Journal of experimental & clinical cancer research: CR Impact Factor & Information

Publisher: BioMed Central

Current impact factor: 4.23

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2013 / 2014 Impact Factor 3.271
2012 Impact Factor 3.066
2011 Impact Factor 2.148
2010 Impact Factor 1.921
2009 Impact Factor 1.274
2008 Impact Factor 1.184
2007 Impact Factor 1.503
2006 Impact Factor 0.869
2005 Impact Factor 0.67
2004 Impact Factor 0.607
2003 Impact Factor 0.574
2002 Impact Factor 0.703
2001 Impact Factor 0.754
2000 Impact Factor 0.54
1999 Impact Factor 0.478
1998 Impact Factor 0.257
1997 Impact Factor 0.232
1996 Impact Factor 0.153
1995 Impact Factor 0.162
1994 Impact Factor 0.207
1993 Impact Factor 0.237
1992 Impact Factor 0.162

Impact factor over time

Impact factor

Additional details

5-year impact 0.00
Cited half-life 4.80
Immediacy index 0.05
Eigenfactor 0.00
Article influence 0.34
Other titles Journal of experimental & clinical cancer research, Journal of experimental and clinical cancer research, CR, C.R
ISSN 0392-9078
OCLC 10009183
Material type Periodical
Document type Journal / Magazine / Newspaper

Publisher details

BioMed Central

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    • Publisher's version/PDF may be used
    • Eligible UK authors may deposit in OpenDepot
    • Creative Commons Attribution License
    • Copy of License must accompany any deposit.
    • All titles are open access journals
    • 'BioMed Central' is an imprint of 'Springer Verlag (Germany)'
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Breast cancer is the most fatal malignant cancer among women, the conventional therapeutic modalities of it are limited. Morusin possesses cytotoxicity against some cancer cells in vitro. The purpose of this study is to test the growth inhibition effect of morusin on human breast cancer growth in vitro and in vivo and to explore the potential mechanism of its action. Methods The growth inhibition effect of morusin on human breast cancer cells in vitro and in vivo were tested by cell cytotoxicity, colony formation inhibition, adipogenic differentiation, apoptosis induction, and tumor growth inhibition in vivo assays. The potential molecular mechanisms underlying the growth inhibition effect of morusin on human breast cancer cells in vitro and in vivo were investigated with Western blotting evaluation of expression levels of transcription factors, C/EBPβ and PPARγ, adipogenic and apoptotic proteins in morusin treated breast cancer cells and tumor tissues. Results Morusin inhibited breast cancer cells growth in vitro and in vivo; it induced adipogenic differentiation, apoptosis and lipoapoptosis of cancer cells. Conclusions Morusin has the potential to inhibit human breast cancer cell growth in vitro and in vivo through C/EBPβ and PPARγ mediated lipoapoptosis.
    Journal of experimental & clinical cancer research: CR 11/2015; 34(1). DOI:10.1186/s13046-015-0252-4
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    ABSTRACT: Dysregulated endocytosis of membrane proteins contributes significantly to several hallmarks of cancer. Basigin can enhance cancer progression, but its precise mechanism remains unclear. CD98 promotes cell spreading and tumorigenicity by triggering integrin clustering and enhancing cell adhesion to the extracellular matrix. The endocytosis and recyle of basigin and CD98 might play critical roles in cancer. The role of CD98 was confirmed in liver cancer cells by cell spreading in vitro and tumorigenicity by nude mice xenograft tumor assay in vivo; membrane expression of basigin and CD98 in SMMC-7721 was measured by FCAS; pull down and SPR analysis were uses to reveal the direct association between basigin and CD98; DsRed1 tagged CD98 was blocked in the cytoplasm in K7721 (whose basigin was knockn out) and had a well colocalization with ER and Rab5a positive recycling endosomes under co-focal; finally, by FRET imaging and FCAS we observed the internalization of basigin and CD98 was flotillin-1-regulated, and their recycle at early steps was Arf6-mediated. Basigin and CD98 were highly expressed and co-localized on the human hepatocellular carcinoma (HCC) cell membrane; basigin can directly bind to CD98, mediating CD98 redistribution on the HCC cell membrane and activating the downstream integrin signaling pathway. Internalization of basigin and CD98 was flotillin-1 regulated the and their recycling was mediated by Arf6. This recycling process for basigin and CD98 promotes cell spreading and tumor growth in liver cancer xenografts. Basigin, as a redistribution chaperone of CD98, plays a critical role in promoting cell spreading and the progression of hepatocellular carcinoma.
    Journal of experimental & clinical cancer research: CR 10/2015; 34(1). DOI:10.1186/s13046-015-0226-6
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    ABSTRACT: Purpose The anti-tumor activity of glucose analogs 2-deoxy-glucose (2-DG) and D-allose was investigated alone or in combination with p38 mitogen-activated protein kinase (MAPK) inhibitor SB202190 or platinum analogs as a strategy to pharmacologically target glycolytic tumor phenotypes. Methods Hypoxia inducible factor-1 alpha (HIF-1α) protein accumulation in pancreatic cell lines treated with SB202190 alone and in combination with glucose analogs was analyzed by Western blot. HIF-1α transcriptional activity was measured in MIA PaCa-2 cells stably transfected with a hypoxia response element luciferase reporter following treatment with glucose analogs alone, and in combination with SB202190. Induction of cleaved poly(ADP-ribose) polymerase (PARP) was measured by Western blot in the MIA PaCa-2 cells. In vitro anti-proliferative activity of 2-DG and D-allose alone, or in combination with oxaliplatin (pancreatic cell lines), cisplatin (ovarian cell lines), or with SB202190 were investigated using the MTT assay. Results SB202190 decreased HIF-1α protein accumulation and transcriptional activity. 2-DG demonstrated greater anti-proliferative activity than D-allose. Pre-treatment with SB202190 enhanced activity of both 2-DG and D-allose in MIA PaCa-2, BxPC-3, ASPC-1, and SK-OV-3 cells. The combination of D-allose and platinum agents was additive to moderately synergistic in all but the OVCAR-3 and HEY cells. SB202190 pre-treatment further enhanced activity of D-allose and 2-DG with platinum agents in most cell lines investigated. Conclusions SB202190 induced sensitization of tumor cells to 2-DG and D-allose may be partially mediated by inhibition of HIF-1α activity. Combining glucose analogs and p38 MAPK inhibitors with chemotherapy may be an effective approach to target glycolytic tumor phenotypes.
    Journal of experimental & clinical cancer research: CR 04/2015; 34(1). DOI:10.1186/s13046-015-0147-4
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    ABSTRACT: Background The role of chemotherapy in the treatment of metastatic male breast cancer patients remains unknown, and the only available evidence stem from small, retrospective series evaluating outdated drugs and/or regimens. Methods In this retrospective study we evaluated the activity of polychemotherapy, consisting of three-drug (anthracycline-containing and anthracycline-free) regimens, as a first-line therapy for metastatic male breast cancer patients who had received at least one prior endocrine therapy. Results Fifty patients treated between 1978 and 2013 were included in the present analysis. Regarding best response, we recorded 1 (2%) complete response and 27 (54%) partial responses, for an overall response rate of 56% (95% CI, 42.2-69.8). Considering stable disease, the disease control rate was 84%. Median progression-free survival was 7.2 months (95% CI, 5.9-8.5), and median overall survival was 14.2 months (95% CI, 12.2-16.2). Albeit we observed some differences for all the outcomes explored when comparing anthracycline-containing and anthracycline-free regimens, they were not statistically significant. Conclusions Chemotherapy, consisting in both anthracycline-containing and anthracycline-free regimens, showed encouraging antitumor activity in metastatic male breast cancer patients previously treated with endocrine therapy.
    Journal of experimental & clinical cancer research: CR 03/2015; 34(1). DOI:10.1186/s13046-015-0143-8
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    ABSTRACT: Pseudogene was recognized as a potential tumor suppressor or oncogene in varies of diseases, however its roles in glioma have not been investigated. Our study was to identify the pseudogene-signature that predicted glioma survival. Using a pseudogene-mining approach, we performed pseudogene expression profiling in 183 glioma samples from the Chinese Glioma Genome Atlas (CGGA) and set it as the training set. We found a six-pseudogene signature correlated with patients’ clinical outcome via bioinformatics analyses (P ≤ 0.01), and validated it in the Repository of Molecular Brain Neoplasia Data (REMBRANDT) containing 350 cases. A formula calculating the risk score based on the six-pseudogene signature was introduced and the patients of CGGA set were classified into high-risk group and low-risk group with remarkably different survival (P < 0.001) based on their scores. The prognostic value of the signature was confirmed in the REMBRANDT set. Though the function of these pseudogenes is not clear, the identification of the prognostic pseudogenes indicated the potential roles of pseudogenes in glioma pathogenesis and they may have clinical implications in treating glioma.
    Journal of experimental & clinical cancer research: CR 03/2015; 34(1). DOI:10.1186/s13046-015-0137-6
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    ABSTRACT: Background To detect genetic expression profile alterations after papillary thyroid carcinoma (PTC) cells transfected with chemokine receptor CXCR7 gene by gene microarray, and gain insights into molecular mechanisms of how CXCR7 regulating PTC growth and metastasis. Methods The Human OneArray microarray was used for a complete genome-wide transcript profiling of CXCR7 transfected PTCs (K1-CXCR7 cells), defined as experimental group. Non CXCR7 transfected PTCs (K1 cells) were used as control group. Differential analysis for per gene was performed with a random variance model and t test, p values were adjusted to control the false discovery rate. Gene ontology (GO) on differentially expressed genes to identify the biological processes in modulating the progression of papillary thyroid carcinoma. Pathway analysis was used to evaluate the signaling pathway that differentially expressed genes were involved in. In addition, quantitative real-time polymerase chain reaction (q-PCR) and Western blot were used to verify the top differentially expression genes. Results Comparative analysis revealed that the expression level of 1149 genes was changed in response to CXCR7 transfection. After unsupervised hierarchical clustering analysis, 270 differentially expressed genes were filtered, of them 156 genes were up-regulated whereas 114 genes were down-regulated in K1-CXCR7 cells. GO enrichment analysis revealed the differentially expressed genes were mainly involved in biopolymer metabolic process, signal transduction and protein metabolism. Pathway enrichment analysis revealed differentially expressed genes were mainly involved in ECM-receptor interaction, Focal adhesion, MAPK signaling pathway and Cytokine-cytokine receptor interaction pathway. More importantly, the expression level of genes closely associated with tumor growth and metastasis was altered significantly in K1-CXCR7 cells, including up-regulated genes FN1, COL1A1, COL4A1, PDGFRB, LTB, CXCL12, MMP-11, MT1-MMP and down-regulated genes ITGA7, and Notch-1. Conclusions Gene expression profiling analysis of papillary thyroid carcinoma can further delineate the mechanistic insights on how CXCR7 regulating papillary thyroid carcinoma growth and metastasis. CXCR7 may regulate growth and metastasis of papillary thyroid carcinoma via the activation of PI3K/AKT pathway and its downstream NF-κB signaling, as well as the down-regulation of Notch signaling.
    Journal of experimental & clinical cancer research: CR 02/2015; 34(1). DOI:10.1186/s13046-015-0132-y
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    ABSTRACT: Background Epithelial-to mesenchymal transition (EMT) involves in metastasis, causing loss of epithelial polarity. Metastasis is the major cause of carcinoma-induced death, but mechanisms are poorly understood. Here we identify differentially expressed in adenocarcinoma of the lung-1 (DAL-1), a protein belongs to the membrane-associated cytoskeleton protein 4.1 family, as an efficient suppressor of EMT in lung cancer.Methods The relationship between DAL-1 and EMT markers were analyzed by using immunohistochemistry in the clinical lung cancer tissues. Quantitative real-time PCR and western blot were used to characterize the expression of the EMT indicator mRNAs and proteins in DAL-1 overexpressed or knockdown cells. DAL-1 combined proteins were assessed by co-immunoprecipitation.ResultsDAL-1 levels were strongly reduced even lost in lymph node metastasis and advanced pathological stage of human lung carcinomas. Overexpression of DAL-1 altered the expression of numerous EMT markers, such as E-cadherin, ß-catenin Vimentin and N-cadherin expression, meanwhile changed the morphological shape of lung cancer cells, and whereas silencing DAL-1 had an opposite effect. DAL-1 directly combined with E-cadherin promoter and regulated its expression that could be the reason for impairing EMT and decreasing cell migration and invasion. Strikingly, HSPA5 was found as DAL-1 direct binding protein.Conclusions These results suggest that tumor suppressor DAL-1 could also attenuate EMT and be important for tumor metastasis in the early transformation process in lung cancer.
    Journal of experimental & clinical cancer research: CR 01/2015; 34(1):3. DOI:10.1186/s13046-014-0117-2
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    ABSTRACT: ABSTRACT: There are no reports in the literature of acute pancreatitis after "one shot" percutaneous ethanol injection (PEI); in contrast, cases of lethal acute pancreatitis are described as a complication of intraarterial PEI. We report a case of a lethal necrotizing pancreatitis resulting from a "one shot" PEI into a multifocal hepatocellular carcinoma (HCC). Deaths after PEI occur between a few hours and a few days after the event because of hemoperitoneum and haemorrhage from oesophageal varices and the major complications are renal insufficiency, hemoperitoneum and hepatic insufficiency. None of these complications occurred in our patient immediately after PEI. We believe that PEI initially caused the edematous pancreatitis through a detrimental metabolic effect. Thereafter, the ensuing treatment with opioids (to reduce the patient's abdominal pain) led to toxic effects causing, together with PEI, the development of lethal necrotizing pancreatitis.
    Journal of experimental & clinical cancer research: CR 07/2008; 27(1):12. DOI:10.1186/1756-9966-27-12
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    Journal of experimental & clinical cancer research: CR 04/2008; 27(1):1. DOI:10.1186/1756-9966-27-1
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    ABSTRACT: Cell cycle progression is mediated by a group of proteins named cyclins that activate a highly conserved family of protein kinases, the cyclin-dependent kinases (CDKs). CDKs are also regulated by related proteins called cdk inhibitors, grouped into two families: the INK4 inhibitors (p16, p15, p19 and p18) and the Cip/Kip inhibitors (p21, p27). Moreover, several tumour suppressor genes (such as Retinoblastoma gene and p53 gene) are implicated in the regulation of the molecular mechanism of cell division. Several studies report the importance of cell cycle regulator proteins in the pathogenesis and the prognosis of mesothelioma. This article will review the most recent data from the literature about the expression and the diagnostic and prognostic significance of cell cycle molecules in mesothelioma.
    Journal of experimental & clinical cancer research: CR 01/2008; 26(4):443-9.
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    ABSTRACT: When HCC is diagnosed at an early stage or liver is affected by a solitary metastasis they can be curable by surgical resection, but this may not be feasible when an extensive tumoural involvement is present. In these cases, possible non-surgical therapies include systemic chemotherapy, chemical ablation (ethanol or acetic acid), radiofrequency ablation, microwave ablation, cryotherapy and transarterial chemoembolisation. All the above mentioned treatments have advantages and disadvantages. In the present paper we reported our experience with selective internal radiation therapy (SIRT) of non-operable HCC and metastatic liver using 99Yttrium (99Y) radioactive microspheres, and our data are compared and discussed with those reported in the literature. A MEDLINE-based review of the literature has been made in the period between 1990 and April 2007. Detailed information on patients selection criteria, SIRT procedure, dose calculation, safety and adverse reactions, follow-up schedule, and clinical efficacy are provided. On the basis of our data, in agreement with those of the literature, SIRT has added another effective method for treatment of primary and secondary liver tumours, being successful in a large number of patients in different experiences. Moreover, SIRT is well tolerated and has minimal adverse effects. Despite being regarded as non-curative, it has been associated with improved survival, reduction in tumour marker, and regression in the number and size of lesions. Follow-up with imaging is essential to assess the response to therapy, and in this respect FDG PET has been shown to be more sensitive than CT, particularly in the early stages.
    Journal of experimental & clinical cancer research: CR 01/2008; 26(4):561-70.
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    ABSTRACT: The L-PAM-ILP procedures under true hyperthermal regime (41.5-41.8 degrees C) require both close control of the physical parameters of the treatment (temperatures profiles and time duration, artero-venous pressure, perfusate flow rate) and medical rationale (drug, dosage, fractioning, timing). All the above essential procedures must be supported by rigorous methodology, reliable operation of the medical devices and apparatus and real-time monitoring of the treatment parameters. Real-time monitoring is essential for proper trimming and modulation of the parameters during treatment. This paper delineates the technical improvements that we have implemented for drug leakage monitoring and control in the systemic circulation aimed at improving the therapeutic efficacy and at reducing the occurrence of unexpected complications.
    Journal of experimental & clinical cancer research: CR 01/2008; 26(4):433-42.
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    ABSTRACT: Metastases to the bones of the hands and feet (acrometastases) represent an uncommon site of recurrence of renal cell carcinoma (RCC). Although challenging, the prompt recognition of solitary acrometastasis from RCC is of crucial importance, since surgical resection of the acrometastasis in the absence of active systemic disease has been reported as beneficial for a subgroup of patients with RCC. Here, we report the case of a patient with RCC metastatic to the left index finger treated with surgical resection of the acrometastasis who shortly thereafter developed progressive disease despite such an aggressive surgical approach.
    Journal of experimental & clinical cancer research: CR 01/2008; 26(4):595-7.
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    ABSTRACT: This study was designed to evaluate the antitumor efficacy and feasibility of postoperative adjuvant metronomic chemotherapy using weekly low-dosage CPT-11 and UFT in colorectal cancer at high risk to recurrence. A total of 49 patients (24 stage IIIb and 25 distant metastasis) who underwent a R0 operation were enrolled in this prospective study. Forty mg/m2 of CPT-11 were administered on day 1, day 8, and on day 15 in 28-day cycles. A dosage of 335 mg/m2/day of UFT was given perorally on daily schedule. Cycles were repeated for 6 months, and were followed by UFT alone for further 6 months. One or more adverse effects were seen in 43 of the 49 patients. However, most of these effects were mild at grade 1 or 2: with only nausea in 3 patients, vomiting in 2, leucopenia in 2 and neutropenia in 2 at grade 3. The overall survival rates were favorable both in the stage IIIb group (5-year: 73%) and in the distant metastases group (5-year: 62%). Postoperative adjuvant metronomic chemotherapy using weekly low-dosage CPT-11 and UFT might be safe and feasible and prolong survival time in colorectal cancer at high risk to recurrence.
    Journal of experimental & clinical cancer research: CR 01/2008; 26(4):475-82.