International Journal of Cancer (INT J CANCER)
Description
The International Journal of Cancer accepts manuscripts for submission under a broad scope of topics relevant to expirmental and clinical cancer research. Subjects we will consider include but are not limited to: cancer cell biology cancer genetics tumor virology tumor immunology cancer therapy and epidemiology and cancer prevention. The six issue topical section Predictive Oncology expands the Journal's coverage into the area of predicting human cancer risk from molecular genetic epidemiologic and statistical data. Predictive Oncology explores the development and application of DNA-based probes that identify biomarkers linked to cancer as well as the results of current investigations using other novel molecular probes as diagnostic and prognostic indicators for cancer detection and therapy.
- Impact factor5.44Show impact factor historyImpact factorYear
- WebsiteInternational Journal of Cancer website
-
Other titlesInternational journal of cancer, International journal of cancer., International journal of cancer., Predictive oncology, Radiation oncology investigations, Journal international du cancer
-
ISSN0020-7136
-
OCLC1753562
-
Material typePeriodical, Internet resource
-
Document typeJournal / Magazine / Newspaper, Internet Resource
Publisher details
-
Pre-print
- Author can archive a pre-print version
-
Post-print
- Author can archive a post-print version
-
Conditions
- See Wiley-Blackwell entry for articles after February 2007
- On personal web site or secure external website at authors institution
- Not allowed on institutional repository
- JASIST authors may deposit in an institutional repository
- Non-commercial
- Pre-print must be accompanied with set phrase (see individual journal copyright transfer agreements)
- Published source must be acknowledged with set phrase (see individual journal copyright transfer agreements)
- Publisher's version/PDF cannot be used
- Articles in some journals can be made Open Access on payment of additional charge
- 'John Wiley and Sons' is an imprint of 'Wiley-Blackwell'
-
Classification green
Publications in this journal
-
Article: Occupational exposure to arsenic and risk of non-melanoma skin cancer in a multinational European study
International Journal of Cancer 04/2013; -
Article: Increased copy-number and not DNA hypomethylation causes overexpression of the candidate proto-oncogene CYP24A1 in colorectal cancer.
International Journal of Cancer 03/2013; -
Article: Sensitivity of endoscopic screening for gastric cancer by the incidence method
International Journal of Cancer 01/2013; -
Article: Fowlpox-based survivin vaccination for malignant mesothelioma therapy.
[show abstract] [hide abstract]
ABSTRACT: Survivin protein is an attractive candidate for cancer immunotherapy since it is abundantly expressed in most common human cancers and mostly absent in normal adult tissues. Malignant mesothelioma (MM) is a deadly cancer associated with asbestos or erionite exposure for which no successful therapies are currently available. In this study, we evaluated the therapeutic efficacy of a novel survivin-based vaccine by subcutaneous or intraperitoneum injection of BALB/c mice with murine fiber-induced MM tumor cells followed by vaccination with recombinant Fowlpox virus replicons encoding survivin. Vaccination generated significant immune responses in both models, leading to delayed tumor growth and improved animal survival. Flow cytometry and immunofluorescence analyses of tumors from vaccinated mice showed CD8(+) T cell infiltration, and real-time PCR demonstrated increased mRNA and protein levels of immunostimulatory cytokines. Analyses of survivin peptide-pulsed spleen and lymph node cells from vaccinated mice using ELISPOT and intracellular cytokine staining confirmed antigen-specific, interferon-γ-producing CD8(+) T cell responses. In addition pentamer-based flow cytometry showed that vaccination generated survivin-specific CD8(+) T cells. Importantly, vaccination did not affect fertility or induce autoimmune abnormalities in mice. Our results demonstrate that vaccination with recombinant Fowlpox expressing survivin improves T cell responses against aggressive MM tumors and may form the basis for promising clinical applications.International Journal of Cancer 01/2013; -
Article: Prognostic factors in gemcitabine/cisplatin polychemotherapy regimens in pancreatic cancer: XPD-Lys751Gln polymorphism strikes back
International Journal of Cancer 01/2013; -
Article: Soluble c-Met protein as a susceptible biomarker for gastric cancer risk: A nested case-control study within the Korean Multicenter Cancer Cohort.
[show abstract] [hide abstract]
ABSTRACT: This study was conducted to evaluate the relevance of the soluble form of c-Met protein, a truncated form of the c-Met membrane receptor involved in the CagA pathway, as a potential biomarker for gastric cancer. Among 290 gastric cancer case-control sets selected from the Korean Multicenter Cancer Cohort, the plasma concentrations of soluble c-Met protein were measured with enzyme-linked immunosorbent assays. Using analysis of variance and covariance models with age, sex, smoking, Helicobacter pylori infection, and CagA seropositivity, the mean concentrations of soluble c-Met protein between cases and controls were compared. To evaluate the association between gastric cancer and a c-Met protein level, odds ratios and 95% confidence intervals were estimated using conditional logistic regression models. Interactions between CagA-related genes and the soluble c-Met protein concentration were also investigated. The overall median plasma concentration of soluble c-Met among cases was significantly lower than those of controls (1.390 vs. 1.610 ng/mL, p < 0.0001). Closer to the onset of gastric cancer, the soluble c-Met protein level decreased linearly in a time-dependent manner (p for trend = 0.0002). The combined effects between the CagA-related genes and the soluble c-Met protein concentration significantly intensified risks for gastric cancer. Restricted analyses including cases that had been diagnosed within 1 year after entering the cohort had a fair degree of ability (area under the receiver operating characteristic curve of 0.73–0.77) to discriminate gastric cancer cases from normal controls. Our findings demonstrate the potential of the soluble form of c-Met protein as a novel biomarker for gastric cancer. The beneficial effects of a high soluble c-Met concentration in human plasma are strongly supported.International Journal of Cancer 10/2012; -
Article: Unbiased estimates of long-term net survival of solid cancers in france.
[show abstract] [hide abstract]
ABSTRACT: In cancer studies, net survival (observed if cancer was the only cause of death) is a useful indicator but survival estimation at five years is insufficient for planning healthcare needs. We estimated the net survivals at 5 and 10 years in a cohort of 387,961 patients who had solid tumours between 1989 and 2004 and were followed-up until January 1, 2008. The cases were actively followed-up. Net survival was estimated with the unbiased Pohar-Perme method. The standardized net survival used the international cancer survival standard weights. In men, the standardized net survivals ranged from 92% at 5 years and 89% at 10 years (testis) to 6% at 5 years and 5% at 10 years (pancreas). In women, it ranged from 91% at 5 years and 88% at 10 years (thyroid) to 10% at 5 years and 7% at 10 years (pancreas). The most frequent cancers had the highest net survivals: 84% at 5 years and 71% at 10 years for prostate and 84% at 5 years and 74% at 10 years for breast cancer. Advanced age was associated with poorer prognosis. In most cancers, the net survivals at 5 and 10 years increased over periods of diagnosis. Net cancer survival is unaffected by mortalities due to other causes. It is the only indicator suitable for comparisons between countries or periods of diagnosis within a given country. The ten-year net survival confirmed the persistent unfavorable role of age in prognosis and the general improvement of cancer management over the last decade. © 2012 Wiley-Liss, Inc.International Journal of Cancer 09/2012; -
Article: Saracatinib (AZD0530) is a potent modulator of ABCB1-mediated multidrug resistance in vitro and in vivo.
[show abstract] [hide abstract]
ABSTRACT: Saracatinib, a highly selective, dual Src/Abl kinase inhibitor, is currently in a phase II clinical trial for the treatment of ovarian cancer. In this study, we investigated the effect of saracatinib on the reversal of multidrug resistance (MDR) induced by ATP-binding cassette (ABC) transporters in vitro and in vivo. Our results showed that saracatinib significantly enhanced the cytotoxicity of ABCB1 substrate drugs in ABCB1 overexpressing HeLa/v200, MCF-7/adr and HEK293/ABCB1 cells, an effect that was stronger than that of gefitinib, whereas it had no effect on the cytotoxicity of the substrates in ABCC1 overexpressing HL-60/adr cells and its parental sensitive cells. Additionally, saracatinib significantly increased the Dox and Rho 123 accumulation in HeLa/v200 and MCF-7/adr cells, while it had no effect on HeLa and MCF-7 cells. Furthermore, saracatinib stimulated the ATPase activity and inhibited photolabeling of ABCB1 with [(125) I]-iodoarylazidoprazosin in a concentration-dependent manner. In addition, the homology modeling predicted the binding conformation of saracatinib within the large hydrophobic drug-binding cavity of human ABCB1. However, neither the expression level of ABCB1 nor the phosphorylation level of Akt was altered at the reversal concentrations of saracatinib. Importantly, saracatinib significantly enhanced the effect of paclitaxel against ABCB1-overexpressing HeLa/v200 cancer cell xenografts in nude mice. In conclusion, saracatinib reverses ABCB1-mediated MDR in vitro and in vivo by directly inhibiting ABCB1 transport function, without altering ABCB1 expression or AKT phosphorylation. These findings may be helpful to attenuate the effect of MDR by combining saracatinib with other chemotherapeutic drugs in the clinic.International Journal of Cancer 05/2012; -
Article: A focused immune response targeting the homotypic binding domain of the carcinoembryonic antigen blocks the establishment of tumour foci in vivo.
International Journal of Cancer 03/2012; -
Article: Hypoxia upregulates ovarian cancer invasiveness via the binding of HIF-1α to a hypoxia-induced, methylation free hypoxia response element (HRE) of S100A4 gene.
International Journal of Cancer 01/2012; -
Article: Hypoxia upregulates ovarian cancer invasiveness via the binding of HIF-1α to a hypoxia-induced, methylation free hypoxia response element (HRE) of S100A4 gene.
International Journal of Cancer 01/2012; -
Article: Low values of 5-hydroxymethylcytosine (5hmC), the "sixth base", are associated with anaplasia in human brain tumours
International Journal of Cancer 01/2012; -
Article: Deregulation of the cell cycle by breast tumor kinase
[show abstract] [hide abstract]
ABSTRACT: Brk is a cytoplasmic nonreceptor tyrosine kinase that is overexpressed in breast tumors but undetectable in normal or benign mammary tissues. Brk promotes proliferation of human mammary epithelial cells and tumor growth in a mouse model, but the role of Brk in cell cycle regulation is not known. In this study, we describe the mechanism of Brk-induced deregulation of the cell cycle. We provide evidence that Brk antagonizes the transcriptional activity of the transcription factor FoxO family of proteins by inhibiting its nuclear localization. As a result, the cell cycle inhibitor p27, a FoxO target gene, is down-regulated. This event is accompanied by G1/S cell cycle progression of quiescent cells. As p27 is a key regulator of the G1/S cell cycle checkpoint, these data suggest that perturbation of p27 expression induced by Brk causes S phase entrance. Deregulation of the cell cycle is a key event in neoplasia, and thus, the mechanism presented here likely contributes to breast cancer development.International Journal of Cancer 12/2010; 127(11):2723-31. -
Article: Type-specific roles of histone deacetylase (HDAC) overexpression in ovarian carcinoma: HDAC1 enhances cell proliferation and HDAC3 stimulates cell migration with down-regulation of E-cadherin.
International Journal of Cancer 09/2010; -
Article: Deregulation of the cell cycle by breast tumor kinase
International Journal of Cancer 01/2010;
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
Keywords
Related Journals
Nature Communications
ISSN: 2041-1723, Impact factor: 7.4
Nutrition research and practice
ISSN: 1976-1457, Impact factor: 1.08
Journal of Periodontology
American Academy of Periodontology
ISSN: 1943-3670, Impact factor: 2.6
Cold Spring Harbor perspectives in biology
ISSN: 1943-0264, Impact factor: 9.4
Human immunology
Elsevier
ISSN: 1879-1166, Impact factor: 2.55
European journal of cancer (Oxford, England: 1990)
Elsevier
ISSN: 1879-0852, Impact factor: 4.12
Current opinion in microbiology
Elsevier
ISSN: 1879-0364, Impact factor: 7.87
Cytokine & growth factor reviews
Elsevier
ISSN: 1879-0305, Impact factor: 6.49