancer risk using data from participants in a randomised controlled trial of screening for breast cancer involving 89,835 women aged 40-59 years at recruitment. Cox proportional hazards models were used to estimate rate ratios (RR) and 95% confidence intervals (CI). During an average of 16.5 years of follow-up, we observed 454 incident cases of ovarian cancer (184 serous, 67 endometrioid, 32 mucinous, 171 other or unknown). We found that women who had smoked for several decades had an approximately two-fold increased risk of epithelial ovarian cancer. Relative to never-smokers, women who had smoked for 40 years or more were at the highest risk (RR = 2.50, 95% CI = 1.37-4.56). The association with non-mucinous tumours was similar to that observed overall. For mucinous tumours, a two-fold increased risk was observed with smoking of shorter duration, although the number of mucinous turnours in our data-set was small. Long-term cigarette smoking may be associated with an increased risk of epithelial ovarian turnours. (C) 2003 Elsevier Science Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 12736118
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  • 6
    Keywords: brain ; CANCER ; Germany ; neoplasms ; PROSTATE ; COHORT ; DISEASE ; EPIDEMIOLOGY ; incidence ; RISKS ; SITE ; SITES ; meningioma ; PATIENT ; FAMILY ; primary ; renal ; tumour ; MEMBER ; MEMBERS ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; AGE ; etiology ; CERVICAL-CANCER ; prostate cancer ; PROSTATE-CANCER ; MELANOMA ; SWEDEN ; DATABASE ; SIR ; familial risk ; NATIONWIDE ; FAMILY-CANCER DATABASE ; CLUES ; CLUSTER ; clustering ; FEATURES ; ONCOLOGY ; ADULTS ; RE ; FAMILIES ; GLIOMA ; TESTICULAR CANCER ; HIPPEL-LINDAU-DISEASE ; astrocytoma ; brain tumour ; ependymoma ; FAMILY-MEMBER ; medulloblastoma ; primary neoplasm ; renal cancer ; SCIENCE
    Abstract: We used the nationwide Swedish Family-Cancer Database to analyse the association of histology-specific brain tumours with other cancers in family members. Among 0-68-year-old offspring, 9414 patients with brain tumours were identified from 1961 to 2000, of whom, 3387 parents were diagnosed with any primary neoplasm. Astrocytoma, meningioma and neurinoma were the main histological types. Increased standardised incidence ratios (SIRs) were found for brain tumours in association with cancers at sites that are known features in recognised syndromes, such as haemangioblastoma and renal cancer in von Hippel-Lindau disease. In addition, an association between astrocytoma and melanoma was recognised. Among as yet unknown clustering, neurinoma was associated with testicular cancer and myeloma; meningioma was associated with cervical cancer; astrocytoma was associated with prostate cancer; ependymoma was associated with breast cancer. Although some of these may feature a true tumour cluster, they need to be confirmed in another setting. (C) 2003 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 14728940
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  • 7
    Keywords: CANCER ; CELLS ; Germany ; SYSTEM ; DISEASES ; HISTORY ; RISK ; ASSOCIATION ; LYMPHOMA ; MALIGNANCIES ; NUMBER ; AGE ; CHILDREN ; non-hodgkin's lymphoma ; Hodgkin's lymphoma ; FOLLICULAR LYMPHOMA ; NON-HODGKINS-LYMPHOMA ; multiple myeloma ; MALIGNANCY ; ADULT ; ADULTS ; case-control study ; CHILDHOOD ; HYGIENE HYPOTHESIS ; SAN-FRANCISCO ; RE ; RHEUMATOID-ARTHRITIS ; allergy ; B-CLL ; case control studies ; diffuse large B-cell lymphoma ; ACUTE-LEUKEMIA ; B-NHL ; LYMPHOMAS ; MALT lymphoma ; T-NHL ; urticaria
    Abstract: Since lymphomas are malignancies of cells of the immune system, associations with disorders characterised by impaired immune functions can be assumed. We investigated the relationship between a history of selected medical conditions and the risk for lymphoma including specified subentities within our population-based case-control study of lymphoma among adults conducted in Germany between 1999 and 2002. Overall, we found decreased risks for a history of repeated diarrhoea, warts, arthrosis, allergies, and appendectomy (at a younger age). Elevated risks for lymphoma correlated with tonsillectomy (at a younger age), whereas null results were found for selected auto-immune disorders in adulthood. Although the numbers are small, most of the results for the subentities corresponded with these findings. These results are compatible with the notion that persistent immunological alterations contribute to the aetiology of lymphoma, but partially inconsistent with the Th1/Th2-shift paradigm. (C) 2004 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15617998
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  • 8
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    European Journal of Cancer 41 (13), 1941-1954 
    Keywords: CANCER ; IN-VITRO ; AGENTS ; COMBINATION ; Germany ; IN-VIVO ; INHIBITION ; VITRO ; SYSTEM ; SYSTEMS ; EPIDEMIOLOGY ; METABOLISM ; COMPLEX ; COMPLEXES ; CARCINOGENESIS ; DNA ADDUCT FORMATION ; WATER ; ALPHA ; ACID ; PROGRESSION ; YEAST ; EFFICACY ; DERIVATIVES ; MASS-SPECTROMETRY ; HUMAN LIVER-MICROSOMES ; LIQUID-CHROMATOGRAPHY ; CONSTITUENTS ; ALCOHOL-CONSUMPTION ; antioxidants ; INITIATION ; cancer chemoprevention ; AGENT ; review ; chalcones ; FLAVONOIDS ; PHASE ; PROFILES ; bioavailability ; BITTER ACIDS ; HOP ; xanthohumol ; PRENYLFLAVONOIDS ; BEER ; 8-prenyinaringenin ; BIOLOGICAL-ACTIVITY ; chalcone ; CHEMOPREVENTIVE ACTIVITY ; hop (Humulus lupulus L.) ; HOPS HUMULUS-LUPULUS ; humulone ; iso-alpha-acids ; isoxanthohumol ; malt ; PHYTOESTROGENS NARINGENIN ; PRENYLATED FLAVONOIDS ; PROMOTION
    Abstract: Beer is a complex alcoholic beverage made from barley (malt), hop, water and yeast. Phenolic constituents of beer are derived from malt (70-80%) and hop (20-30%). Structural classes include simple phenols, benzoic- and cinnamic acid derivatives, coumarins, catechins, di-, tri- and oligomeric proanthocyanidins, (prenylated) chalcones and flavonoids as well as alpha- and iso-alphaacids derived from hop. Compounds belonging to different structural classes have distinct profiles of biological activity in in vitro test systems, and in combination might lead to enhanced effects. Scientific evidence has accumulated over the past 10 years pointing to the cancer preventive potential of selected hop-derived beer constituents, i.e., prenylflavonoids including xanthohumol and isoxanthohumol, and hop bitter acids. Chemopreventive activities observed with these compounds relevant to inhibition of carcinogenesis at the initiation, promotion and progression phases, as well as results from in vivo studies on metabolism, bioavailability and efficacy are summarised in this review. (c) 2005 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15953717
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  • 9
    Keywords: CANCER ; Germany ; DISEASE ; POPULATION ; RISK ; GENOME ; PATIENT ; ASSOCIATION ; FREQUENCY ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; BRCA1 ; WOMEN ; MUTATION ; REPAIR ; cancer risk ; MUTATIONS ; DNA-DAMAGE ; case-control studies ; RISK ASSESSMENT ; PREVALENCE ; BRCA1/2 ; EUROPE ; ONCOLOGY ; case control study ; case-control study ; ASSOCIATIONS ; RE ; ALLELE ; case control studies ; NEED ; EUROPEAN POPULATIONS ; breast cancer patients selected for family history and age ; CHEK2 GENE ; CHEK2*1100delC variant ; population-based study
    Abstract: CHEK2*1100delC is associated with a twofold increased breast cancer risk. This was shown in a collaborative analysis of European populations, but not in other populations from Europe and the US. Accordingly, there is a need to clarify the role of CHEK2*1100delC in breast cancer. We established its prevalence in two German populations GENICA (Northrhine-Westphalia, it = 724) and KORA (Bavaria, n = 600) and in women with breast cancer. The latter included cases (n = 688) from the GENICA breast cancer case-control study, patients with early-onset breast cancer (n = 86) and patients with familial breast cancer (n = 71). The latter patient groups were previously investigated for BRCA1/2-mutations and tested negative. Mutation analysis was performed by combined PCR/DHPLC methodology. CHEK2*1100delC was found in 0.9% of GENICA controls and was absent in the KORA controls indicating a significant difference between the two populations (P = 0.03). The frequency of CHEK2*1100delC in age-matched cases of the GENICA collection was 0.8% and thus not different from controls (OR 0.88, 95% CI 0.21-3.50). In patients with early-onset disease CHEK2*1100delC was found at a frequency of 2.3% referring to an increased breast cancer risk of 2.56 (95% Cl 0.25-14.58). In patients with familial disease the frequency was 1.4% referring to an increased risk of 1.53 (95% CI 0.03-12.93). Our data showed variations in CHEK2*1100delC prevalence within German populations suggesting possible inaccuracies in breast cancer risk assessments from non population-based studies. In patients with a high-risk profile however, CHEK2*1100delC was indicative for this risk and highest for early-onset breast cancer. (c) 2005 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16239104
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  • 10
    Keywords: CANCER ; CELL ; DISEASE ; DISEASES ; incidence ; liver ; RISK ; RISKS ; GENE ; kidney ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; AGE ; MELANOMA ; SWEDEN ; DATABASE ; MUTATIONS ; familial risk ; CHILDREN ; FAMILY-CANCER DATABASE ; CHONDROSARCOMA ; CHILDHOOD ; ASSOCIATIONS ; AGGREGATION ; LI-FRAUMENI-SYNDROME ; Ewing's sarcoma ; osteosarcoma ; familial aggregation ; BONE ; CANCERS ; PROBAND ; familial disease ; KIDNEY CANCER ; HISTOLOGICAL TYPE ; bone cancer ; EARLY-ONSET ; EWINGS-SARCOMA ; giant cell sarcoma ; NEUROECTODERMAL TUMORS ; soft-tissue sarcoma
    Abstract: We used the nation-wide Swedish Family-Cancer Database to examine the familial risks of histology-specific bone cancers in offspring by parental or sibling probands. Adjusted standardised incidence ratios (SIRS) were used to measure the risk. Among the 1327 offspring bone cancers, only two parent-offspring pairs and one sibling pair were noted with concordant bone cancer but the SIRS were not significant. Significant associations were observed in specific histological types or specific age groups, some of which may be chance findings arising from multiple comparisons. However, the risk of early-onset (〈 25 years) osteosarcoma in offspring was significantly increased when mothers presented with breast cancer (1.7) and melanoma (2.9), suggesting that Li-Fraumeni syndrome could partly explain this familial aggregation. Other associations, such as childhood osteosarcoma with parental liver cancer, Ewing's sarcoma with kidney cancer and giant cell sarcoma with maternal breast cancer, were novel findings and may be related to other familial diseases. (c) 2006 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16859907
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