Neoplasia (NEOPLASIA)

Publisher: Elsevier

Journal description

Neoplasia is published bimonthly. Neoplasia publishes the results of novel investigations in all areas of oncology research. The journal encompasses the traditional disciplines of cancer research as well as emerging fields and interdisciplinary investigations. Neoplasia is interested in studies describing new molecular and genetic findings relating to the neoplastic phenotype. Laboratory and clinical studies will also be an important part of the journal's coverage where creative applications of the advances in the basic science to risk assessment, prognostic indications, detection, diagnosis, and treatment are demonstrated. In addition to regular Research Articles, the journal also publishes Brief Articles, Reviews, and Meeting Articles. All members of the oncologic research community are invited to submit their work to Neoplasia.

Current impact factor: 4.25

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 4.252
2013 Impact Factor 5.398
2012 Impact Factor 5.47
2011 Impact Factor 5.946
2010 Impact Factor 5.476
2009 Impact Factor 5.025
2008 Impact Factor 5.191
2007 Impact Factor 5.674
2006 Impact Factor 4.913
2005 Impact Factor 3.85
2004 Impact Factor 4.377
2003 Impact Factor 4.312
2002 Impact Factor 5.917

Impact factor over time

Impact factor

Additional details

5-year impact 4.92
Cited half-life 6.10
Immediacy index 0.60
Eigenfactor 0.01
Article influence 1.57
Website Neoplasia website
Other titles Neoplasia (Online)
ISSN 1522-8002
OCLC 42678887
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • 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
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: ATM-Chk2 network is critical for genomic stability and its deregulation may influence breast cancer pathogenesis. We investigated ATM and Chk2 protein levels in two cohorts [cohort 1 (n=1650) and cohort 2 (n= 252)]. ATM and Chk2 mRNA expression was evaluated in the Metabric cohort (n=1950). Low nuclear ATM protein level was significantly associated with aggressive breast cancer including larger size tumours, higher tumour grade, higher mitotic index, pleomorphism , tumour type , lymphovascular invasion, ER- , PR-, AR-, triple negative and basal-like phenotypes (ps<0.05). BRCA1 negative, low XRCC1, low SMUG1, high FEN1, high MIB1, p53 mutants, low MDM2, low Bcl-2, low p21, low Bax, high CDK1 and low Chk2 were also more frequent in tumours with low nuclear ATM level (ps<0.05). Low ATM protein level was significantly associated with poor survival including in patients with ER- negative tumours who received adjuvant anthracycline or CMF based adjuvant chemotherapy (ps<0.05). Low nuclear Chk2 protein was likely in ER-/PR-/AR-, HER- 2 positive, BRCA1 negative, low XRCC1, low SMUG1, low APE1, low polβ, low DNA-PKcs, low ATM, low Bcl-2 and low TOPO2A tumours (p<0.05). In patients with ER+ tumours who received endocrine therapy or ER- negative tumours who received chemotherapy, nuclear Chk2 levels did not significantly influence survival. In p53 mutant tumours, low ATM (p<0.000001) or high Chk2 (p<0.01) was associated with poor survival. When investigated together, low ATM/high Chk2 tumours have the worst survival (p=0.0033). Our data suggests that ATM-Chk2 levels in sporadic breast cancer may have prognostic and predictive significance.
    Neoplasia 09/2014; In Press.
  • [Show abstract] [Hide abstract]
    ABSTRACT: The hepatocyte growth factor receptor (c-Met) and a constitutively active mutant of the epidermal growth factor receptor (ΔEGFR/EGFRvIII) are frequently overexpressed in glioblastoma (GBM) and promote tumorigenesis. The mechanisms underlying elevated hepatocyte growth factor (HGF) production in GBMare not understood. We found higher, coordinated mRNA expression levels of HGF and c-Met in mesenchymal (Mes) GBMs, a subtype associated with poor treatment response and shorter overall survival. In anHGF/c-Met–dependentGBMcell line, HGF expression declined upon silencing of c-Met using RNAi or by inhibiting its activity with SU11274. Silencing c-Met decreased anchorage-independent colony formation and increased the survival of mice bearing intracranial GBM xenografts. Consistent with these findings, c-Met activation by ΔEGFR also elevated HGF expression, and the inhibition of ΔEGFR with AG1478 reduced HGF levels. Interestingly, c-Met expressionwas required for ΔEGFR-mediated HGF production, anchorage-independent growth, and in vivo tumorigenicity, suggesting that these pathways are coupled. Using an unbiased mass spectrometry–based screen, we show that signal transducer and activator of transcription 3 (STAT3) Y705 is a downstream target of c-Met signaling. Suppression of STAT3 phosphorylation withWP1193 reduced HGF expression in ΔEGFR-expressing GBM cells, whereas constitutively active STAT3 partially rescued HGF expression and colony formation in c-Met knockdown cells expressing ΔEGFR. These results suggest that the c-Met/HGF signal- ing axisisenhancedby ΔEGFR through increased STAT3-dependent HGF expression and that targeting c-Met in Mes GBMs may be an important strategy for therapy.
    Neoplasia 01/2013; 15(1):73-84. DOI:10.1593/neo.121536