European journal of cancer (Oxford, England: 1990) Impact Factor & Information

Publisher: Elsevier

Journal description

Current impact factor: 4.82

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 4.819
2012 Impact Factor 5.061
2011 Impact Factor 5.536
2010 Impact Factor 4.944
2009 Impact Factor 4.121
2008 Impact Factor 4.475
2007 Impact Factor 4.454
2006 Impact Factor 4.167
2005 Impact Factor 3.706
2004 Impact Factor 3.302
2003 Impact Factor 3.694
2002 Impact Factor 3.562
2001 Impact Factor 3.46
2000 Impact Factor 2.725
1999 Impact Factor 2.537
1998 Impact Factor 2.743
1997 Impact Factor 2.407
1996 Impact Factor 2.017
1995 Impact Factor 2.095
1994 Impact Factor 0.789
1993 Impact Factor 1.959
1992 Impact Factor 2.191

Impact factor over time

Impact factor
Year

Additional details

5-year impact 0.00
Cited half-life 6.70
Immediacy index 1.44
Eigenfactor 0.05
Article influence 1.36
ISSN 1879-0852

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
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    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, arXiv.org or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Currently about 160 population-based cancer registries (CRs) in Europe have extensive experience in generating valid information on variation in cancer risk and survival with time and place. Most CRs cover all cancers, but some are confined to specific cancers or to children. They cover 15-55% of the populations in all of the larger member states of the European Union (EU), except the United Kingdom (UK), and 100% coverage in 80% of those with populations below 20million. The EU FP 7 EUROCOURSE project, which operated in 2009-2013, explored the essential role of CRs in cancer research and public health, and also focused attention on their programme owners (POs) and stakeholders (e.g. cancer societies, oncological professionals, cancer patient groups, and planners, providers and evaluators of cancer care and mass screening). Generally, all CRs depended on their regional and/or national oncological context and were increasingly involved in population-based studies of quality of cancer care, long-term prognosis and quality of life, one third being very active. Within the public health domain, CRs, in addition to describing the variety of environmental and lifestyle-related cancer epidemics, have also contributed actively to aetiologic research by a European databases that showed wide discrepancies in cancer risk and survival across the EU, and in more depth by follow-up of cohorts and recruitment for case-control studies. CRs were also actively contributing to independent evaluation of mass screening as an intervention which affects quality of care and cancer mortality. The potential of CRs for clinical evaluation has grown substantially through interaction with clinical stakeholders and more incidentally biobanks, also with greater involvement of patient groups - with a special focus on elderly patients who generally do not take part in clinical trials. Whereas 25-35% of CRs are active in a range of cancer research areas, the rest have a low profile and usually provide only incidence and survival data. If they are unable to do so because POs and stakeholders do not demand it, they might also be inhibited by data protection restrictions, especially in German and French speaking countries. The value of population-based studies of quality of oncologic care and mass screening and the flawless reputation with regard to data protection of intensively used CRs in the northwest of Europe offered a sharp contrast, although they also follow the 1995 EU guideline on data protection. CRs thus offer a perfect example of what can be done with sensitive and minimal data, also when enriched by linkages to other databases. Intensive use of the data has allowed CR research departments to take on a visible expertise-based profile but a neutral in many public controversies in preventive oncology. Their management and fundability also appeared to benefit from externally classifying the wide array of tumour- or tract-specific intelligence and research activities for the various users in oncology and public health and also patients - who are the source of the data - are better informed. Transparency on what CRs enable may also improve through programmes of research have been deemed essential to our funding POs (ministries, cancer charities, cancer centres or public health institutes) who might benefit from some guidance to - often suboptimal -governance. Therefore, a metaphoric RegisTree® has been developed for self-assessment and to clarify CR working methods and domain-specific performance to stakeholders and funding agencies, showing much room for development in many CRs. All in all, CRs are likely to remain unique sources of independent expert information on the burden of cancer, indispensable for cancer surveillance, with increased attention to cancer survivors, up to 4% of the population. Investments in the expanding CR network across Europe offer an excellent way forward for comparative future cancer surveillance with so many epidemiologic and clinical changes ahead. Copyright © 2015 Elsevier Ltd. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.02.017
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    ABSTRACT: Large variability in the clinical outcomes has been observed among the nasopharyngeal cancer (NPC) patients with the same stage receiving similar treatment. This suggests that the current Tumour-Node-Metastasis staging systems need to be refined. The nomogram is a useful predictive tool that integrates individual variables into a statistical model to predict outcome of interest. This study was to design predictive nomograms based on the clinical and pathological features of patients with NPC. Clinical data of 270 NPC patients who underwent definitive radiation therapy (RT) alone or concurrent with chemotherapy were collected. Factors predictive of response to RT and overall survival (OS) were determined by univariate and multivariate analyses, and predictive nomograms were created. Nomograms were validated externally by assessing discrimination and calibration using an independent data set (N=122). Three variables predictive of response to RT (age, histology classification and N classification) and four predictive of OS (age, performance status, smoking status and N classification), in addition to T classification, were extracted to generate the nomograms. The nomograms were validated externally, which showed perfect correlation with each other. The designed nomograms proved highly predictive of response to RT and OS in individual patients, and could facilitate individualised and personalised patients' counselling and care. Copyright © 2015. Published by Elsevier Ltd.
    European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.04.003
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    ABSTRACT: The oral neurokinin-1 antagonist aprepitant is recommended in several guidelines for preventing chemotherapy-induced nausea & vomiting (CINV) due to highly emetogenic cancer chemotherapy. Little is known about the feasibility and safety of aprepitant in patients treated with oxaliplatin. In this multicentre, open label, randomised, phase 3 trial, we recruited patients with colorectal cancer who underwent an oxaliplatin-based chemotherapy. Patients were centrally randomised in a 1:1 ratio to the control group (5-HT3-receptor antagonist+dexamethasone) or aprepitant group (5-HT3-receptor antagonist+dexamethasone+aprepitant or fosaprepitant) in the first course. All patients were treated with aprepitant/fosaprepitant therapy in the second course. The primary end-point was the proportion of patients with no emesis. A total of 413 patients entered this clinical trial from 25 centres in Japan. Significantly more patients in the aprepitant group achieved no vomiting overall and delayed phase than those in the control group (95.7% versus 83.6%, and 95.7% versus 84.7%, respectively). The aprepitant group also had statistically significantly higher percentages of no significant nausea, complete response and complete protection than the control group overall. In the control group, the percentages of no vomiting were higher in the second cycle than in the first cycle. The incidence of vomiting occurred day 7 or later was significantly higher in the control group compared with the aprepitant group. Other adverse events were not significant between the groups. The aprepitant therapy was more effective than the control therapy for prevention of CINV in colorectal cancer patients receiving an oxaliplatin-based regimen. Copyright © 2015 Elsevier Ltd. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.03.024
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    ABSTRACT: Endoscopy based screening programmes for colorectal cancer (CRC) are being implemented in an increasing number of countries. In Germany, screening colonoscopy at age 55 or older has been offered since the end of 2002. We aimed to estimate the long-term impact of this offer on CRC prevention. We estimated numbers of prevented CRC cases by expected age and year of their (prevented) occurrence over four decades (2005-2045) by four state Markov models (non-advanced adenoma, advanced adenoma, preclinical CRC, clinically manifest CRC). Estimates are based on screening colonoscopies reported to the German screening colonoscopy registry in 2003-2012 (N=4,407,971), transition rates between the four states and general population mortality rates. Numbers of prevented clinically manifest CRC cases are projected to increase from <100 in 2005 to approximately 6500 in 2015, 12,600 in 2025, 15,400 in 2035 and 16,000 in 2045, compared to approximately 58,000 incident cases observed in 2003. The annual number of prevented cases is expected to be higher among men than among women and to strongly vary by age. The vast majority of prevented cases would have occurred at age 75 or older. Despite modest participation rates, the German screening colonoscopy programme will lead to substantial reductions in the CRC burden. The reductions will be fully disclosed in the long run only and predominantly affect numbers of incident cases above 75years of age. Screening offers would need to start at younger ages in order to achieve more effective CRC prevention at younger ages. Copyright © 2015 Elsevier Ltd. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.03.020
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cancer is relatively rare in childhood, but it contributes considerably to childhood mortality, years of life lost per person and late effects in survivors. Large populations need to be covered to set up meaningful studies of these rare conditions. Cancer registries ensure cancer surveillance, thus providing the basis for research as well as policy decisions. In this paper we examine coverage of childhood population by cancer registries in Europe and encourage national cancer registration. Over 200 cancer registries in various stages of development were identified as collecting data on childhood cancer patients in Europe. They cover 52% of the childhood population in the World Health Organisation (WHO) European region and 83% in the European Union (EU). More than 80% of this coverage is ensured by nationwide data collection, which is ongoing in 29 European countries. Overall coverage of the childhood population could increase to around 98%, if the recently established cancer registries start producing results and others improve their quality and dissemination plans. Paediatric cancer registries are being established with increasing frequency even in the areas covered by general cancer registries, and they tend to be national. Compared with regional registration, national cancer registries are more cost-effective, record larger number of cases, they can achieve higher completeness, less biased incidence and survival estimates and they are conditioned for national and international research. National registration of childhood cancer should be the rule in Europe, so that accurate regional, nation-wide and international statistics can provide solid baselines for research, clinical practice and public health policy. Governmental support and stakeholders' involvement are indispensable to guarantee optimal data quality and completeness. Copyright © 2015 Elsevier Ltd. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.03.009
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    ABSTRACT: Adult body size is positively associated with aggressive and fatal prostate cancers. It is unknown whether these associations originate in early life. Therefore, we investigated if childhood height, body mass index (BMI; kg/m(2)) and growth are associated with prostate cancer-specific mortality and survival. Subjects were 125,208 men from the Copenhagen School Health Records Register, born 1930-1969 with height and weight measurements at ages 7-13years. Linkage to the Danish Cancer Registry and the Register of Causes of Death enabled identification of incident and fatal prostate cancers. Cox proportional hazards regressions were performed. 630 men had prostate cancer recorded as the underlying cause of death. Childhood height at age 13years was positively associated with prostate cancer-specific mortality (hazard ratio [HR]per z-score=1.2, 95% confidence interval [CI]: 1.1-1.3). Associations were significant at all other childhood ages. Growth analyses showed that height at age 13years had a stronger association with prostate cancer-specific mortality than height at age 7, suggesting the association at age 7 is largely mediated through later childhood height. The tallest boys at age 13years had a significantly worse survival, but only when restricted to a diagnosis at <60years of age (HRz-score of 1=1.7, 95% CI: 1.3-2.4). These associations were significant at all other childhood ages. Childhood BMI was not associated with prostate cancer mortality or survival. Childhood height was positively associated with the hard end-point of prostate cancer-specific mortality, which strengthens prior epidemiologic observations of a positive association with prostate cancer incidence. Copyright © 2015 Elsevier Ltd. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.03.022
  • [Show abstract] [Hide abstract]
    ABSTRACT: Drug-induced liver chemistry abnormalities, primarily transaminase elevations, are commonly observed in pazopanib-treated patients. This meta-analysis characterises liver chemistry abnormalities associated with pazopanib. Data of pazopanib-treated patients from nine prospective trials were integrated (N=2080). Laboratory datasets were used to characterise the incidence, timing, recovery and patterns of liver events, and subsequent rechallenge with pazopanib. Severe cases of liver chemistry abnormalities were clinically reviewed. Multivariate analyses identified predisposing factors. Twenty percent of patients developed elevated alanine aminotransferase (ALT) >3×ULN. Incidence of peak ALT >3-5×ULN, >5-8×ULN, >8-20×ULN and >20×ULN was 8%, 5%, 5% and 1%, respectively. Median time to onset for all events was 42days; 91% of events were observed within 18weeks. Recovery rates based on peak ALT >3-5×ULN, >5-8×ULN, >8-20×ULN and >20×ULN were 91%, 90%, 90% and 64%, respectively. Median time from onset to recovery was 30days, but longer in patients without dose interruption. Based on clinical review, no deaths were associated with drug-induced liver injury. Overall, 38% of rechallenged patients had ALT elevation recurrence, with 9-day median time to recurrence. Multivariate analysis showed that older age was associated with development of ALT >8×ULN. There was no correlation between hypertension and transaminitis. Our data support the current guidelines on regular liver chemistry tests after initiation of pazopanib, especially during the first 9 or 10weeks, and also demonstrate the safety of rechallenge with pazopanib. Copyright © 2015. Published by Elsevier Ltd.
    European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.03.019
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    ABSTRACT: Second line endocrine therapy has limited antitumour activity. Fulvestrant inhibits and downregulates the oestrogen receptor. The mitogen-activated protein kinase (MAPK) pathway is one of the major cascades involved in resistance to endocrine therapy. We assessed the efficacy and safety of fulvestrant with selumetinib, a MEK 1/2 inhibitor, in advanced stage breast cancer progressing after aromatase inhibitor (AI). This randomised phase II trial included postmenopausal patients with endocrine-sensitive breast cancer. They were ramdomised to fulvestrant combined with selumetinib or placebo. The primary endpoint was disease control rate (DCR) in the experimental arm. ClinicalTrials.gov Indentifier: NCT01160718. Following the planned interim efficacy analysis, recruitment was interrupted after the inclusion of 46 patients (23 in each arm), because the selumetinib-fulvestrant arm did not reach the pre-specified DCR. DCR was 23% (95% confidence interval (CI) 8-45%) in the selumetinib arm and 50% (95% CI 27-75%) in the placebo arm. Median progression-free survival was 3.7months (95% CI 1.9-5.8) in the selumetinib arm and 5.6months (95% CI 3.4-13.6) in the placebo arm. Median time to treatment failure was 5.1 (95% CI 2.3-6.7) and 5.6 (95% CI 3.4-10.2) months, respectively. The most frequent treatment-related adverse events observed in the selumetinib-fulvestrant arm were skin disorders, fatigue, nausea/vomiting, oedema, diarrhoea, mouth disorders and muscle disorders. The addition of selumetinib to fulvestrant did not show improving patients' outcome and was poorly tolerated at the recommended monotherapy dose. Selumetinib may have deteriorated the efficacy of the endocrine therapy in some patients. Copyright © 2015 Elsevier Ltd. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.03.016
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    ABSTRACT: Lynch syndrome, the most common inherited colorectal cancer syndrome in adults, is an autosomal dominant condition caused by heterozygous germ-line mutations in DNA mismatch repair (MMR) genes MLH1, MSH2, MSH6 and PMS2. Inheriting biallelic (homozygous) mutations in any of the MMR genes results in a different clinical syndrome termed biallelic mismatch repair deficiency (BMMR-D) that is characterised by gastrointestinal tumours, skin lesions, brain tumours and haematologic malignancies. This recently described and under-recognised syndrome can present with adenomatous polyps leading to early-onset small bowel and colorectal adenocarcinoma. An important clue in the family history that suggests underling BMMR-D is consanguinity. Interestingly, pedigrees of BMMR-D patients typically show a paucity of Lynch syndrome cancers and most parents are unaffected. Therefore, a family history of cancers is often non-contributory. Detection of BMMR-D can lead to more appropriate genetic counselling and the implementation of targeted surveillance protocols to achieve earlier tumour detection that will allow surgical resection. This review describes an approach for diagnosis and management of these patients and their families. Copyright © 2015 Elsevier Ltd. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.02.008
  • European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.03.012
  • European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.03.017
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    ABSTRACT: Several somatic mutation hotspots were recently identified in the telomerase reverse transcriptase (TERT) promoter region in human cancers. Large scale studies of these mutations in multiple tumour types are limited, in particular in Asian populations. This study aimed to: analyse TERT promoter mutations in multiple tumour types in a large Chinese patient cohort, investigate novel tumour types and assess the functional significance of the mutations. TERT promoter mutation status was assessed by Sanger sequencing for 13 different tumour types and 799 tumour tissues from Chinese cancer patients. Thymic epithelial tumours, gastrointestinal leiomyoma, and gastric schwannoma were included, for which the TERT promoter has not been previously sequenced. Functional studies included TERT expression by reverse-transcriptase quantitative polymerase chain reaction (RT-qPCR), telomerase activity by the telomeric repeat amplification protocol (TRAP) assay and promoter activity by the luciferase reporter assay. TERT promoter mutations were highly frequent in glioblastoma (83.9%), urothelial carcinoma (64.5%), oligodendroglioma (70.0%), medulloblastoma (33.3%) and hepatocellular carcinoma (31.4%). C228T and C250T were the most common mutations. In urothelial carcinoma, several novel rare mutations were identified. TERT promoter mutations were absent in gastrointestinal stromal tumour (GIST), thymic epithelial tumours, gastrointestinal leiomyoma, gastric schwannoma, cholangiocarcinoma, gastric and pancreatic cancer. TERT promoter mutations highly correlated with upregulated TERT mRNA expression and telomerase activity in adult gliomas. These mutations differentially enhanced the transcriptional activity of the TERT core promoter. TERT promoter mutations are frequent in multiple tumour types and have similar distributions in Chinese cancer patients. The functional significance of these mutations reflect the importance to telomere maintenance and hence tumourigenesis, making them potential therapeutic targets. Copyright © 2015 Elsevier Ltd. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 04/2015; DOI:10.1016/j.ejca.2015.03.010
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    ABSTRACT: The high failure rate in phase III oncology trials is partly because the signal obtained from phase II trials is often weak. Several papers have considered the appropriateness of various phase II end-points for individual trials, but there has not been a systematic comparison using simulated data to determine which end-point should be used in which situation. In this paper we carry out simulation studies to compare the power of several Response Evaluation Criteria in Solid Tumours (RECIST) response-based end-points for one-arm and two-arm trials, together with progression-free survival (PFS) and testing the tumour-shrinkage directly for two-arm trials. We consider six scenarios: (1) short-term cytotoxic therapy; (2) continuous cytotoxic therapy; (3+4) cytostatic therapy; (5+6) delayed tumour-shrinkage effect (seen in some immunotherapies). We also consider measurement error in the assessment of tumour size. Measurement error affects the type-I error rate and power of single-arm trials, and the power of two-arm trials. Generally no single end-point performed well in all scenarios. Best observed response rate, PFS and directly testing the tumour-shrinkages performed best for a number of scenarios. PFS performed very poorly when the effect of the treatment was short-lived. In scenario 6, where the delay in effect was long, no end-point performed well. A clinician setting up a phase II trial should consider the likely mechanism of action the drug will have and choose an end-point that provides high power for that scenario. Testing the difference in tumour-shrinkage is often powerful. Alternative end-points are required for therapies with a long delayed effect. Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 03/2015; 3. DOI:10.1016/j.ejca.2015.03.002
  • European journal of cancer (Oxford, England: 1990) 03/2015; DOI:10.1016/j.ejca.2015.03.006
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    ABSTRACT: Chemotherapeutic regimens for elderly patients with metastatic colorectal cancer (mCRC), such as bevacizumab combined with 5-fluorouracil (5-FU) and leucovorin, often exclude oxaliplatin and irinotecan owing to the risk of toxicity. However, treatment with infusional 5-fluorouracil and leucovorin requires percutaneous port-catheter placement and other precautions, causing unnecessary stress for patients as well as healthcare workers. We conducted a phase II study to evaluate the efficacy and safety of bevacizumab plus S-1 in elderly patients with previously untreated mCRC. Bevacizumab was given intravenously every two weeks, and S-1 was administered orally on days 1-28 of a 42-day cycle. The primary end-point was progression-free survival (PFS). The secondary end-points were time to treatment failure, response rate (RR), overall survival (OS), treatment completion status and safety. From October 2007 through March 2010, 56 patients were enroled. The median PFS was 9.9months, the median OS was 25.0months, and the RR was 57%. The main adverse events of grade 3 or higher were hypertension (11%), diarrhoea (9%) and neutropenia (7%). Our results suggest that combination chemotherapy with S-1 and bevacizumab can be administered safely and continuously on an outpatient basis and is therapeutically effective in elderly patients with mCRC. Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.
    European journal of cancer (Oxford, England: 1990) 03/2015; 15. DOI:10.1016/j.ejca.2015.03.007
  • European journal of cancer (Oxford, England: 1990) 03/2015; DOI:10.1016/j.ejca.2015.03.005