Neoplasia: Where We Have Been and Where We Are Going

IF 6.3 2区 医学 Q1 ONCOLOGY Neoplasia Pub Date : 2006-12-01 DOI:10.1593/NEO.08EDI
A. Rehemtulla
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Abstract

Neoplasia was launched in 1999 with the mission of providing a high-quality publication venue for the rapid dissemination of novel and exciting advances in cancer research. The journal has grown, in a very rapid fashion, from a bimonthly publication to a monthly publication by publishing a broad-based range of articles ranging from apoptosis to angiogenesis, as shown in Table 1. This table categorizes articles published by Neoplasia by general topic for publication years 2004 to 2006. Cancer genetics, cell and tumor biology, experimental therapeutics, and cancer imaging continue to be significant components of article growth published over these years. The number of submissions and published articles has continually increased over the year, and, next year, Neoplasia will enter its ninth year of publication (Vol. 9). The success of Neoplasia has affirmed to the editorial staff and editorial board that there was and continues to be a significant need for a broad-based cancer journal. During the past year, Neoplasia has further adapted and taken the lead in online peer-reviewed publication of cancer research articles. Table 1 Major Research Topics Published in Neoplasia from 2004 to 2006. In 2006, Neoplasia adopted the open access (OA) model for all articles published. This allows for all articles to be made available free to the scientific and layman communities through online electronic access. All articles are linked through PubMed (www.PubMEd.gov) to a Web-based database, which hosts all Neoplasia articles published to date. Moreover, beginning in 2007, all Neoplasia articles published in Neoplasia will also be freely available through the Biomedcentral portal (http://www.biomedcentral.com/) beginning on the day of publication, rather than after 6 to 12 months like most journals. Of 8700 selected journals currently covered in Web of Science, only 160 are available through Biomedcentral. The effect of immediate OA on the impact of Neoplasia is anticipated to dramatically improve the citation impact factor in terms of the frequency with which an article is cited in the literature (http://dlib.org/dlib/june04/harnad/06harnad.html) [301]. Overall, OA will provide for dramatically increased readership due to access to articles, which would traditionally be unavailable due to costs associated with access tolls to the journal in which it was published because their affiliated institution could not afford the price of subscription. Overall, providing OA to all past, present, and future articles published in Neoplasia should significantly improve the quality and speed at which cancer research advances will be made due to more rapid dissemination of knowledge. Neoplasia is committed to meeting the challenges and emerging needs of the cancer research scientific community. This commitment has been met through the early establishment of a rapid online peer-review system, which has facilitated review of submitted articles. Moreover, the recent OA in 2006, with expansion onto Biomedcentral in 2007, will provide maximal international dissemination of all manuscripts published by Neoplasia. This forward-looking approach allowing for immediate OA availability of all published articles should provide authors using Neoplasia as their publication venue with maximal impact of their exciting research findings.
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肿瘤学:我们已经做了什么,我们要去哪里
《肿瘤》杂志于1999年创办,其使命是提供一个高质量的出版场所,以便快速传播癌症研究方面令人兴奋的新进展。通过发表从细胞凋亡到血管生成的广泛的文章,该杂志以非常迅速的方式从双月刊发展到月刊,如表1所示。本表按2004至2006年出版年度Neoplasia发表的文章按一般题目分类。癌症遗传学,细胞和肿瘤生物学,实验治疗学和癌症成像继续是这些年来发表的文章增长的重要组成部分。投稿和发表的文章数量在过去的一年中不断增加,明年,Neoplasia将进入其出版的第九个年头(第9卷)。Neoplasia的成功向编辑人员和编辑委员会证实了对一本基础广泛的癌症期刊的巨大需求。在过去的一年里,Neoplasia进一步适应并在在线同行评审的癌症研究文章发表方面处于领先地位。表1 2004 - 2006年肿瘤学发表的主要研究课题。2006年,Neoplasia对所有发表的文章采用开放获取(OA)模式。这使得所有的文章都可以通过在线电子访问免费提供给科学界和非专业人士。所有文章都通过PubMed (www.PubMEd.gov)链接到一个基于web的数据库,该数据库包含迄今为止发表的所有Neoplasia文章。此外,从2007年开始,所有发表在Neoplasia上的文章也将从发表当天开始通过生物中心门户网站(http://www.biomedcentral.com/)免费提供,而不是像大多数期刊那样需要6到12个月。在Web Of Science目前收录的8700种精选期刊中,只有160种可以通过Biomedcentral找到。直接开放获取对Neoplasia影响的影响预计将显著提高文献中文章被引用的频率(http://dlib.org/dlib/june04/harnad/06harnad.html)[301]。总的来说,开放获取将极大地增加读者数量,因为他们可以访问文章,而这些文章在传统上是无法获得的,因为他们的附属机构无法负担订阅费用,而这些费用与发表文章的期刊的访问费用相关。总的来说,为Neoplasia杂志上发表的所有过去、现在和未来的文章提供OA应该会显著提高癌症研究的质量和速度,因为知识的传播更加迅速。肿瘤学致力于满足癌症研究科学界的挑战和新兴需求。通过早期建立快速在线同行评议系统实现了这一承诺,该系统促进了对提交文章的评议。此外,2006年的开放获取,以及2007年扩展到生物医学中心,将最大限度地提供Neoplasia发表的所有手稿的国际传播。这种前瞻性的方法允许所有已发表文章的即时OA可用性,应该为使用Neoplasia作为其发表场所的作者提供其令人兴奋的研究成果的最大影响。
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来源期刊
Neoplasia
Neoplasia ONCOLOGY-
自引率
2.10%
发文量
82
期刊介绍: Neoplasia publishes the results of novel investigations in all areas of oncology research. The title Neoplasia was chosen to convey the journal’s breadth, which 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 and in laboratory and clinical studies demonstrating creative applications of advances in the basic sciences to risk assessment, prognostic indications, detection, diagnosis, and treatment. In addition to regular Research Reports, Neoplasia also publishes Reviews and Meeting Reports. Neoplasia is committed to ensuring a thorough, fair, and rapid review and publication schedule to further its mission of serving both the scientific and clinical communities by disseminating important data and ideas in cancer research.
期刊最新文献
Non-redundant roles of the CCR1 and CCR2 chemokine axes in monocyte recruitment during lung metastasis. Sequential treatment of anti-PD-L1 therapy prior to anti-VEGFR2 therapy contributes to more significant clinical benefits in non-small cell lung cancer. DCZ0014, a novel compound in the therapy of diffuse large B-cell lymphoma via the B cell receptor signaling pathway. Corrigendum to "Hodgkin Lymphoma Cell Lines Are Characterized by a Specific miRNA Expression Profile." Neoplasia 2009, Feb;11(2):167-176. The dual PI3K/mTOR inhibitor NVP-BEZ235 is a potent inhibitor of ATM- and DNA-PKCs-mediated DNA damage responses.
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